Categories
Calquence (acalabrutinib) Mantle Cell Lymphoma (MCL) Non-Hodgkin Lymphoma

Mantle Cell Lymphoma| Jason’s Story

Mantle Cell Lymphoma:
Jason W.’s Story

Jason is a New York entrepreneur, tennis player, a theater-goer, and traveler who says he loves the lights of Las Vegas. But he is most passionate about his work.

Things shifted in 2019 when Jason, at only 39 years old, was diagnosed with stage 4 mantle cell lymphoma, a rare blood cancer that is more common in men over 60 years old. His diagnosis almost turned his world upside down, and he was thankful he had become an entrepreneur prior to his own treatment.

In this video series, Jason shares his story of diagnosis, clinical trial and treatment, and how cancer changed his life. His story is such an inspiring example of patient self-advocacy!

Explore his 3-part story series below. Thank you so much for sharing, Jason!

The Mantle Cell Lymphoma Diagnosis

His blood work and everything seemed normal. Except for the increasing itch and pain from hives and inflamed arms, Jason and his primary doctor thought it was nothing serious.

Specialists couldn’t find anything until he was referred to a hematologist. Learn how Jason was finally diagnosed.

Read more→

Treatment & Clinical Trial Experience

Jason used to be afraid of needles and procedures. And watching his mom battle breast cancer through chemo, he was determined to try a different course of treatment.

Luckily, Jason got into a clinical trial which proved to be working for him.

Read more→

Life After Cancer (Quality of Life)

For more than two years now, Jason diligently writes in his clinical trial journal every single day. Staying on his course of treatment outside of the formal trial gives him hope of full remission from mantle cell lymphoma.

Jason’s story is also an inspiring example of patient self-advocacy—making informed decisions for better quality of life.

Read more→

  • Name: Jason W.
  • Diagnosis (DX)
    • Mantle cell lymphoma
  • 1st Diagnosis:
    • Age at DX: 39 years old
    • Symptoms
      • Hives
  • Tests for DX: Bone marrow biopsy, PET CT
  • Treatment:
    • Acalabrutinib
    • Lenalidomide
    • Rituxan

Inspired by Jason's story?

Share your story, too!

Other mantle cell lymphoma stories


Tim H., Mantle Cell Lymphoma (MCL), Stage 3/2



1st Symptoms: Lump on left-side of neck that grew bigger over a couple years, new lump on right side
Treatment: 6 cycles Nordic chemo protocol, alternating cycles of R-CHOP and rituximab + high-dose cytarabine, autologous stem cell transplant

Sheryl B., Mantle Cell Lymphoma (MCL), Stage 4



1st Symptoms: (Over 15 years) Skin irritation from temperature changes, rising WBC levels, unexplained fatigue, retinal hemorrhage, hardened abdomen (from enlarged spleen)
Treatment: 6 cycles Hyper-CVAD chemotherapy

Shari B., Mantle Cell Lymphoma (MCL), Stage 4



1st Symptoms: None, lymphoma discovered at unrelated doctor appointment
Treatment: 6 cycles R-CHOP, 5 cycles Phase 3 trial of Velcade + Rituxan (normally for multiple myeloma), allogeneic bone marrow transplant (BMT)

Bobby J., Mantle Cell Lymphoma (MCL), Stage 4



1st Symptoms: Fatigue, enlarged lymph nodes
Treatment: Clinical trial of ibrutinib + rituximab, consolidated chemo of 4 cycles of Hyper-CVAD

Jason W., Mantle Cell Lymphoma (MCL), Stage 4



1st Symptoms: Hives, inflamed arms



Treatment: Calabrutinib, Lenalidomide, Rituxan
Favorite0
Categories
Multiple Myeloma Relapsed/Refractory Tagrisso (osimertinib)

Multiple Myeloma | Connie H.

Multiple Myeloma:
Connie H.’s Story

Connie is a self-described Wyoming cowgirl—not the rough type, but someone who balances it with gentle self-care. She’s happily married to her high school sweetheart, Greg. Together, they’ve raised three wonderful children.

In 2001, she survived thyroid cancer. In 2012, at age 46, she found herself with yet another diagnosis – this time, the rare blood cancer called multiple myeloma.

In this video series, Connie shares her story of diagnosis, numerous treatments and clinical trials, relapse, and the side effects she endured. But Connie’s journey is not yet over—a continuing quest for treatment while living life to the fullest with her family.

Explore her inspiring 3-part story series below. Thank you so much for sharing, Connie!

How I Got Diagnosed

Connie was in denial. She had constant pain in her ribs, shoulder, and hips. It hurt so bad she was limping at work and even unable to clap at her daughter’s sport’s games.
When she finally went to the doctor, she had broken ribs, a hole in sternum, soft tissue vertebrae tumor, spine hip skull lesions. At 46, she was diagnosed with Multiple Myeloma.

Read more→

Relapse, Treatment, and Clinical Trials

Connie underwent a series of IV chemo. She endured devastating side effects that took 50 pounds off her weight. There was remission but her cancer keeps coming back. This led her to try a number of clinical trials.

Read more→

Living with Multiple Myeloma

Even with initial successes from the treatments, Connie’s battle vs relapsed, refractory multiple myeloma continues. She is tireless in looking for clinical trials, going after her insurance company to make sure she gets her treatments.

Connie is such a strong and inspiring example of patient self-advocacy.

Read more→

  • Name: Connie H.
  • Diagnosis (DX)
    • Multiple Myeloma (Relapsed/Refractory)
  • 1st Diagnosis:
    • Age at DX: 46 years old
    • Symptoms
      • Chronic pain on ribs, shoulder and hips
      • Cough, bronchitis
  • Tests for DX: CT scan, Bone marrow biopsy
  • Treatment:
    • Stem Cell
    • IV Chemo (CyBorD)
    • Busulfan
    • Velcade + Revlimid (VR)
    • Cytoxan + Pomalyst
    • Darzalex
    • Bendamustine
    • Kyprolis
    • CAR T cell therapy
    • Blenrep
    • Isatuximab

Inspired by Connie's story?

Share your story, too!

Other relapsed/refractory multiple myeloma stories


Donna K.



Diagnosis:Multiple myeloma, refractory
1st Symptoms:None, found by blood tests
Treatment: Total Therapy Four, carfilzomib+pomalidomide, daratumumab+lenalidomide, CAR T, selinexor-carfilzomib

Connie H.



Diagnosis: Multiple myeloma, relapsed refractory
1st Symptoms: Chronic bone pain
Treatment: IV Chemotherapy, CAR T cell therapy

Elise D.



Diagnosis:Multiple myeloma, refractory
1st Symptoms:Lower back pain, fractured sacrum
Treatment: CyBorD, Clinical trial of Xpovio (selinexor)+ Kyprolis (carfilzomib) + dexamethasone

Beth A.



Diagnosis:Multiple myeloma, relapsed/refractory
Subtype: Non-secretory (1-5% of myelomas)
1st Symptoms:Extreme pain between shoulder blades, sternum, head, burning sensation
1st Line Treatment:VAD chemo, radiation, stem cell transplant
RR Treatment: 8 chemo regimens, successful combo→selinexor+bortezomib+dexamethasone
Scott

Scott C.



Diagnosis: Multiple myeloma, relapsed/refractorySubtype:IgG lambda (majorityof myelomas)
1st Symptoms: Pain in hips and ribs, night sweats, weight loss, nausea
Treatment:
Clinical trial, chemo, kyphoplasty, stem cell transplant
Favorite0
Categories
Integrative Therapies Medical Experts

Integrative Cancer Therapies | Dr. Donald Abrams

Integrative Cancer Therapies

Dr. Donald Abrams, Integrative Oncologist, UCSF

Dr. Donald Abrams is a leading integrative oncologist at the Osher Center for Integrative Medicine at UC San Francisco (UCSF).

Dr. Abram shares with us some of his most recommended resources for those of us navigating cancer. From cancer nutrition and diet to natural supplements and discussions around medical cannabis and how to use mind, body, spirit practices, from physical activity, yoga, traditional Chinese medicine, to meditation.


Dr. Abram’s Recommendations on Resources

Cancer nutrition and diet

Dr. Donald Abrams, a leading integrative oncologist at the Osher Center for Integrative Medicine at UCSF, leads us through topics across nutrition in cancer—good cancer diet, sugar, inflammatory foods, and more.

Natural Supplements (Vitamins, Cannabis, Mushrooms)

Dr. Abrams shares his insights and recommendations on different kinds of natural supplements. He also discusses his insights on CBD and medicinal mushrooms.

Mind, Body & Spirit Practices

Dr. Abrams, being a leading integrative oncologist at the Osher Center for Integrative Medicine at UCSF, also discusses mind, body and spirit practices for integrative healing.

About Dr. Donald Abrams

An integrative oncologist at the UCSF Osher Center for Integrative Medicine, and Professor Emeritus of Medicine at the University of California San Francisco. He was one of the original clinicians/investigators to recognize many of the early AIDS-related conditions.  

His integrative oncology interests are in medicinal mushrooms, Traditional Chinese Medicine interventions, and nutrition.  He co-edited the Oxford University Press textbook Integrative Oncology with Andrew Weil, M.D. Dr. Abrams is a member of the National Cancer Institute PDQ CAM Editorial Board. He was President of the Society for Integrative Oncology in 2010.

Education and Training
  • Fellowship in Hematology-Oncology, UCSF Cancer Research Institute 
  • Fellowship in Integrative Medicine, University of Arizona, Arizona Center for Integrative Medicine
  • Internal Medicine Residency Training, Kaiser Foundation Hospital, San Francisco
  • MD, Stanford University
  • AB, Molecular Biology, Brown University 

Thank you so much, Dr. Abrams!

More from Experts on Integrative Therapies


Dr. Donald Abrams



Integrative Medicine:



Experience: 30 years



Institution: UCSF Osher Center for Integrative Medicine
...
Favorite0
Categories
Medical Experts Prostate Cancer

Leanne Burnham, PhD Prostate Cancer | The Patient Story

My Dad Was Diagnosed with Prostate Cancer. Now I’m Fighting It.

Dr. Leanne Burnham: A Caregiver, Patient, and a Doctor’s Journey

Motivated by her father’s prostate cancer journey, Dr. Leanne Burnham, scientist and community program coordinator at the City of Hope, dedicates her time and expertise so that communities of people of color could better understand prostate cancer and its specific risk factors.

Not only has Dr. Burnham been been a caregiver to both parents with cancer, she’s a lymphoma survivor, herself.

Her mission has been to raise more conscious and open conversations among families about their risks of cancer. That makes her a perfect fit in her department: Division of Health Equities at City of Hope.

Dr. Leanne Burnham is doing such amazing and inspiring work, not just in prostate cancer diagnosis and treatment clinical trials but also in patient self-advocacy, support, and other important socio-cultural factors around cancer. Explore our entire conversation below.


Introduction: Dr. Leanne Burnham

I am Leanne Burnham. I was born and raised in Akron, Ohio. Home of Lebron, we like to say. I live in California now. I am a wife and a mom of three. I have a 17-year-old, a 12-year-old and a 10-year-old. 

I’m a scientist at the City of Hope, that’s what I do. I do experiments at the bench for sure. We call it at the bench when we’re in the lab, but I also do a lot of community work and work in clinical trials.

Prostate Cancer

What is prostate cancer?

There’s a lot to unpack. But first of all, women don’t have prostate, so it’s just a male disease.

Another thing that seems silly to say, but the prostate and the colon are two separate things. A lot of times people think they’ve had a colonoscopy means they’ve gotten their prostate checked. But that’s not the case.

According to the American Cancer Society, prostate cancer is one of those diseases with a 100% cure rate at five years if you catch it when the disease is still localized or confined in the prostate.

That’s amazing because not a lot of cancers are like that. Many people would hear, “Prostate cancer is one of the better cancers to get,” or they hear, “Prostate cancer happens to older men,” which is true.

It’s a disease of age, and there have been some studies that by the time men reach their 70s and 80s, many men, if not most, have prostate cancer at some point. But prostate cancer isn’t what ultimately kills a lot of men that have it.

For that reason, a lot of people tend to not get so stressed when they think about prostate cancer and their risk of it.

But it’s important to realize that the second you have prostate cancer cells escape out of the prostate and spread in the body, you go from a 100% cure rate in five years to there is no cure.

There’s no in-between, so all of the treatments we have once the cancer cells have escaped are to prolong life or improve quality of life.

We’ve got some really great treatments out there. We’ve got cutting-edge treatments nationwide that are really extending the lives of many patients, and they’re living great lives. But I’m at the City of Hope, so, of course, I’m partial. 

It is also important to point out that, yes, prostate cancer is very curable, it happens a lot to older men, but that doesn’t mean it doesn’t happen in younger men.

It doesn’t mean that there are no aggressive forms in younger men. It certainly doesn’t mean that if you have prostate cancer, you’re just going to be cured and be fine because it’s not that way for everyone.

Diagnosing and Staging

First of all, you start with a PSA test. That’s testing your prostate-specific antigen, which is a protein secreted by the prostate. It’s circulating in your blood, so that’s one of the first markers they can test and say, “Hey, something is going on with your prostate. It might not be cancer, but something is going on.”

After a PSA test, men will get a biopsy, then they get a Gleason score. Pathologists look at the tumor under the microscope and assign a score based on how cancerous the cells are looking.

The higher your Gleason score, the more aggressive your cancer is.

There are genetic mutations that not everyone has access to, but some physicians provide that for their patients. Especially if they have a lot of family members that have had prostate cancer.

You can look at the genetics and see if there are some mutations that make the tumors more aggressive. What makes it hard to pinpoint treatments for prostate cancer, and to find a cure ultimately, is that prostate cancer tumors are very heterogeneous.

If you’re taking a sample from one part of the prostate and another sample from another part of the prostate and you’re looking under the microscope, they look different. There are different genetic mutational landscapes in those tumors.

Prostate cancer cells are very smart. Every cancer cell is smart. I’ve had cancer but I also have tremendous respect for the cancer cell, its ability to navigate its way and go undetected by the immune system, its ability to receive treatments and figure out ways to resist those treatments and form mutations.

The ability of resistant cells to keep growing is truly amazing. Cancer cells find a way, I tell you, but the key to its science is when they find a way, we have to tackle that new way.

»MORE: Read more prostate cancer stories

What inspired you to focus on prostate cancer?

It was totally unfamiliar to me. I don’t really have a family history of cancer at all. My dad was relatively young. He was like 50 at the time. He worked out a lot, he ate very well, he was going to Mustard Seed (organic grocery store) and things like this.

One day, he called me as I walk out of a physics class. I picked up the phone but he wasn’t talking; he was just crying.

I was like, “What in the world is happening?”

I just heard him crying on the phone, and he said, “I have prostate cancer. You’re the first person I’m telling. I haven’t told your sisters, so if you can come to the house when you get out of class and I’m going to talk to all of you guys. I’m just letting you know.” 

At the time, I was a premed student, so he was reaching out to see if I had any advice, which I didn’t know about prostate cancer at all.

That experience really kicked off my passion for understanding what was going on with him. But beyond his diagnosis of prostate cancer, I started to notice that Black men in our community were getting that, as well.

It was just something I hadn’t noticed before, so I’m like, “Oh wow, this person at church has it. Oh wow, this person at the grocery store has it.” Different men were getting prostate cancer in their 40s and 50s. It was younger than what I would have thought.

So since I was a student and I had some shadowing opportunities and some research opportunities, I decided to get those hours at Cleveland Clinic, which is number one in urology in the nation, and that’s where my dad is a patient.

I went, and I was able to spend quite some time there. I was with a physician one time when he walked into a room with a Black patient with prostate cancer, and when he walked in the hallway with me, he said, “I hate these cases.”

He said, “Because every time I see a Black man in their 40s, or 50s with prostate cancer, it’s almost like it’s a different disease than other prostate cancers.” He was like, “You have to treat it so much more aggressively. It’s just a different ballgame.”

That’s when I thought, “Wow. I never had thought about it. Was there a difference in race and all that?”

From that point, when I went on to Loma Linda University to get my doctorate, I decided that I was going to focus my dissertation on prostate cancer and Black men specifically, and looking at reasons why their tumors might be more aggressive.

Prostate cancer in Black men

There are so many reasons why that is, and there’s been a lot of research that goes into looking at the multifactorial reasons behind that. We do know that Black men are much more likely to get prostate cancer.

Different numbers float around.

The American Cancer Society says that Black men are 76% more likely to be diagnosed. We do know that Black men are much more likely to be diagnosed at younger ages. When they show up to the clinic, they’re at a more advanced stage.

We also know that they are more than two times more likely to die from prostate cancer.

But what’s new on the forefront that we have found in the past five years doing clinical trials that include Black men is that when Black men are given cutting-edge treatments that are out, they actually respond better to treatments than men of other ethnicities, which is really exciting for any disease that you look at.

You can look at breast cancer, colon cancer, or others. If you have a certain demographic that is most high risk and doing the worse, if you can show that if you give them medications, they’ll do better, that’s a win-win for everybody at the end of the day.

Disproportionate risk to prostate cancer

Watching him go through his surgery and radiation and seeing his medications and things that he was on made me realize how private prostate cancer can be.

I really have never even talked to him about this, so dad, don’t get mad when you watch. I noticed some issues come up that maybe men would be embarrassed about. That was the first time I saw it with him.

Now that I’ve worked with hundreds of men with prostate cancer, that appears as a common theme.

Men are scared of certain treatments. They don’t want to have the side effects and don’t necessarily feel comfortable talking to people. They feel isolated sometimes.

That was the first time I saw my dad not be such a superhero. He became more human at that moment. Maybe he was embarrassed or nervous. I wasn’t used to seeing him like that.

DNA and genetic component

In terms of different reasons why he got prostate cancer younger, or Black men in general, for sure, there is a genetic component. I’ll start with the things you can’t change.

You can’t change your DNA. The reason that Black men in the United States specifically are at increased risk for aggressive prostate cancer is because their DNA happens to trace back to the DNA of West African men.

This makes sense because, in the history of the US, the transatlantic slave trade, Black people in the US came from the western portion of Africa. Not surprisingly, men in West Africa have very high rates of aggressive prostate cancer as well, so that DNA matches.

There are certain variations on certain chromosomes that we know that are more likely to occur in Black men than other ethnicities that makes them more likely to get aggressive prostate cancer.

Role of Vitamin D

In addition to that, my boss, Dr. Rick Kittles, the Director of the Division of Health Equity at the City of Hope and an internationally known geneticist and prostate cancer researcher, has shown for a decade that there’s a link between vitamin D deficiency and prostate cancer risk.

People may have heard about COVID going on, like, “If you’re vitamin D deficient and have COVID, that’s not a coincidence.” Vitamin D deficiency leads to a lot of pathogenic trends.

With prostate cancer specifically, we know that vitamin D deficiency leads to tumor aggressiveness. But how that relates to Black men is that our bodies make vitamin D from the sun, and our bodies are dependent on sunlight.

The more melanin you have in your skin, the less vitamin D your body can synthesize.

If you have darker skin, and then in our lifestyles now, we’re not outside in the sun as much as we used to be, we’re much more likely to be vitamin D deficient.

In the African-American population, about 70% are vitamin D deficient or insufficient. There’s a vitamin D link to prostate cancer as well, then we know that there’s diet and lifestyle, of course.

It’s always good to have a healthy diet, of course. But we’re doing studies at the City of Hope right now where we’re looking at the link between charred foods, like barbecue or grilled foods, and the ability of the consumption of that to contribute to more aggressive tumors.

Socioeconomic factors

There’s also socioeconomic status, which goes a lot of different ways. But first of all, it controls your access to healthcare that you have.

Of course, if you have better access to healthcare, you’re going to have earlier screening, maybe a better team of doctors who will treat your case with a precision medicine approach, and you’ll have access to newer cutting-edge treatments.

But the other part of socioeconomic status that we’ve really dived into in 2020, given our nation’s culture, is looking at discrimination, especially in healthcare and medicine and in science really.

We know that stress kills, literally. And there are studies out there, and I published on it, on how much cumulative stress somebody’s taken on over their lifetime. We know it occurs more often in Black people.

If you have that cumulative stress, it dysregulates your HPA axis. It dysregulates how much cortisol your body is making and how your body responds to that cortisol and looks at glucocorticoid receptors. But that’s real science; we don’t have to go all into that.

Comparing cancer cells in Black and white men

Basically, what I’ve shown previously is that when I treated Black prostate cancer cells that I was growing in the lab with cortisol and compared them to Caucasian cells. I had Black cells and I had White prostate cancer cells.

The Black cancer cells grew more aggressively, and they upregulated these genes in these proteins that made them more likely to resist therapy. You could have this cumulative stress that would dysregulate your stress hormone system, making you more likely to get cancer. Then once you do get cancer, it makes you less likely to respond well to treatment.

That’s a very interesting concept that’s being studied right now. There’s a lot of research dollars going into that nationwide. I’m not working on that anymore, but I can’t wait to see like the results that come out of that.

Ignoring the risk factors

This is something that infuriates me, for sure. I’ve also published on this.

First of all, in Southern California, where I live, we did a study looking at more than 400 men and found that with 54% of Black men, their doctors never even talked to them about prostate cancer screening. We have to start with that.

A lot of men are not even getting screened when they should. That is because prostate cancer screening recommendations for a while we’re saying, “Okay, screen every man at 50,” and then in 2012, the US Preventive Taskforce said, “We’re not screening men at 50 anymore.”

The problem is that it really hurt Black men, and that recommendation was based on studies that looked at 200,000 men that did not have prostate cancer.

They had done the PSA test to see if it was indicative that they would get prostate cancer in the future, but the studies say over 95% were men of European ancestry.

This recommendation is applied to everyone, but it didn’t consider a racial difference in prostate cancer risk.

The American Cancer Society and Prostate Cancer Foundation says that if you’re Black, and you’re 45, you need to get your PSA tested. If you’re Black, and you have family members that have prostate cancer, you need to get tested at 40.

This is the recommendation, and then you go to the doctor and your doctor says, ‘Actually, no, you don’t need to be screened.’ That’s a big problem.

That happens so many times. Of course, if you go to the doctor and the doctor says you don’t need to test, who would want to get the test? You’re just like, “Okay, I’m good. I don’t need to get the test.”

That’s the first thing. But then once you do get the test and you get your PSA results back, there are differences in how those numbers should translate based on race.

For a while, the number that men would look at is four nanograms per milliliter of your PSA. If it’s higher than four, then maybe you want to do some follow-up.

It’s actually 2.5 for Black men, according to the American Cancer Society. Dr. Rick Kittles has published that, actually. You can look at numbers of 1.5 in Black men and it can be predictive years down the road that it’s going to transform into prostate cancer.

A PSA of 14 is quite alarming and then by the time he was diagnosed, it was 64, as far as I can remember.

When you go to the doctor, and you have an elevated PSA, and a high Gleason, I can’t tell you how many times where I’ve had people reach out to me and they’ll say, “Hey, my Gleason score is seven and my doctor says that I should do watchful waiting.” I say, “Did they look at you? Do they know that you’re Black? Did they get the memo?”

It’s not a one-size-fits-all blanket approach sometimes. You really want to make sure that your physician, first of all, is referring you to a urologist. I would definitely say, go to a urologist at that point and have them help you make the decision and hopefully with somebody that’s well-versed in how this disease affects men differentially.

Watching out your genetics and mutations

You hear about BRCA mutations of breast cancer. Not surprisingly, if you have a high risk of breast cancer in your family, that also translates to prostate cancer.

They’re both hormonal cancers, but particularly, if you have BRCA mutations that run in families, we can treat patients with those mutations with PARP inhibitors. There are different kinds of PARP inhibitors that are in clinical trials right now. You’d have to check and see what’s available for you.

Oftentimes, we know that these mutations lead to more aggressive tumors. But sometimes, it’s like hitting the jackpot because then you have access to an additional line of therapy compared other patients that don’t have those mutations.

Genetic Testing

I think it would be individualized, and that the urologist would discuss with the patient their family history and just get a sense of how high their risk is. I don’t believe that it’s offered to everyone. Just because you want it, I’m not sure that you can necessarily get it or your insurance would cover it.

You could always pay for it out of pocket, but not everybody has that luxury. But if you have multiple family members that have prostate cancer, it is definitely something worth looking into.

Ongoing studies on PARP inhibitors

Dilemmas and decisions

I love working on clinical trials, because to me clinical trials, how I try to explain it to people, is like a VIP access to cutting-edge treatment.

Many people can be afraid of clinical trials because you might think that you’re going to be a guinea pig. There’s a lot of mistrust in clinical trials in the Black community, for sure. Number one, because of the Tuskegee syphilis experiment that was just a trial gone completely wrong for 40 years.

There’s a lot of mistrust about clinical trials and who’s funding it and who’s behind it, and if I will be a guinea pig or get a placebo.

A lot of people have an idea that they’re going to get a placebo when in actuality, if you participate in a clinical trial, you are either going to get standard of care, which is what’s offered in the clinic to anybody that have your particular disease, or have the option get the VIP treatment on top of the standard of care or in place of the standard of care.

The VIP drugs don’t get to that stage just like that. It’s years and years in the making so by the time it’s to that point, we, scientists and physicians, feel very confident that this is going to work.

Thus, it is important to point where it’s at in a clinical trial and that there are different phases of clinical trials too. There’s phase 1, phase 2, phase 3. Obviously, the later the phase, the more people have used that drug in that disease setting before. So you can decide if you want to do a phase 1 trial or feel better with a phase 2 or phase 3.

Stratified Clinical Trials

With clinical trials, they typically, in the past, have not included a lot of minority populations—Black, Latino, Asian, Native American, for sure. So it really does a disservice to everyone because you need to know how a drug would work in the context of different genetic variations.

One drug may work really well in one demographic, and it might not work as well in another, so we really try to accrue.

This means recruiting and enroll Black men in prostate cancer clinical trials, which makes sense because they’re more likely to get the disease and die younger.

It’s important to look at these new VIP cutting-edge drugs and Black men could really benefit from them. As I mentioned before, some recent trials enrolled a lot of Black men. We call it race stratified clinical trials.

There were a few studies where one was looking at hormone therapy, one was looking at chemotherapy, and one was looking at immunotherapy. In all three of them, the Black men that participated in the trial had longer survival than men of other races and ethnicities.

When we looked at that, scientists like me who do health disparities research were like, “Wow, that’s so encouraging.”

At the City of Hope, we have a team of scientists and physicians and clinical research nurses, and statisticians who come together and think about diseases and ways to help people who suffer the most from that disease.

Talazoparib clinical trial

Alongside Dr. Rick Kittles, Dr. Tanya Dorff, who’s the Director of the Genital Urinary Program there, and Dr. Zijie Sun, who’s another prostate cancer researcher, we designed a clinical trial to use a PARP inhibitor called talazoparib. It’s a newer-generation drug that Pfizer makes.

This trial is also sponsored by Prostate Cancer Foundation and we’re going to be using PARP inhibitors in a racially diverse group of patients so we are going to have a third of the patients be white men, a third of the patients be Black men, and a third of patients be Asian-American.

The Asian population is very heterogeneous, so I just hate to throw it all into one.

Many Asian-American men actually do better with prostate cancer than white men. Black men do the worst. So we want to see how this drug works in different races. But we’re not just picking races just to see; there has to be some sort of a scientific reason.

Racial Differences in Androgen and Androgen Receptors

The reasoning there is an interplay at the cellular level between PARP and androgen receptor. Androgen receptor has some variations that affect its function.

Androgen and androgen receptors are crucial for prostate cancer cells to grow. That’s why if you get prostate cancer, one of the treatments is hormone therapy because we want to block androgen and the androgen receptor.

There are racial differences due to genetics where different trinucleotide repeats that exist in the antigen receptor. There’s different links, so they’re shorter repeat links and there’s longer repeat links.

Asian men, not just American, tend to have longer repeats, and African-American men tend to have shorter repeats. The repeat length may affect the men’s response to this PARP inhibitor with the talazoparib. We’re going to see.

The study just kicked off this past month and we’re starting to accrue patients. It would be one more drug in the arsenal because as I said, this is going to be offered to patients who already have metastasis.

They can do different drugs that are out there, but this PARP inhibitor could be something that’s extra added to their hormone therapy, and that’s what we’re looking at. We’re looking at the Talazoparib specifically with Abiraterone acetate at this point in time.

Developing targeted therapy according to race

That’s something that we could check in the future. We could look at their androgen receptor, look at your trinucleotide repeats, then we could say, look, you’ll be a great candidate for this drug in the future beyond clinical trials.

But it’s not going to target the shorter. It’s the same with everyone. We think that there may be differences in response in the androgen receptor and the trinucleotide repeats within that receptor, within that gene. But we don’t know what to expect.

It may work well for everyone, but if there is a difference, we want to tease that out.

This is a two-year study, and we assess the study. You don’t just start the study and then just let it go and check at the end. You’re constantly tracking your progress as it goes, so we should have a good idea by the end of the year.

Building trust in clinical trials

That to me is the most important part of it.

In the past 20 years, there has not been an increase in the number of Black physicians accepted into medical school. That’s the problem. It’s not making it through medical school; it’s getting accepted into it.

A study came out of Oakland last year that showed how much better the outcomes were and how much more the diseases were addressed when Black people went to Black physicians.

We look at it in Black maternal death rates and infant mortality, and we know that just by the presence of a Black nurse or a Black physician in the room, the mortality rates go down, just by them being in the room.

That is a lot to unpack on why that is, but there is a trust factor when you have cultural competency in the room. Race doesn’t have to match all the time as long as your physician is culturally competent and sensitive to different communication styles and cultural contexts. It can work just fine, but we know that there are still many barriers, for sure.

When they go into the office, the patients feel the bias going both ways. There’s bias on the part of the patient, and then there’s bias on the part of physicians.

»MORE: Learn more about the process of clinical trials from one program director

First of all, increasing the number of minority physicians, in general, would help. But what we like to do is to have a diverse team—diversity, in terms of race, gender, age, and occupation. We have physicians, nurses, scientists, and many of us who work within the Division of Health Equities at the City of Hope have personal ties to how we even got into this.

I got into this because of my dad, and so I’m speaking to Black men, and they’re saying:

  • “Oh, I feel fine. I don’t have any symptoms.”
  • “Really? Because my dad didn’t have any symptoms either.”
  • “Oh, I don’t know if I get that done. I’m not going to have a normal life.”
  • “My dad had that, and he’s doing great.”

That works on these teams who have personal ties, and so it comes across as more genuine, for sure.

We’re not just going to collect samples for research and just leave. We are there to help the men. We do actual prostate cancer screening in the community.

I know people freak out. We don’t do digital rectal exams in the community, but we do the blood tests, we provide the men their results and then we offer follow-up care and it’s not just at the City of Hope.

We partner with community clinics for men who may not have insurance or under-insured to make sure that they get that follow-up care, especially if their numbers are low enough that we think it could be caught early.

That’s really the goal of everything that we do. But, yes, the mistrust is a real thing and we try to tackle it that way.

Another way to really increase minority enrollment in clinical trials is just to provide access in communities of color.

Not everybody can travel to your main clinical trial center. I know at the City of Hope, we’re very fortunate to have community sites in Pasadena, Antelope Valley, or Santa Clarita, Pomona.

There are different locations to make it easier for patients to go from their neighborhood to a closer location to get treatment, which helps.

There’s financial incentives as well, and that can be controversial for sure.

Some of our trials offer them, and some of them don’t. But a lot of times, when you’re a cancer patient, getting to clinical trials is expensive. You and your caretaker have to call off work, you might have to get lodging, have transportation costs, and so a clinical trial can provide some financial incentive to help overcome that. It can really open the door for a lot of people.

Telemedicine as a tool

Telemedicine definitely has its pros and cons we’ve all learned during quarantine, for sure.

That translates to prostate cancer as well. If you don’t live close and have the technology and the app you need to communicate with your provider, it can give you access to perhaps more than you were exposed to before.

City of Hope Work in Communities

It’s our community-based prostate cancer program directed by Dr. Rick Kittles. I am lucky and blessed that he allows me to be the project coordinator for that. I work under him to recruit licensed phlebotomists. We recruit volunteers.

It is not hard to recruit volunteers because these events are the highlight of our week. They’re so fun. We get so much more out of these events.

Anything that we give back, we receive back in the energy of the individuals that we meet and we touch.

First of all, we provide education.

Let’s say we’re at a church. Usually, the pastor will let us get on stage for five minutes to say what we are doing and why it is important.

We know in the literature that, unfortunately, the men who are most at risk for aggressive prostate cancer don’t think that they are. So the first piece is letting people know they belong to the high-risk group.

Then a lot of men are afraid of the digital rectal exam. We let them know that it’s the PSA test now. You can get the DRE when you go to the doctor, but since 2017, you lead with the PSA. 

A lot of times, when they find that out, they say, “Oh, okay. You don’t have to do that. Then I’ll do the blood test.” That’s the next part of it.

We also let them know that most of the time, with prostate cancer, you don’t have any symptoms. Men will be at Taste of Soul or the Long Beach Jazz Festival and are sitting there with their drinks and their cigars, and they’re, “I feel great. I feel great.” On the other hand, you might frequently be urinating at night.

We go into the communities, educate, interact, do the blood tests, and then follow up within two weeks. And we tell them, “Don’t freak out. That doesn’t mean you have prostate cancer. But either way, you just want to stay on top of your prostate health.”

We send every person an individualized letter. By individualized, it’s an official letter from the City of Hope. It gives them their PSA level. Based on their race and age, we translate to them what that means for them. Not everybody’s letter is going to look the same.

If they are at a younger age but they are showing a 2.5 or a 3 PSA, we’re like, “You really want to follow up and get this double-checked.” We follow up within two weeks.

If a man has very high PSA levels, we will call to make sure they got that letter. We tend to follow up after a few weeks for everyone who has elevated PSA, anyway, just to see, “What have you done with that?”

Many men find out and haven’t told anybody and they’re nervous to take the next step. So we help them with that.

Then we have social workers that help to navigate them getting to their next follow-up person. Whether it’s at the City of Hope, we would love to offer the different treatments that we have there.

But not everyone can travel that far, or maybe their insurance doesn’t allow them to. We partner with community clinics in the LA area where patients can go there as well.

Lessons from Community Work

I’ve learned how much people trust their doctor without knowing their personal risk. They trust their doctor knows their risk. It’s scary how often it doesn’t necessarily seem to be the case.

I’ll talk to men sometimes, and they’ll say, “Oh, I had that test done.” Then I’ll say, “You went and got the blood test?” They’ll say, “No.” Then I find out they’re talking about the colonoscopy. That’s one thing.

A lot of times, I hear, “I got all my blood work. My doctor does all my blood work every year.” Then I’ll say, “Well, did they include that in your blood work?”

A lot of times, it’s not included. They’re checking your blood sugar and your enzymes but not the PSA. Now that you have medicine apps on your phone, they’ll say, “No, I did it. My doctor ordered it.” They’ll pull it up. I say, “If you don’t mind, let’s look and see. What was your PSA?” Then it’s not in there, and then they’re like, “What? My doctor was not testing?”

It’s endearing how a lot of people do trust their doctor. Then it is sad to see sometimes they’re let down, but it’s like, “Now you have the tools. Now you email your doctor, and next time you’re in there, you let them know that you want to have this test, but actually, you don’t have to because we’re going to do the test now, and we’re going to give you a letter, and you can show your doctor.”

Hopes and prospects in prostate cancer research

I think we’re so close. When I got into this when my dad was sick, his doctor told him at that time, “Oh, you have a set amount of years.”

He’s passed that amount of years, and he’s doing well. We know he’s not curable still, but I hope to change that. When I got into this, I said, “I’m going to find a cure for my dad,” many people say. That’s the goal of a lot of scientists. They have a loved one, and that’s why they got into it in the first place.

I’m at a place at City of Hope where we have so many clinical trials, so many cutting-edge treatments, and we’re seeing patients that are really doing well. I just feel like we’re just at the cusp of it.

I’m just like, “Dad, hold on. Just hold on. We’re at the cusp of it.” I do think that it’s around the corner. I don’t think that it’s something that’s decades away. I think it’s sooner than we think and I’m really hoping that’s the case.

Being on both sides: Survivorship and cancer research

I was in science before I got cancer. My dad had cancer first. Then I was in science. But I was walking around with cancer for six months myself, and then I had to do chemo in the whole nine yards.

After that, it just completely changed my thought process and my approach. It changed my outlook on life, first of all. Everything I did became urgent. I don’t know if I’ll be here tomorrow. Everything is urgent.

One in two men is diagnosed with cancer, one in three women. I walk through life like, “Listen, it’s morbid as it sounds.” I’m like, “It’s not a matter of if you’re going to get cancer. It’s just like, ‘When? At what age?'” It’s just so common. We really need to get a handle on something, and I’m so glad we have so many scientists really dedicated to that cause.

It changed my outlook on life, and then it changed my outlook on scientific approaches. I used to sit in scientific meetings, and it’s like, ‘Oh, we can use this drug. Let’s try this and that.’

Sometimes I would open my mouth and say, ‘These are people. Imagine what all of those drugs are going to feel like.’

I know with my lymphoma, I had four chemo drugs at each session. That just was not fun. The idea of like, “You really want to be able to treat your patients with the least invasive method. You don’t want to go so hard on the pain all the time. You want to find something that works, but it’s not so toxic to the patient.”

Then I also think I know what it’s like to walk around with cancer and not know that you have it. You think it could be anything else, and that applies to a lot of people.

When I’m out in the community and people will say, “Oh, I don’t feel like I have cancer.” Sometimes you don’t feel like it, but sometimes you get used to those nagging little symptoms that have formed over a few weeks or a few months. You never want to go off of how you feel when it comes to screenings. 

Another thing, because I’m a cancer survivor, I have to go to my oncologist. But that’s always so weird to me. I’m in the lab and working in the hospital then, “Oh, it’s now my turn to go to the oncologist.” It’s just always weird.

When I went, they said, “Listen, we want to do a colonoscopy on you.” I was young. I wasn’t 40 yet. I’m like, “Fine. Another test.” So I did it. When I woke up, they said, “You know what? We found several pre-cancerous polyps.” I was like, “What?”

I was so happy that I did that colonoscopy that young. If I hadn’t had lymphoma, they wouldn’t have thought to do it that young. Now I know. I don’t wait as long as other people. Now I’ll be referred for a colonoscopy much more frequently than anybody else.

Don’t put off symptoms. If your doctor thinks that you have a reason to be screened for something, don’t be afraid because trust me, you want to be diagnosed at an earlier stage and save yourself some of the hassles, please.

Especially with prostate cancer because it’s curable if you catch it early. That’s literally life or death. You want to screen for that sooner rather than later.

Approaching conversations on cancer risks

I try not to freak out on him all the time. He’s 17 so it’s like, “Oh, everything’s fine.”

Just the other day, he texted me and said, “Oh mom, I’m having an allergic reaction to like 30 things.” Then I responded, “Oh my gosh, what are your symptoms?” Then he didn’t respond. Then I’m calling his girlfriend, calling every everybody to see, “Is he gone into anaphylactic shock?” I just assumed the worst all the time.

He’s used to, “Oh, mom’s just freaking out,” but I look at every symptom as like, “Oh my goodness.” He did have some swollen lymph nodes at one point. I thought it’s lymphoma because it’s hereditary. But it was not the case.

I don’t really talk to him because I take action. We’re going to see what happens when he becomes an adult and has to make decisions independently. 

At that point, he knew his grandfather, who’s my dad. He was like, “Oh, well, he has cancer, and he’s okay.” I don’t know if he thought, “Oh, she has cancer. She’ll be okay.”

He saw my hair fall out and he saw me being sick and tired from the chemo all the time, and he seemed okay.

On my final PET scan, the day that I found out that there was no evidence of disease, I sat him on the couch, and I showed him the picture. Because at that point, my son is a little nerd like me, so he knew like, “Oh my mom. I’ve seen her cancer cells. There’s two nuclei instead of one.” He knew what the cancer cell looked like.

I said, “Let me show you the PET scan. This one, this is the before, and this is the after.” He said, “[gasps] there’s nothing there.” I said, “Yes.”

His shoulders just dropped. It’s like he sighed. I didn’t realize, in that moment, that he had been walking around like this for months.

»MORE: Parents describe how they handled cancer with their kids

I saw it, and I was like, “Oh my gosh. It’s the little boy Beck that I remember that’s worried for you.” I don’t think he worries about it anymore right now. It doesn’t seem like it. That’s going to be something interesting to navigate as he will not be missing any screenings.

Normalize these conversations

It’s super important. I hope it changes with younger generations because my sister-in-law just beat triple-negative breast cancer last year during COVID, and she’s only 40, the same age as me. 

When she was asked about family history, it was difficult to think who had what cancer? I know it’s the same with me. People died, and you don’t really know what they died of.

I hope that really changes moving forward and we become more open to sharing. I know in my family and my husband’s family, prostate cancer is not limited to one person. It’s rampant. The more you talk about it, the more you normalize it.

It’s difficult because a lot of older generations may have had prostate cancer, treatments are not the same as they were then. Maybe you hear horror stories, and then the younger guys are like, “Oh, I really don’t want to do it.”

We really try to stress that the testing is different, the treatments are different, the outcomes are different. The side effects after the treatments are different because things are improving. It is important to talk about it as a family to know that your individual risks are based on your family members.

Patient Self-Advocacy

I am just so grateful that Al Roker shared his story like that. A lot of people know him, and they’re going to think, “Wow. He had this, and he’s doing well. I can get a screening for this. If I get that diagnosis, it’s not the end of the world. I can come through it on the other side.”

It’s important, and I recognize that importance. When we’re out in the community, I recognize my limitation. I’m a woman. I don’t have a prostate.

I can talk, turn blue in the face, but it’s not a one-person job. I make sure I show up with people who have been previous patients because men want to see somebody they can relate to that has been through and come out on the other side.

»MORE: How to be a self-advocate as a patient

I really think support groups are a great thing as well for men who have been diagnosed with prostate cancer. Just seeing men talk about it and be open about it definitely helps with anything in life, for sure.

We see it with the COVID vaccine now, too.

One person in the family gets it, you talk about it, now the cousins get it. I was the first person in my family. Now everybody’s gotten it. But it’s taken weeks and weeks to get to that point. That’s an example of you just talk about it and then it normalizes it for everybody else.

Message to Black men cancer community

Well, that’s something I hear in the community a lot too. Men will say, “Oh, I don’t want to have this treatment because I’m afraid that I won’t be able to have sex anymore.” That is true for a lot of different treatments.

One thing I tell men, it’s funny, but it’s not, but I’ll say, “Listen, if you don’t treat it at all, you won’t be able to have sex anyway, and you’re definitely not going to have sex when you’re six feet underground. It’s just not going to happen.” I make sure that they know that, but that’s just more on the joking side.

There are nerve-sparing surgeries offered now where results are not the same as they were 10 years ago. Your chances of regaining that function are so much better. Al Roker spoke about how he was able to regain that function. So don’t let that hinder you.

At the same time, I’ve been a patient, and I firmly believe that it’s the patient’s choice. Some patients decide, “I don’t want to do any treatment.” It’s their life, and that’s totally fine.

I’ll never forget when I spoke to a man who had a very elevated PSA and a Gleason of 9, and he was like, “I don’t want to have anything done.”

He was in a support group, and other men—it was a room of all black men —were telling him, “Oh, I had this treatment, and I had that treatment,” and at the end of the day, he was like, “I just would rather just see what happens, and I’m just going to live with my decision.”

You just have to respect that at the end of the day. I don’t know if I could have done that before I was a patient myself.

That is an example of you just wanting somebody to be able to make an informed and educated decision.

If you know all that and that’s what you want to do, do you boo. Because you’re going to have to live with that. You should be allowed to make your own choice.


Read Other Prostate Cancer Stories


Clarence S., Early Stage



Cancer Details: PSA levels fluctuated but were never extremely elevated, cancer contained to prostate
1st Symptoms: No symptoms, caught at routine physical with PSA test
Treatment:Radical prostatectomy (surgery)

Steve R., Stage 2



Cancer Details: Started at stage 2 and gradually progressed to stage 3, and then to stage 4 with metastasis to lymph nodes
1st Symptoms: Rising PSA score
Treatment: IMRT (radiation therapy), brachytherapy, surgery, and lutetium-177

Al Roker, Gleason 7+, Aggressive



Cancer Details: Aggressive but caught early
1st Symptoms: No symptoms, caught at routine physical with PSA test
Treatment: Radical prostatectomy (surgery)
Bruce

Bruce M., Gleason 8/9, Stage 4A



Cancer Details: Staged Gleason 6/7 pre-surgery, post-surgery changed to 8/9, PSA level at 27
1st Symptoms: Urination changes, brother's prostate cancer diagnosis
Treatment: Radical prostatectomy (surgery), salvage radiation, hormone therapy (Casodex & Lupron)
Dennis Golden

Dennis G., Gleason 9 (Contained)



Cancer Details: Staged Gleason score 9
1st Symptoms: Urinating more frequently middle of night, slower urine flow
Treatment: Radical prostatectomy (surgery), salvage radiation, hormone therapy (Lupron)

Theo W., Prostate Cancer, low-end high-risk



Cancer details:
Low-end high-risk prostate cancer, early kidney cancer
1st Symptoms: PSA level of 72
Treatment: Surgery, radiation

Jeffrey P., Gleason Score 7



Cancer Details: Diagnosed at 59, biopsy had not detected it
1st Symptoms:None, routine PSA test, then IsoPSA test
Treatment:Laparoscopic prostatectomy

More Medical Expert interviews


Dr. Christopher Weight, M.D.



Role: Center Director Urologic Oncology
Focus: Urological oncology, including kidney, prostate, bladder cancers
Provider: Cleveland Clinic
...
Dr. Babis Andreadis of UCSF shares his approach with patients, the importance of patient self-advocacy, whether to ask for a second opinion, and more on shared treatment decision-making. ...

Doug Blayney, MD



Oncologist: Specializing in breast cancer | HER2, Estrogen+, Triple Negative, Lumpectomy vs. Mastectomy
Experience: 30+ years
Institution: Stanford Medical
...

Dr. Kenneth Biehl, M.D.



Role: Radiation oncologist
Focus: Specializing in radiation therapy treatment for all cancers | Brachytherapy, External Beam Radiation Treatment, IMRT
Provider: Salinas Valley Memorial Health
...

James Berenson, MD



Oncologist: Specializing in myeloma and other blood and bone disorders
Experience: 35+ years
Institution: Berenson Cancer Center
...

Jacqueline Barrientos, MD



Role: Hematologist, researcher
Focus: Chronic lymphocytic leukemia (CLL), lymphoma, 17p Deletion (Ibrutinib, Acalabrutinib, Venetoclax), IgHV mutation
Provider: Northwell Health (NYC)
...

Dr. D. Ross Camidge, M.D., Ph.D.



Role: Thoracic oncologist, Director of the Thoracic Oncology Clinical Research Programs
Focus: Lung cancer, small cell (Immunotherapy), EGFR (Osimertinib), ALK (Alectinib), ROS1 (Crizotinib), BRAF (Dabrafenib & Trametinib), NTRK
Provider: Univ. of Colorado
...

Edmund Tai, M.D.



Role: General oncologist, hematologist
Focus: Specialist in treating Chinese-speaking patients
Provider: Sutter Health (Bay Area, CA)
...

Irene Ghobrial, MD



Role: Clinical investigator and professor of hematological oncology
Focus: Multiple myeloma, Waldenström’s Macroglobulinemia, early screening, clinical trials
Provider:Dana-Farber Cancer Institute (Boston)
...

Tim Fenske, MD, MS



Role: Hematologist-Oncologist
Focus: chronic lymphocytic leukemia (CLL) & leukemia and lymphoma | CAR T, targeted therapy
Provider: Medical College of Wisconsin
...

David Miklos, MD



Date: Jan. 2021
Focus: Who benefits from CAR T, ZUMA-2 clinical trial, Stanford's CAR 22 Work
Provider: Stanford Medical
...

Kimmie Ng, MD, MPH



Role: Gastrointestinal oncologist
Focus: Young-onset colorectal cancer, microbiome
Provider: Dana-Farber Cancer Institute (Boston)
...

Farrukh Awan, MD



Role:Hematologist-oncologist, associate professor
Focus:Leukemias, Lymphomas, BMT
Institution:UT Southwestern
...
Mark Lewis, MD, is not just an oncologist, he's a cancer survivor, himself. This gives him a unique perspective as both physician and patient. Hear more about his thoughts on second opinions and importance of self-advocacy. ...

Kerry Rogers, MD



Role: Hematologist, researcher
Focus: Chronic lymphocytic leukemia (CLL), Hairy Cell Leukemia (HCL)
Institution: OSUCCC-The James
...

Nina Shah, MD



Role: Hematologist-oncologist, researcher
Focus: Multiple Myeloma
Institution: University of California, San Francisco (UCSF)
...

Rafael Fonseca, MD



Role: Interim executive director, hematologist-oncologist
Focus: Multiple myeloma, new drug development
Institution: Mayo Clinic
...

William Wierda, MD, PhD



Role: Hematologist, Med. Dir., Dept of Leukemia
Focus: Chronic lymphocytic leukemia (CLL), other leukemias
Provider: MD Anderson
...

Latest on CLL Treatment (2022)



Featuring: Nicole Lamanna, MD; William Wierda, MD, Ph.D 
Hosted by: Michele Nadeem-Baker
Topics: Pirtobrutinib, new oral combinations, venetoclax updates, CAR T
...

David Miklos, MD, Ph.D



Role: Hematologist, researcher
Focus: How MCL treatments have improved, importance of clinical trials
Provider: Stanford Medical Center
...
transplant patient in hospital

David Miklos, MD, Ph.D



Role: Hematologist, researcher
Focus: Role of allogeneic BMT, response to graft versus host disease (GVHD)
Provider: Stanford Medical Center
...

CAR T Cell Therapy in Myeloma



Dr. Fonseca shares his insights on emerging T-cell therapies for multiple myeloma, describing the role T-cells play in our bodies and then focusing on chimeric antigen receptor (CAR) T-cell therapy and bispecific T-cell engagers.
...

How Do Clinical Trials Work?



In this episode, Dr. Fonseca details the process of clinical trials, as well as how patients and families can better understand what goes on during each of the main parts of the study.
...

Joseph Mikhael, MD



Role: Dir. Myeloma Research, CMO at International Myeloma Foundation (IMF)
Focus: Multiple myeloma
Provider: TGen/City of Hope
...

Ruben Mesa, MD



Role: Executive Director, Mays Cancer Center; Prof. of Medicine
Focus: Myeloproliferative neoplasms (MPN)
Institution: UT Health San Antonio MD Anderson
...

Srdan Verstovsek, MD, PhD



Role: Director, Clinical Research Center for MPNs at MD Anderson; Section Chief, MPNs; Prof., Dept. of Leukemia
Focus: Myeloproliferative neoplasms (MPN)
Institution: MD Anderson
...
Favorite0
Categories
Acute Myeloid Leukemia (AML) Leukemia Tagrisso (osimertinib)

Acute Myeloid Leukemia | Michele G.

Acute Myeloid Leukemia: Michele G.’s Story

Michele loved the outdoors and the beach. At 24, she was living a vibrant and active life until she was diagnosed with relapsed refractory Acute Myeloid Leukemia.

In this video series, Michele shares her story of diagnosis, chemo and stem cell treatment, relapse, and the side effects she had to endure. Her continuing journey through AML is such a shining light of inspiration, especially for young cancer patients.

Explore her incredible 4-part story series below. Thank you so much for sharing, Michele!

How I Got Diagnosed

Michele tried to ignore the bruising, tiredness, and shortness of breath.

At 24, she was living an active and healthy lifestyle. Michele enjoyed playing sports and exploring the outdoors with friends.

But the persistent bruises and itching prompted her to several doctor’s visits. And her labs eventually revealed she had Acute Myeloid Leukemia (AML)

Read more→

Going Through AML Treatment

Michele underwent series of IV chemo and an allogeneic stem cell transplant, which means her brother donated his stem cells as a perfect match

The side effects were devastating for her—she couldn’t keep any food down, she lost so much weight, and her hair was gone.

Read more→

Relapse and Treatment

Determined to get back to normal, Michele worked on and off. But her AML relapsed.

Perplexed how come a perfect donor match could not work, Michele underwent another stem cell transplant, rounds of chemo, and then a targeted chemo pill.

Read more→

Her bright young mind couldn’t have comprehended her fate at first, but Michele chose to see the positive side of things.

With the love and support of family and friends, meditation, enthusiasm to meet new friends, Michele now shares her story to give hope and inspiration to fellow young cancer patients.

Read more→

  • Name: Michele G.
  • Diagnosis (DX)
    • Acute Myeloid Leukemia (Relapsed/Refractory)
  • 1st Diagnosis:
    • Age at DX: 24 years old
    • Symptoms:
      • Bruising
      • Tiredness, shortness of breath
      • Itching
    • Tests for DX:
      • Blood tests
      • Bone marrow biopsy
    • Treatment
      • 2 stem cell transplants
      • IV Chemo
      • targeted therapy (XOSPATA)

Inspired by Michele's story?

Share your story, too!

Favorite0
Categories
Lung Cancer Non-Small Cell Lung Cancer Tagrisso (osimertinib)

Lung Cancer Patient Stories | Ashley’s Story

Lung Cancer Patient Stories: Ashley R.

Ashley was leading a career in her local community college, enjoying being around students when she was diagnosed with stage IV non-small cell EGFR+ lung cancer.

In this video series, she shares about how getting her kind of lung cancer was like hitting the jackpot in the lung cancer lottery—the good and the bad in getting diagnosed with such, taking a daily pill instead of infusion chemo and diving into how hey journey changed her perspective and outlook.

Explore her incredible 3-part story series below. Thank you so much for sharing, Ashley!

Getting Diagnosed with Non-Small Cell Lung Cancer

Ashley describes how seeing her OB-GYN doctor for a cyst turned out to be a news and journey that would change her life.

While working a career in her local community college and being an amazing wife and fur-mom, she was diagnosed with Stage IV non-small cell EGFR+ lung cancer.

Read more→

Testing + Targeted Therapy

Here, Ashley takes us through the endless tests, treatment decisions, and how she is actually navigating her new take-a-daily-pill life.

Sad as it is, Ashley tells us about how she even felt like winning the lottery when she found out she’s EGFR+ which means taking a daily pill and no infusions.

Read more→

Living with Lung Cancer (Survivorship)

Finally, Ashley bares how lunch cancer changed her perspective, outlook—how it changed her life.

To Ashley, she was lucky enough to be taking the daily pill road and having a sense of normalcy. And so, despite her odds, she shares the gift of reflections and hopes with her cancer community.

Read more→

  • Name: Ashley R.
  • Diagnosis (DX)
    • Stage IV Non-Small Cell EGFR+ Lung Cancer
  • 1st Diagnosis:
    • Age at DX: 36 years old
    • Symptoms:
      • Tiny nodules on both lungs
    • Tests for DX:
      • CT Scan
      • Tissue removal – sent to Mayo Clinic for genomic testing
    • Treatment
      • Tagrisso (Osimertinib) – 80 mg/day

Inspired by Ashley's story?

Share your story, too!

Favorite0
Categories
Chronic Lymphocytic Leukemia

CLL Diagnosis Stories | Stephen’s Story

Stephen’s Story: CLL Diagnosis & Treatments

Stephen was 45 years old when he felt his first symptoms that sent him to the doctor. After seeing specialists and undergoing several scans, he was diagnosed with chronic lymphocytic leukemia or CLL.

Now on ongoing targeted therapy, Stephen shares the details of his CLL diagnosis story to help others go through their own CLL treatment and experience. He shares everything from

Explore his story below. Thank you for sharing your story, Stephen!

  • Name: Stephen B.
  • Diagnosis (DX)
    • Chronic lymphocytic leukemia (CLL)
  • Age at DX: 45 years old
  • 1st Symptoms:
    • difficulty swallowing
    • fatigue
  • Treatment
    • Rituxan
    • Bendamustine
    • Targeted therapy BTK inhibitor

Episode 01:
1st Symptoms

From being a very fit and active triathlete, Stephen started feeling the first symptoms of what changed his life forever – getting diagnosed with CLL.

Episode 02: CLL Diagnosis

Diving deeper into his story, Stephen shares his insights about patient self-advocacy, and how he managed processing the news of cancer with himself and loved ones.

Episode 03: 1st Line Treatment

With a positive outlook, and by taking it moment by moment, Stephen was able to get through longer-term treatment, including two years of rituxan.

Episode 04: CLL Relapse

While staying focused and positive, and with the support of his family, Stephen confronts relapse and moves on from one treatment to another.

Episode 05: Targeted Therapy

Stephen lends his experiences and insights to getting ahead of his cancer, saying yes to a newer treatment (ibrutinib), how he managed the side effects, and why he finds it so important to use his voice to help others.


Inspired by Stephen's story?

Share your story, too!


Other CLL Patient Stories


Tony D., Chronic Lymphocytic Leukemia (CLL)



Cancer details: ~25% of new cases of leukemia, also classified as non-Hodgkin lymphoma (slow-growing)
1st Symptoms: Lump in back of neck that got bigger in a couple weeks
Treatment: Targeted therapy - orall pill (Imbruvica), takes 3 pills a night

Lacey B., Chronic Lymphocytic Leukemia (CLL)




1st symptoms: Extreme fatigue and elevated WBCs
Treatment: FCR chemo and Venetoclax+R

Sean R., Chronic Lymphocytic Leukemia (CLL)



1st symptoms: No apparent symptoms; went to ER for unrelated shoulder pain
Treatment: Clinical trial, Ibrutinib & Venetoclax

Stephen B., Chronic Lymphocytic Leukemia (CLL)



1st symptoms: difficulty swallowing and fatigue
Treatment: Rituxan, Bendamustine, targeted therapy BTK inhibitor (ibrutinib)
Favorite0
Categories
Cancers Prostate

Prostate Cancer Diagnosis Stories | The Patient Story

Prostate Cancer Stories

Theo W: Getting Through Cancer (Gleason Score 7)

Theo shares his story of getting diagnosed with relapsed and metastatic prostate cancer, undergoing surgery, and radiation.

Having rampant cancer in his family and the African-American community, Theo lends a voice to advocate awareness. early diagnosis and open conversations.

Explore his story below to hear all about his experience and very timely message. Thank you for sharing your story, Theo!

  • Name: Theo W.
  • Diagnosis (DX)
    • Prostate Cancer
    • early Kidney cancer
  • Age at DX: 52 years old
  • 1st Symptoms
    • PCP, PSA of 72
  • Treatment
    • Surgery
    • Partial nephrectomy
    • Radiation


Theo’s Story on Video


Life outside Cancer

I’ve always adopted the mantra: You get to live a day at a time, and you get to choose how you live it. That’s really all we get.

I’m happily married to my wife of 42 years, Beth. We have three daughters. Leanne is the oldest. Randy is a middle child. She’ll tell you the dreaded middle child. Lauren is the youngest. We now have seven grandchildren.

I run a business in Akron, Ohio. My business is to manage money for people that are about to retire or retired, make sure they have enough for the rest of their lives, and leave a legacy to some institution or some people.

Learning about prostate cancer

I have no symptoms of anything whatsoever. My doctor is also a dear friend of mine, and who also happens to suffer from prostate cancer.

During my routine annual exam, he said, “Theo, your PSA is elevated. I’m going to refer you to a urologist.”

I went to the urologist. He got the results of a blood test. He asked me a few questions and said, “Let’s do another blood test in about three or four days.” We did another one and my PSA rose again from 12 to 14 very quickly. So they did the biopsy.

I remember where I was and what I was doing when I got the phone call on a Saturday morning from my doctor at the Cleveland Clinic. Incidentally, my wife had been diagnosed with melanoma the day before.

We’re in the car, and I get the phone call. He says, “Theo, it’s prostate cancer. Let’s set up a time to talk. I want you to interview me, the surgeon, talk to a radiologist, and determine a plan of action.”

I think it was the following week that we went to the Cleveland Clinic. That began the process of my prostate cancer journey.

Getting diagnosed

It was 2003 when I had the first biopsy. That biopsy was inconclusive. It said I did not have prostate cancer.

But it was not the Cleveland Clinic then. It was a local hospital and doctor here in the Akron area, a local nephrologist. Knowing what I know now, there should have been some type of phone call. I left that doctor’s office and there was no follow-up appointment of any kind.

Normally, I guess there should be a three-month or six-month routine biopsy scheduled. I missed a couple of years of getting my annual exam from my primary care physician. So when I went to the primary care physician, he said, “Your PSA is up in the 60, 70s range. You need to see a urologist.”

My doctor, my primary care physician, being a person that had prostate cancer himself and was able to keep his numbers low, possibly should have been more alarmed about it and said, “Get back there every six months.”

I was instructed by no one and at that point, I didn’t know enough about the disease on my own to say get back in there every six months.

I was diagnosed in 2009 at 52. High-end of intermediate-risk and the low-end of high-risk. No staging. That’s with aggressiveness and that’s pretty aggressive, especially at 52.

Family history of prostate cancer

No. My dad did not. His dad did not. My brother did not and he’s an older brother. This came out of left field on us here.

Receiving the bad news

He looked at me and said, “Don’t panic.” He literally said, “Mine has been up close to 1,000.”

He took a new prime shot and took them the rest of his life and his PSA remained low. He did not die from prostate cancer. He lived into his early ’90s. 

I thought about two things. He’d always told me in my early 30s that I had an enlarged prostate. In my mind, I said, “Maybe that could be part of the PSA issue. No one is being really urgent about it, getting back in there after 2003.” 

I was hoping so I said, “Maybe it’s just a high PSA because of that.” Of course, I was very nervous that it could be prostate cancer.

»MORE:Patients share how they processed a cancer diagnosis

Describe the biopsy

Be grateful that times have changed since my biopsy then. Currently, they give you a shot literally in the prostate that numbs it, and so it’s not painful. That was not the case with my biopsy. There was nothing.

I think they do three to four snippets per quarter. It’s in quadrants. By the time you hear the clip, it’s too late. It’s a very painful, uncomfortable but short procedure and process, which has changed now.

Getting the results

We got the call. The surprising thing is neither one of us broke into tears right away.

We ran a stoplight, actually, when I received the information. We looked at each other. I think one of us said, “What are the chances of both of us having cancer at the same time?” That’s how our relationship is. She tells me even to this day, “If cancer doesn’t kill you, I might.” That’s the kind of relationship we have.

We finished our errands. Of course, we kept the conversation going, and talked about what the next steps may be, and that we had to call the girls. They were naturally pretty devastated. The ones that were close to home came over as quickly as  they could.

We just started plotting out when and what. They were all for surgery. My whole family was, I quite frankly was not interested in surgery at all, wanted to do the radiation instead because it was less invasive.

At the end of the day, I never really had peace about it.  I opted for the surgery.

Breaking the bad news to the family

It’s difficult as the process was literally to put everybody on speakerphone and called everyone.

We did joint calls with all of our close friends, our pastors, our family, and our parents. That really took a few days because at that point, there’s some crying on your own you’re doing. You’re physically exhausted and you’re saying, “We’ve talked to eight people today, and let’s just pick this up tomorrow.”

»MORE: Breaking the news of a diagnosis to loved ones

Just make sure you talk directly to your closest friends whether it’s phone or face to face. You do not want them to find out secondhand at all. They show up and they go way beyond the call of duty to make sure you’re okay.

What support was most helpful

You have to make the assumption that people want to help. I’m more of the person that is the helper and less likely to call and say, “Help.”

We would meet a group of guys at Einstein’s for breakfast. Leanne can tell you about this. She says, “I don’t believe you have 10 to 12 guys that meet every morning and just talk. No, guys don’t do that.”

Because I was at home with a catheter, I couldn’t get out. One friend says, “Is there anything I can do for you?” I said, “Yes. Go to Einstein’s, get me a cup of coffee and a bagel, and bring them to my house and sit with me and have breakfast.” That did as much for him as it did for me.

People just want to help. That’s a story is an example of you needing your friends, and your friends needing you. The opposite end, for kids, it could be scary.

Antonio, Leanne’s son, was five. He walked into the library and saw me in my bathroom, sitting there. I think Leanne had to tell him, “It’s okay to go over there and sit in his lap. He’s fine. He has cancer. Number one, he’s not going to get on you. Number two, he’s not fragile at this point. It’s perfectly okay to go sit in his lap.”

He was very cautious. With kids, when you see them, you need to tell them, “I’m okay. Come over here and give me a hug.”

Why was that an emotional moment for you?

I’ll tell you exactly why. “I want you to look at this chart.” He literally put his head down and wouldn’t look at me.

I took the chart and I said, “Is this me right here?” He says, “Yes.” I said, “I’m at the high-end of intermediate-risk and the low-end of high-risk.” I said, “This is saying the average life expectancy is 11 years?” He says, “Yes.” I said, “Explain that to me.” He says, “Well, eight years will be great, two years you’ll be on hormones, last year you’ll be miserable.”

The very first thing I thought was Antonio is five. Where will I be when he’s 16? I did the calculations and I said, “I’ll live long enough to see him turn 16 and get his driver’s license. If I make it that far, I’ll be fine.”

That was my first thought. Will he be driving? Will I get to see him drive? Will I get to see him become a 16-year-old?

Of course, we’re beyond that now, but that was my first thought when I calculated those numbers.

First of all, if they’re really close to you, you’re more forgiving.

Most times, people don’t need to say anything. Just an, “I’m sorry. I feel bad. I’m here for you. If there’s anything I can do, let me know. This is terrible. This is devastating. I don’t know what to say. I don’t know what to do. I feel horrible.” Leave it at that, for the most part.

Treatment Decisions and Surgery

I have a very good friend in Chicago who incidentally was also going through prostate cancer.  This gentleman was retired. I called him up.

He was at his vacation home. He said, “All the treatments are pretty much the same success level. If I were you, I would strongly consider radiation, because, by the time you add up all the side effects, that one in your situation with your PSA number,that’s what you should do.”

Monday morning at eight o’clock, my cell phone rings. “Hi. I’m Dr…. head of urology at the Cleveland Clinic.”  

I said, “Well, doctor, he told me that you said radiation makes the most sense.” He goes, “No. I don’t think so.”I think here at the clinic, you need to do surgery because if you do surgery and you have a relapse or recurrence, then we can do radiation.” He said, “We do a nerve-sparing surgery, so you don’t have issues going down the road.”

Once I heard that I said, “I don’t know where this is going, but I’d rather have more than one shot at it if this is not going to go well.” That’s what I did. I did the surgery.

Fears with surgery

You’re always concerned about your sex life going forward. But a nerve-sparing surgery makes it more possible for a man to maintain an erection, to have sex. That’s a big concern for a lot of guys.

I did have one of my buddies tell me, “Hey, at the end of the day, your wife may prefer just a lot of cuddling and you will be alive. That was great advice. 

Cleveland Clinic made sure to tell me that. It was also one of the discussions that I had with the second opinion doctor. He kind of felt like if you went with the radiation, then you would have less issues in later and it would not affect your sex life now. That was his reason for it.

He says, if we’re going to come up with the same success rate, then why impact your life in that way now?

Then again, as I said before, for me, it was more important to do the surgery, and then the added bonus was when he said they could do the nerve-sparing. I said well, okay then that’s it. That makes it less of an issue.

Describe the surgery

My doctor said this is going to be a pretty routine surgery. We will be using robotics that will help with less bleeding and a much quicker recovery.

I am told that my father accosted him when he came out because the surgery ended up being about six or seven hours. It was substantially longer than it should have been, and my father just was not too happy about that.

He told me the recovery would be three to four days and I’d be out of there. He said, “You’ll have a catheter for several weeks, come back and we’ll take that out.”

He said, “You should be off and running, for the most part. You can start back to work in a month and a half or so.” He felt that the surgery would be pretty routine, with very few complications that ended up not being totally true.

But you never know until you get in there. So I’m glad he did. Things took a little longer, the surgery and the recovery. Getting out of the hospital took longer than normal.

How long was the surgery

Three to four hours.

He always talked about the nerve-sparing and one of my seminal vesicles actually had cancer, so he had to remove that, and then the margins. When you do the surgery, you remove lymph nodes and they usually do a few, but they ended up doing 10 or 11 removals of those. That’s what took the time.

The recovery was supposed to be four to five days, but I stayed for eight days in the hospital.

How you were able to get through

My issue was my creatinine levels were higher than they needed to be, and so they were worried about kidney function. It took a while to get those belts under control.

My advice is, if you’re in a hospital, you need to have your family guard how often people come and go.

They really have to look out for you in terms of your rest and be able to delicately say, “He’s glad you came to see him, but he really needs to sleep right now, because I’m sure you know, you do not get any rest of the hospital.”

Every three to four hours, someone’s coming to do something to you, and so therefore the only time you get a rest is when you get out of the hospital.

They’re going in at all hours of the day and night, checking your blood pressure, checking all the different stuff you’re hooked up to.

Post-surgery Care

One of my main issues is I could not pass gas. When I finally did, no one was in the room but me. I got my phone and I text to my wife. It’s a girl.

She said, she read it out loud and everybody knew what it meant, and everybody out there just erupted and they want you to go. I tried prune juice, everything and nothing worked. They said you cannot leave, and so that was the last thing I had to do before I left. After that, I went home.

Taking it lightly helps. You just have to.

I did have another kind of strange experience. There was one person that I have a temporary rift with. But sometimes when you’re sick, they feel a need to come around and try to fix it all before.

She told me that someone wanted to come and my blood pressure went up. She had to kindly tell them no, and that’s difficult. But I will say people will come to see you for the right reasons and people will come to see you for the wrong reasons.

»MORE: Read more patient experiences with surgery

Dealing with extended period of time at home

I think I ended up going two weeks longer than I should have, but I thought the catheter was great. You don’t have to get up to go to the bathroom because you’re sore after surgery.

Every time I tried to lift myself off of a chair, it’s just painful. So with that, I didn’t have to get out of bed and go to the bathroom at night. I was reluctant to let it go but I had to.

When I found out it didn’t come out the day it was supposed to, it quickly became irritating because I was mobile. I was in less pain, and now it became an inconvenience because I can’t go running around outside and although I did around the house. I was living in the country at the time.

The last week or so was really, really hard. “Just get this thing out.” Initially, it was very convenient.

If was supposed to have it for two weeks, I think I had it double that. If it was supposed to be a week, it was two. But I’m pretty sure it was close to a month that I had that catheter.

I have to just be careful of infection, just have to keep it clean. Other than that, I didn’t have any issues with it whatsoever.

Radiation therapy

First of all, I made a very dear friend in this process. I was going to my first radiation treatment and I got out of my car in the parking deck. I’m about 6’7, and Black obviously, and there was this 5’7 White guy who got out of his car and we both went through the door out the deck.

We went to the building for cancer treatment. We got on the elevator.  He said, “Are you following me?” I said, ‘It depends on where you’re going.”

He said, “I’m going to start my radiation treatment for cancer. You’re the last person I want because you should not be following me.” I said, “I actually am following you because that’s where I’m going too.”

We’re dear friends up to this day. I had a buddy who got treatment sometimes around the same time.

It was treatments every day, Monday through Friday for seven weeks.

At that point in time, my youngest daughter worked downtown near the clinic. She would just show up unannounced. I never knew what day she was coming, what day she wasn’t coming.

She wouldn’t tell me. She would show up and I would be in there for probably 20 to 30 minutes. It wasn’t long. Out and back in the car and back home or back to work.

It was an inconvenience from a travel standpoint but there was a certain amount of comfort.

 The hospital is about a half hour from my house. It was a highway drive, mostly. It was a good time.

Until this day, I get comfort when I drive under the main campus of the Cleveland Clinic. Seven weeks out, you know you’re done and you ring the bell and you just hope your PSA doesn’t climb.

Describe the process of radiation

For prostate cancer, you just get on the table, they put a tarp over you, you pull your pants down to your knees. You’re on this flatbed and the radiation machine just goes around. It actually tilts and goes around and hits specific areas that they’ve targeted and certain margins outside of where they think the prostate cancer may have spread to.

You see the same three or four nurses so you develop relationships with them.

That’s really the process. You’re done and you leave and go back to your life.

Side Effects

I had no side effects until the last two weeks.

I would have some burning during urination. Women have urinary tract infections so they may be used to that. 

That was my first experience. It gets to the point where you tell yourself you don’t want to drink water because you don’t want to have to go to the bathroom, but you have to.

You let them know and then they give you things like pills you can take to help with that and they did work. It was very surprising when I first started and I was very glad to take those pills after I got to.

The doctor did tell me that could happen. I was actually surprised that it took as long as it did and thought maybe it wouldn’t, but it did.

Outside of that, no burns, no rashes, no irritations of any type.

The issue with me was when they check my PSA after the surgery and it started to rise again. That’s evidence that I have a recurrence. We don’t know how far.

They looked at the surgery and said, “Let’s do an additional margin of X.” They feel they can go so far before they start affecting the lymph nodes. Once they affect the lymph nodes, then you have a whole different set of side effects.

The radiation itself was targeting a specific area with the idea of not having issues with your lymph nodes down the road.

Signs of recurrence

I think when it got up to about two, it was when they said, “Okay. Hey. We need to start doing something,” Because, at one point, it was almost undetectable right after the surgery. Then within two weeks, it started declining.

Addressing the recurrence

It was, “Hey. Let’s start every three months and see where this goes.”

Unfortunately, it went from two to four and from four to six, and then they said, “You’re going to be dealing with this the rest of your life. You need to talk to a medical oncologist.”

I went to his office, my wife and I, he reared his chair back and put up his cowboy boots on the desk and he says, “Do you know why you’re here?” I said, “Yes. I have prostate cancer and my PSA is still climbing.” 

He goes, “Do you understand that from now on, we’re monitoring this and that you are going to be dealing with this the rest of your life?” I reluctantly said, “I do.”

He started out and he just wanted me to know the gravity of it. We’re just going to be maintaining this for the rest of your life, and that’s when it really hit me.

When the doctor said, you’ve got eight good years, two years of hormone treatments, your last year is miserable. That’s when it hit me. I said this really could be me.

Managing a chronic disease

That’s the case, it was a chronic disease. He told me what we would need to introduce, when, and what things they would use, and then went on through, talk to them about clinical trials.

He said, “For now, we’ll monitor it, and then that’s what starts the CT scans, the bone scan once a year, and I’d heard about kidney cancer also. I was getting the chest X-rays and then all ended up fine. So I’ve got to stop the checks

2nd Cancer

Getting diagnosed with kidney cancer

I was diagnosed with kidney cancer five years after the radiation. They removed it and of course, the concern is if it returns, it could spread to the lungs. So I have to do the scans, basically chest X-rays because I was already getting a CT scan.

That kind of doubled for both the kidney issue and the prostate issue. I had to get the X-rays and five years and that was done. That was totally successful, and I had a recurrence there. I’ve had some cysts on my kidneys that I didn’t know I had until then, and so they’ve watched them and that’s how they discovered it.

It was at a very early stage.

In fact, I had a colonoscopy and was out to dinner, getting ready to go to a Todd Rundgren concert. My side started hurting me so off to emergency I went, didn’t go to the concert.

They said, “You have cysts on your kidneys. That’s not why you have pain, though. You have pain from the gas that is stuck in your body from your colonoscopy. But you have cysts in your kidneys and probably want to get those watched.

That’s when I started getting them washed and not too long after that, they figured that it’s all that the colon cancer and not the kidney cancer.

I had a PSA check every three months, every half a year, every six months a CT scan, and then every 12 to 18 months a bone scan. That’s just because they’re watching to make sure it doesn’t spread to the bones.

So far, it’s been all good.

PSA levels so far

It’s crazy. They continue to climb until 2019, it got to 52. Since 2019 it has gone up and down, which is really strange.

It sits at 57 now, so I called my doctor because I was supposed to have a bone scan in December, and said, “I don’t see a bone scan on my chart. Shouldn’t I be having the bone scan about now?” He said, “Well, think about it. In 2019, your PSA was 52, and now it’s 57. Percentage-wise there has been very little movement. I don’t see any reason to do one right now.”

There’s a couple of philosophies, and his philosophy is if hormone treatments after metastasis do not prolong your life any more than taking hormone treatments before metastasis, why subject yourself to the side effects?

That’s what we’ve done. I have not started hormone treatments at all, and they have not found any metastasis at all.

 Now I did mention my dear friend, who I’ve met, the little 5’7 guy, and he’s a worrywart. He started his hormone treatments when he hit 10, and so it’s different for different people. I talked to him often, and he tells me, “Theo, I’d be a nervous wreck.”

I said, “I know you with time and I’m glad you’re taking hormone treatments. It’s different and the doctors are different. I have a different oncologist now than I did then—Dr. Timothy Gilligan. He’s a white gentleman, but he specializes in prostate cancer for African Americans.”

I really feel like I’ve got an individualized treatment plan that is geared towards the quality of life, according to the risks that the patient wants to take. You just have to say, “Hey, I don’t feel like taking any additional risks by not starting these hormonal treatments. I just don’t, I haven’t.”

I think Lan said there’s a Dr. Pan. I can’t really recall the guy’s name, but he knows a doctor that’s out there at the City of Hope, and the previous doctor ended up taking a job somewhere else. Then I just got on the Cleveland Clinic website and fell upon his name and then called him and said, hey, I need you to come to be my doctor.

Homeopathy and naturopathy

What supplements to you take?

I have a bunch of supplements that I take, but the real key is a machine called a hocatt. It’s designed to get in there for about a half-hour.

They shoot oxygen and carbonics into your nose which drains you, but more importantly, they raise the temperature. It gets very hot, and the idea is it stimulate your white blood cells because it says my body has a fever. I need to run and attack anything that is suspect, and I get that.

I go every Friday at 2:30 or three o’clock, what’s called my spa treatment at the end of every week.

They told me it will raise my PSA temporarily, so I don’t want to get my PSA check when I get out of this thing, but overall, it should slow down the process and give my body the best fighting chance that it has.

 I also take vitamin D and fish oil.

Deciding on integrative treatment

I just did it and then told them, and fortunately, Cleveland Clinic is adopting some of that on their own at this point. He’s perfectly fine. There’s no, “Hey, you know, what’s in these supplements, do you know what you’re taking? Is this going to counteract what we’re trying to do here?”

No resistance, judgment, or anything of any kind from him at all. It’s been great.

When to start hormone therapy

For him, it’s just whenever the bone scan shows metastasis. It’s cut and dry with him. I did ask him a question. I didn’t want to ask him, “Doc, at what point in time are you pretty sure you’re going to find something?” But he said at 50.

The next time I see him after I ask him. I’ve been over 50 for a while, especially if my next bone scan is clean. I said, what does that say? I don’t know what that says, but he says, he goes, “Most people were going to find something when they start getting a PSA of 50.” I’ve had scans since it’s been 50 in 2019.

Managing “scanxiety”

I don’t do very well with that one because of my charts. If I get my PSA checked today, I know I’m probably going to get an answer within 24 hours.

If I get up to go to the bathroom at 3:00 AM, I’m checking my phone and, there’s a certain amount of anxiety once you do the password, I get an email that says test results. That’s also stressful.

I had a very dear friend who died from prostate cancer. It was caught in the latest of late stages and did a lot of experimental stuff.

He told me the best advice I’ve had. He said, “You have to thoroughly enjoy the highs.” You’ll have the highs and you’ll have the lows. But you got to celebrate every high you’d get.

Whenever my PSA stays the same or goes down, I keep a chart. I look at that graph and I look at how fast it goes. If it’s doubles in three months, you’re in trouble. I’m always looking at what rate is it doubling? Is it nine months? Is it 10 months? Is it a year? That affects me emotionally.

You don’t really want the information, but you do. It’s a mixed bag there. I don’t do a good job of handling that part of the anxiety.

»MORE: Patients describe dealing with scanxiety and waiting for results

Caregiver support and survivorship

You keep your plans and your dreams until you can. From a caregiver’s standpoint, being the guy messes with my wife’s security.

We do talk about that. Her statement now is, “You may end up living longer than me.” That could be true.

I don’t know. We don’t know. You have to have people, whether it’s a spouse or a good friend, or both, that you really can talk about everything you’re feeling.

We’re both type A personalities to the point that, if I get up in the middle of the night to go to the bathroom, I’ll come back and my pillow will be on the floor, and she’ll say “Go make some money.”

I’m like, “It’s 4:00 am, I can’t. Let me sleep for another hour or two.”

Humor has a lot to do with everything in terms of hightailing. Find somebody safe with whom you can express how you really feel and will let you express that.

I don’t get a lot of sympathy and I don’t want a lot of sympathy. I don’t feel like I need it, there may be a time that I do.

Life is normal, because as long as you are able to, you still get to choose what you’re going to do and what your outlook on life is going to be in the end.

Some friends and I have a saying, “Your tombstone should have three dates on it, not two dates—the date you were born, the date you stopped living, and the date you died. Hopefully, the last two will be the same day.

My wife has been the best thing for me. Because if I wanted to have a pity party, which I typically don’t, I couldn’t have one anyway.

Having children as support

Leanne and I are a lot alike, and we do things without really talking about it a lot.

She didn’t really tell me she was going to start doing the research. I found that out almost secondhand. That was the inspiration for it.

I remember when she was in prep school in high school and brought home straight A’s, the first semesters as a freshman and I asked her, “Do you feel any pressure to get straight As?” She said, “No. This is okay.” “Good. That’s all I want to know.” I’m floored.

She’s never been afraid of things. She likes the limelight. I’m just impressed by her all the time. I’m just, “Damn. She’s an impressive woman.” That’s why I’m proud of her, that she is on a mission.

Advocating in the community

We do now, but nobody talks about it until you get it. Then all of a sudden, out of the woodwork comes “Well, I had prostate cancer three years ago.” “Well, I had prostate cancer four years ago.”

You’re walking around with all these guys, 3 out of 10, 80% African American, which have had it and nobody knows anybody else has had it. Now they’re support groups, that type of thing.

Not having it in my family, I was not that exposed to it.

Then having a doctor that had prostate cancer that was doing okay, and died in his ’90s and not from prostate cancer. There just wasn’t as big of a fear of it, but then once I got it, and you start looking around, you’re like, “Whoa, wait a minute, this is everywhere.”

At the Cleveland Clinic, they told me they had a kid in his late 20s, a black kid that had prostate cancer. Do you start checking in your 20s? They say no. I learned about the process after I was already in it, and the numbers after I was already in it.

Conversations in the Black community

Men generally, but especially men of color, don’t go to the doctor. A lot of them don’t. Some of it is because they don’t have insurance. Some of them are macho. Some of them fear the doctor. They don’t want a rectal exam.

I think getting out there like getting your blood drawn. If you can do that, and you could start doing that when you’re 40 it’s going to save your life. I think the education process.

 You’ve got to look at the hand of the government with the Tuskegee issues saying, “I don’t know if I can trust.” Which by the way is a whole other story with COVID, because I’m finding more middle and upper-class white men not wanting to take it, which is strange to me.

A lot of my black friends have gotten the shots, I’ve had my first shot. That’s a whole another story.

Just the lack of trust for doctors, the absence of African-American doctors.

Again, I’m 63 now, and so I’m talking for my age group. It may be different for people 20 years younger than me, but those are some of the reasons.

My mom to this day calls me when my dad goes to the doctor and asks me to go, because he does not want her in the room, while she’s in there with a doctor.

The last two times, I told her,” Yes, that’s the macho thing.” It’s the “keep her in the dark” thing. So if I get bad news, she doesn’t have to think about it.

I just convinced her, “You just barge in there and hear what the doctor has to say.” That’s what she’s doing now. She’s 91 and he’s 88. There’s just this fear of doctors.Is there anything that you think the industry,  like healthcare industry, Could they do something differently to reach people especially in communities of color, who may have trust issues, or lack of access even to health care with insurance barriers, this kind of thing.

What needs to change

I asked Leanne about that at one point in time. Can’t some medical association or some medical say, “Hey, all the doctors in Summit County, and such, every African-American that comes in here, tell them that we have to do a blood test. We have to draw blood as part of your health. Not just for PSA.

I don’t know if that’s an oversimplification, but it should be almost demanded that doctors do that for people that are at risk. Because that is the first step; it’s the least costly, it’s the least invasive. It’s the least threatening thing you could do that gives you the information you need to take care of yourself.

Prostate cancer is one of those cancers that are very treatable if you can catch it. My prostate and kidney cancer was that example. They caught it quickly, did it and I’m done with it.

Cultural differences and doctor training

I think it’s a great conversation. The way that conversation in a perfect world should have gone is, “Theo, your PSA is at 14, that’s high. You are a candidate for getting prostate cancer.

However, the success rate if we find it early is you basically get to live your life as if you never had it. As scary as this sounds Theo, I need you to come back every three months, do this so we can catch it and do something about it and then you can have a normal life.”

I would have been scared to death walking around feeling I’m a walking prostate cancer. That’s a whole different psychology, but coming out on the other end of that with less risk at the end of life. That’s a difficult discussion that the doctor should have with the patient.

Opening the conversation of risks to kids and grand kids

I have not, but I will. I’m 62; 20 years puts me at 82 if I live that long. 17 put him at 37. I’ve done the math.

We’ll have the discussion before he’s a candidate for getting diagnosed with prostate cancer. Whether that’s him and I talking over an ice cream cone, or me telling him goodbye in his life. I feel there’s time, but having had this discussion with you, I’ll approach the subject with him now. Why not?

The critical part is you’re at a higher risk than most because I’ve had it. It is 100% curable if they catch it on time. Just stay in front of it. Promise me at 35-36, if not sooner, that you’ll get an annual exam. That if you do not hear from your doctor about a blood test by a certain age, you’ll ask for it.

Normalizing the conversation

We’re all interested in living as long as we can. Part of that is taking steps to assure that. One of the easiest things you could do is just go get an annual physical exam.

When you get one, ask for a blood test to find out what your PSA is. I don’t care what number they give you, you want to know that number today, more than you want to know that number tomorrow.

Diversity in clinical trials

I think I would try, and my doctor, Dr. Timothy Gilligan, that’s another thing. He is well on top of clinical trials and will suggest one at the appropriate time.

I am all for anything that could prolong and improve the quality of life.

With prostate cancer, chemotherapy does not. Chemotherapy with a lot of cancers is curative. I don’t feel that I would opt for that if they said, “We can give you three more months.” I’d rather have the quality of life.”

Now, if I can go into his office and he tells me, you have to start chemotherapy, all bets may be off, I may be retracting everything saying right now because, at the end of it, everybody wants to live as long as they can.

I’ve seen a few people elect not to get chemotherapy. I looked at them and I said, they went out the way they wanted to go out; they looked the way they wanted to look.

I’m also concerned about what view will your grandchildren have of you before you die? What will you look like? I know that could be vain, but I am concerned about it because those imprints stay on your life for the rest of your life.

I think we should go online and look for doctors that talk about doing clinical trials and specialize in dealing with African-American prostate cancer. They’re out there. I had four that I was looking at, and that’s why I chose him.

All of us get a day at a time. Relationships are the most important thing in this world, period, and that’s it.


Inspired by Theo's story?

Share your story, too!


Other Prostate Cancer Diagnosis Stories


Clarence S., Early Stage



Cancer Details: PSA levels fluctuated but were never extremely elevated, cancer contained to prostate
1st Symptoms: No symptoms, caught at routine physical with PSA test
Treatment:Radical prostatectomy (surgery)

Steve R., Stage 2



Cancer Details: Started at stage 2 and gradually progressed to stage 3, and then to stage 4 with metastasis to lymph nodes
1st Symptoms: Rising PSA score
Treatment: IMRT (radiation therapy), brachytherapy, surgery, and lutetium-177

Al Roker, Gleason 7+, Aggressive



Cancer Details: Aggressive but caught early
1st Symptoms: No symptoms, caught at routine physical with PSA test
Treatment: Radical prostatectomy (surgery)
Bruce

Bruce M., Gleason 8/9, Stage 4A



Cancer Details: Staged Gleason 6/7 pre-surgery, post-surgery changed to 8/9, PSA level at 27
1st Symptoms: Urination changes, brother's prostate cancer diagnosis
Treatment: Radical prostatectomy (surgery), salvage radiation, hormone therapy (Casodex & Lupron)
Dennis Golden

Dennis G., Gleason 9 (Contained)



Cancer Details: Staged Gleason score 9
1st Symptoms: Urinating more frequently middle of night, slower urine flow
Treatment: Radical prostatectomy (surgery), salvage radiation, hormone therapy (Lupron)

Theo W., Prostate Cancer, low-end high-risk



Cancer details:
Low-end high-risk prostate cancer, early kidney cancer
1st Symptoms: PSA level of 72
Treatment: Surgery, radiation

Jeffrey P., Gleason Score 7



Cancer Details: Diagnosed at 59, biopsy had not detected it
1st Symptoms:None, routine PSA test, then IsoPSA test
Treatment:Laparoscopic prostatectomy
Favorite0
Categories
Hematology Medical Experts Myeloma Oncologist

Dr. Nina Shah, Multiple Myeloma

Nina Shah, MD

The Latest in Multiple Myeloma Treatment & Clinical Trials (2021)

Nina Shah, MD brings hope to multiple myeloma patients with news of standard of care trends and updates.

She lends here her expertise in managing multiple myeloma and experience improving patients’ quality of life.

Read Dr. Shah’s insights on the treatment decision-making process, patient and provider communication, and more.

Thank you, Dr. Shah, for the work you do and for sharing your incredible voice!

Dr. Nina Shah on Video


Introduction

Introduction of you and your work

My name is Dr. Nina Shah and I’m a professor of clinical medicine at the University of California, San Francisco, or UCSF. That’s where I focus mainly on multiple myeloma clinically.

That’s what I see in my clinic, but on the inpatient side, we see everything including leukemia and lymphoma. I’m particularly interested in immunotherapy, as it relates to multiple myeloma and cellular therapy.

This would include things like chimeric antigen receptor T-cells, or CAR T-cells, as well as natural killer cells, dendritic cell vaccines, antibodies, and T-cell engagers. All those exciting immunotherapies that are coming down the line.

I also have a secondary interest in patient experience, including quality of life, patient-reported outcomes, and some life coaching applications that we’re trying to use to improve patient experience.

Understanding Multiple Myeloma

What is multiple myeloma in human terms?

Multiple myeloma is a cancer of a cell called plasma cell. A plasma cell is part of your immune system. Normally your immune system is made to fight viruses and bacteria and one of its soldiers is called a plasma cell.

Particularly, plasma cells are supposed to produce antibodies, which we’ve heard a lot about recently. COVID antibodies, antibodies to zoster, all these things. 

These antibodies are proteins that help you fight and tag bad things so your immune system can know to kill those things.

In the case of multiple myeloma, one of these plasma cells goes haywire. It grows out of proportion to the other cells, and that’s really the definition of cancer.

When one cell gets selfish and replicates its own clone, it takes up the resources of the other cells. That’s what happens in multiple myeloma.

One plasma cell grows and it starts taking up the space in the bone marrow. It starts producing a protein that eats the bone around it and that’s why people can have holes in their bones, or lytic lesions.

Then the protein that it produces—that antibody is now one antibody. It’s not a variety of antibodies. It’s just that one clone.

That’s why you will often hear the term monoclonal protein or monoclonal or clonal protein, M protein. That’s something that we can use to measure how many plasma cells there are.

It’s like the petals on the flower; the more petals you see around, the more you know they have flowers and that’s what we often use to measure in the blood.

The proteins that are produced from these cells can be in such high quantities that they also can have detrimental effects. That’s why some people with myeloma will say, “Well, my light chains were really up.”

That’s part of that M protein, those antibodies, and they can clog up the kidneys.

You hear about multiple myeloma as a disease that affects almost every part of the body—the bones, the kidneys, the blood system, and it all comes from having this one immune cell get a little out of whack. It’s supposed to help you, but in this case, it’s harming you.

What are the chances of it relapsing or being refractory

Unfortunately, multiple myeloma is considered an incurable disease, but it is a disease that one person can live with for a very long time.

We have patients who’ve lived 10, 15 years with it. It really depends on where that myeloma is going and what it’s like.

Sometimes we can predict that and sometimes we can’t, but on average, our standard myeloma patients are living longer than 10 years, at least, because we have new therapies.

What I tell all myeloma patients I meet is that, “You’ve been newly diagnosed and we’re starting therapy on you. We’re hoping that we can stretch out this time as long as possible so that we can have this first remission, meaning the first time you have a response that lasts as long as possible so that you don’t have to worry about it and you get back to your life and start being a person and not a patient.”

First Line Treatment

First line of myeloma treatment

For anybody who’s been newly diagnosed with multiple myeloma, it is very overwhelming because there’s a lot of information about what this disease is, then what is your life going to look like, what treatments are there and how can you predict what’s going to happen to you.

Those are all unknowns and if we had a crystal ball, of course we would be able to tell you as best as we could, but we often don’t know.

Combination (induction) therapy

What I usually tell the patients is that we’ll start off with some combination therapy. This is called induction therapy, and it’s usually a three-drug combination.

The backbone of that usually is some steroids, like dexamethasone, the drug everyone loves to hate, and then two other drugs. We usually combine those three drugs and we give them for three or four-week cycles. Those are pockets of time.

VRd induction therapy

There can be a variety of choices that we may give upfront, and this is really dependent on what the physician’s style is. The standard treatment is VRd, or Velcade or bortezomib (they’re the same thing), Revlimid or lenalidomide, and dexamethasone.

VRd side effects and management
  • bortezomib (Velcade) side effects: neuropathy or numbness in hands and feet
  • lenalidomide (Revlimid): fatigue, diarrhea
  • dexamethasone: energy level changes

The major side effects from the bortezomib or Velcade are potential neuropathy, or numbness, tingling, and a weird sensation in your hands and feet. A lot of times patients will say it’s worse at night.

We’ve tried to get around this by changing the dosing schedule and doing it weekly instead of twice weekly, although it was originally approved in a twice-weekly fashion. Sometimes, for older patients, we may reduce the dose.

The Revlimid often can make patients experience fatigue or diarrhea, but it’s generally well-tolerated when you do it upfront and when newly diagnosed. I would say more of the Revlimid symptoms happen after the transplant.

The dexamethasone can make you nutty. It’s like people are cleaning up their house all day long on the first day, and then on the second day, they crash. Their spouses now avoid the dexamethasone day.

Alternatives

There are other alternatives to the first one. Sometimes instead of using Velcade or bortezomib, we’ll use a drug called carfilzomib. This also works in the same mechanism of action, but has been studied in later lines. It’s also a very effective drug that has another side effect. It affects the blood pressure and has potential slight effects on the heart.

For example, if a patient comes to me and they’re healthy, except they have diabetes and they have really bad neuropathy from their diabetes, maybe a better choice for them would be the carfilzomib and not the bortezomib with Kyprolis and not Velcade, as their trade names.

That’s how we go about thinking about the side effects of these therapies.

High-dose chemotherapy and autologous stem cell transplant

After several cycles, if you’re healthy enough, we often would take you to a high-dose chemotherapy autologous transplant, or just transplant for short.

Stem cell transplant is what I would consider to be part of the standard of care for newly diagnosed multiple myeloma patients. You may not hear that from every doctor, but I like to do transplants.

The reason for that is that while those three drugs at the upfront, the Velcade, Revlimid, and dexamethasone, are like the soap and sponge for cleaning a dirty pot.

But the melphalan, which is the transplant drug, is the Brillo pad. It really digs in and gets the deep myeloma cells that you couldn’t get. It’s another way of being smarter than the myeloma.

This process involves two things. Since we can’t give you a very high dose of chemotherapy without damaging normal cells, before we even give that dose of chemotherapy, we have first to collect blood stem cells so that your blood will recover from having that dose of chemotherapy.

We always initially do a stem cell collection. This is an outpatient procedure and can take about a few days. We put a big catheter, usually in your chest wall, or a big IV in your arm. Then we take out a bunch of blood and filter out those stem cells after having given you some medication to get those to your blood.

Usually about a week for it between the injections and the procedure. Then after that, we do part two, which is the actual transplant. That’s when patients are, in our case, admitted to the hospital, although you can do it as an outpatient.

They get one dose of this chemotherapy. Two days later, they get replaced with those stem cells. We thaw them and give them just like a blood transfusion; it’s pretty anticlimactic.

For the next two weeks or so, these patients recover from these traditional chemotherapy yucky side effects:

  • nausea
  • vomiting
  • diarrhea
  • hair loss
  • infections.

Of course, they need transfusions because we’ve completely obliterated the blood system and we have to take time for those stem cells that we gave to come back and grow and repopulate. 

That’s the time that you’ll feel those traditional chemotherapy side effects that are less present with the newer Velcade, ReV/Dex.

Those are the new chemos, but this is like the old-school chemo. It does its job because we know that patients who get transplants early and get it upfront as a planned procedure actually do better as far as how long their disease is in control.

Maintenance therapy

After that people would generally go on to maintenance therapy, which right now is just one pill of low-dose lenalidomide, also known as Revlimid.

That pill and that factor can go on for five years or as long as they can tolerate the revlimid. It’s not always easy to tolerate it, but most of my patients can tolerate some of it.

You can go back to work, go back to having a life, go back to their family life. 

»MORE: Read more patient experiences with Revlimid (lenalidomide)

Shared Decision-Making

What to ask your hematologist 

As far as understanding what they should know and what they should ask their doctors, it’s important to know what kind of myeloma you have because you want to be able to follow your own labs.

Being able to follow your own labs when you get them is an empowering thing.

Sometimes it’s an anxiety-provoking thing, but I find in general it’s empowering because you and your doctor can have a really good conversation about trends and where things are going.

You feel like you’re really a part of the decision-making, which you always should be.

The second thing is that it’s important to know what your cytogenetics or FISH studies are. These are DNA characteristics of the myeloma cells and how those myeloma cells are prone to grow or not grow based on what we find in these studies. That can help us determine the risk. 

When we talk about risk, it’s how aggressive the myeloma really is, how likely it is to come back sooner than later. These are all parts of the discussion that are important to have with your doctor at the time.

There’s also other parts of discussion you want to have like supportive care. Other things you should be doing, for example, to make your bones stronger and to make you stronger to go through this process.

Higher risk versus standard risk

When we think about high risk versus standard risk in general, that means the malignancy is more aggressive.

In the case of multiple myeloma, high risk is defined by factors like a staging criteria. This staging criteria is called the revised ISS (international staging system). We use the beta 2 microglobulin and the DNA characteristics as well as LDH to determine. That’s a lab value that’s often overlooked, but is useful to help us figure out how myeloma cells like to grow.

Then there’s what we call cytogenetic risk. These are very specific findings in the DNA studies, you’ll see most commonly called cytogenetics or FISH. That’s a short term to talk about how these pieces of DNA look.

When we find things like 17p deletion, or deletion 17p, or translocations, that’s when two pieces of DNA break off and hook back up with each other. You may see that there’s a piece of 11 with a piece of 14 or a piece of chromosome 14 with a piece of chromosome 16.

We often see that there are some patterns of high-risk cytogenetic or FISH findings. Then we can say to the patient, “Your myeloma cells are getting a genetic signal that tells them to grow,” or, “They’re not getting a signal that tells them to stop growing.”

Then we know that those patients may have more aggressive disease. That’s what we talk about risk—either by disease burden or by what propensity or likelihood it is for these cells to grow.

Is it standard that doctors pursue these tests

Thankfully, we have grown a majority over the past 10 years and it’s almost always standard. In fact, I can’t remember the last time I didn’t have a bone marrow test that had this. At least FISH is sent, sometimes cytogenetics. They’re two sides of the coin. It is very critical that it is sent.

Even for patients who may have had a biopsy done, for example, on a bone in their back, because there was something that was biopsied by a neurosurgeon that turned out to be consistent with myeloma.

I still insist on FISH being run either on that specimen if it’s possible, or repeating with the bone marrow biopsy. It is so critical to get that DNA information.

Describe how you manage the treatment decision-making process with patients

It’s really important for the doctor and the patient to be partners in this process. It must also involve the caregivers because they’re part of the story too. 

What I do is I try to give the patient background information so they can understand the pathophysiology. It makes them understand what’s happening in their bodies. Then we talk about what to consider when picking one treatment over the other.

A lot of times treatment decisions are based on what the patient himself or herself looks like. Some people may have kidney dysfunction, some may be older and frailer. Some people may have preexisting conditions like diabetes, et cetera. This information helps us to understand what treatment will do the least harm.

Many of these treatments do equal good, but we want to do the least harm.

It’s really important for me to know a patient’s medical history and what are the symptoms that he or she has. I can understand what would be a good fit for treatments and I can explain that to the patient.

Oftentimes, the patient and I, having spoken about their symptoms and some of their medical history, can come to an agreement based on the choices.

It’s hard because sometimes you don’t want to ask for recommendations that you don’t plan on taking. But you should always feel free to do that because it’s our job to give you the choices that exist and make recommendations.

Ultimately, you have to be okay with the path going forward.

Newer Multiple Myeloma Treatments

Proteasome Inhibitors

It’s a very interesting thing that the proteasome inhibitors exist at all, because it’s one of the few times where you can take advantage of something going wrong in the cancer cell.

The myeloma cells—the plasma cells—love to make proteins. They make that one antibody which is a real problematic thing, but it is a way for us to measure it. Because of that, their protein machinery is on overdrive.

The proteasome inhibitors work by irritating the garbage disposal of fat protein machinery. That then makes the cell extremely mad and it makes it die because it can’t get rid of all its waste.

That’s why these proteasome inhibitors are particularly good for myeloma cells because those cells produce a lot of protein. You generally hear about these drugs specifically for multiple myeloma.

New CAR-T-cell therapy

This is the BCMA-directed CAR-T-cell therapy and idecabtagene vicleucel or ide-cel. The trade name is ABECMA. You can look at any of those, we call it bb2121. Everything has five names. 

It’s a way to take a patient’s own T-cells and genetically engineer them so that they will express a protein on the surface. That protein will specifically target a protein on the myeloma cell that’s called BCMA. It stands for B-cell maturation antigen and it happens to be a very specific protein that is on the surface of the myeloma cells.

These T-cells are engineered to recognize specifically that protein and those T-cells see the myeloma cells and they think, “Oh, you’re an infection, I better kill you.” That’s what they do. We take advantage of the T-cell ability to kill things that they consider foreign and these T-cells will bind to these BCMA plasma cells and kill them.

That’s what’s so exciting about it—it’s taking your own immune system and repurposing it to do its job of killing its myeloma cells.

This product was FDA-approved just this March of 2021. We’re very excited to start rolling in our clinic to make this available for patients as a standard of care after having received four prior lines of therapy.

Abecma side effects and management that you have to offer to patients and caregiver

Acutely, Cytokine Release Syndrome, or CRS, does happen and is like the worst flu you ever had. It’s appropriate because your T-cells are having a party with all the myeloma cells and that’s good. That means the T-cells are trying to fight the myeloma cells as they would any infection.

You do have fever and potentially lower blood pressure. Over 84% of patients had this in the pivotal trial, but very low grade, manageable with a drug called tocilizumab. It usually happens within the first day or so of getting these cells for Abecma. After that, it’s boring in the hospital thereafter, which is good.

There’s also an 18% chance of having neurotoxicity or confusion that’s also very treatable with steroids. After the first two weeks, it’s actually much better.

There is fatigue and some low blood counts, but we’ve just had an analysis of primary and secondary quality of life measures.

It showed that over time, going from time zero all the way to 6, 9, and 12 months, patients actually had improved quality of life with decreased pain and fatigue, and increased emotional and social functioning. This is very important in maintaining who you are, not just what you are as a patient.

Patient Response

The pivotal KarMMa study, which is the study that ultimately got this product approved, had patients with very heavily pre-treated myeloma. Median, so at least half the patients, had six prior lines of therapy. That’s a lot of therapy that people have had.

Usually, drugs get approved by the FDA for myeloma with a 30% response rate. That’s the bar, but here you have something with a 70% response rate and it’s actually upwards of over 80%, for the actual dose level that has been recommended to go forward. We think we can get 8 out of 10 people to respond, hopefully.

For those people, they can have a year without getting any therapy. Again, the progression pre-survival for most drugs with FDA approval in this setting is like two, three months. It’s not very long at all. To get 12 months a year without any other therapy is something that we’re looking forward to because our patients definitely want a break. They’d love to see our faces, but maybe not at the chemo suite.

This is something that is unprecedented, but we’re hoping that we can even improve upon this with future products.

Wave of Therapies

I think what we’re going to see now is this wave of T-cell therapy and immune therapy, which includes bispecific T-cell engagers (BiTEs). Those are like antibodies, but they engage T-cells and these are really exciting drugs.

Both of these are going through a lot more clinical trials. Although we have one product approved for T-cells, we have another one coming down the line, and we have to also alginate, which would be off-the-shelf T-cells, so patients don’t have to go through a T-cell collection. That will be coming down the line, not this year or next year, but soon.

In a concurrent way, we’re also going to have these T-cell engagers, which are not cell therapies. They’re actual drugs but they’re off-the-shelf drugs that can be given. The first dose or two needs to be given maybe in a hospital or monitored setting, but after that, it’s very well-tolerated. People will be able to receive this at their local oncologist’s office.

As we get more data for all of these drugs and understand safety and what’s best for treating patients, these will hopefully get FDA approved. There are already ongoing clinical trials to look at these agents, including the CAR-T cells in earlier lines of therapy, so we don’t have to wait for people to be on their fifth line of therapy to reap the benefits from this particular treatment.

Clinical trials enrollment process

If they want to set up a consultation, they can get to our new patient consult service and we try to see everybody within a week or two. Especially now with Zoom, it’s much easier. We can plug them in and we’re starting a queue now for people to get ready for this treatment.

At first, there will be a big line of people because we have people waiting and have been waiting for a year now, but we’re hoping that as 2021 rolls out, we’ll have a better way to space everybody.

Soon, we’ll be able to be in line as patients have relapsed disease, taking them and quickly getting them set up for Abecma.

»MORE:Learn more about the process of clinical trials from one program director

What is your message to the world and to patients

We are all limited by the same human things: time, cells, mutations, everything. I think this journey is one that has to be a journey of partnership between the provider and the patient. 

It’s not anyone talking to you. It should be you having a conversation with your provider. The more that each of you is educated—and I get plenty of education from my patients—helps us understand each other better and ultimately make a better integrated and informed decision for your care path going forward.


Thank you, Dr. Shah!

More Hematologist Interviews


Rafael Fonseca, MD



Role: Interim executive director, hematologist-oncologist
Focus: Multiple myeloma, new drug development
Institution: Mayo Clinic
...

Farrukh Awan, MD



Role:Hematologist-oncologist, associate professor
Focus:Leukemias, Lymphomas, BMT
Institution:UT Southwestern
...

Nina Shah, MD



Role: Hematologist-oncologist, researcher
Focus: Multiple Myeloma
Institution: University of California, San Francisco (UCSF)
...

Kerry Rogers, MD



Role: Hematologist, researcher
Focus: Chronic lymphocytic leukemia (CLL), Hairy Cell Leukemia (HCL)
Institution: OSUCCC-The James
...

Tim Fenske, MD, MS



Role: Hematologist-Oncologist
Focus: chronic lymphocytic leukemia (CLL) & leukemia and lymphoma | CAR T, targeted therapy
Provider: Medical College of Wisconsin
...

Irene Ghobrial, MD



Role: Clinical investigator and professor of hematological oncology
Focus: Multiple myeloma, Waldenström’s Macroglobulinemia, early screening, clinical trials
Provider:Dana-Farber Cancer Institute (Boston)
...

Edmund Tai, M.D.



Role: General oncologist, hematologist
Focus: Specialist in treating Chinese-speaking patients
Provider: Sutter Health (Bay Area, CA)
...

Jacqueline Barrientos, MD



Role: Hematologist, researcher
Focus: Chronic lymphocytic leukemia (CLL), lymphoma, 17p Deletion (Ibrutinib, Acalabrutinib, Venetoclax), IgHV mutation
Provider: Northwell Health (NYC)
...

James Berenson, MD



Oncologist: Specializing in myeloma and other blood and bone disorders
Experience: 35+ years
Institution: Berenson Cancer Center
...
Favorite0
Categories
CLL Hematology Medical Experts Oncologist

Dr. Kerry Rogers, CLL

Kerry Rogers, MD

On Latest CLL Research & Treatments

Kerry Rogers, MD shares the latest news and opinions on treatment options for CLL (chronic lymphocytic leukemia) patients.

Lending her vast expertise and research experience as an assistant professor in the Division of Hematology at The Ohio State University (OSUCCC – James), specializing in chronic lymphocytic leukemia (CLL) and hairy cell leukemia (HCL), Dr. Rogers sheds light on participating in clinical trials and the community’s efforts to move the mark in the standard of care.

Explore below for Dr. Rogers’ insights on everything from the latest in CLL treatment, decision making throughout treatment, importance, and prospects of clinical trials. Full written version below the video.


Introduction: Dr. Kerry Rogers

I currently live in Columbus, Ohio, and I’m from the Midwest, but I grew up in the Chicago area.

I have a guinea pig, and I like college football. That’s huge at the Ohio State University, but I did my residency at the University of Michigan.

Don’t tell anyone, but I went to Northwestern for an undergrad, so that’s really my football team. That’s just a bit of me.

I work at The James (OSUCCC), and I enjoy taking care of people with chronic lymphocytic leukemia (CLL) and hairy cell leukemia (HCL).

My major interest academically is on improving targeted agents for the treatment of both these diseases.

Chronic Lymphocytic Leukemia (CLL)

What is CLL

Chronic lymphocytic leukemia or CLL is a blood cancer. It’s a cancer of cells called B lymphocytes. Don’t ask me why they’re called B lymphocytes! Those are white blood cells or immune system cells that have turned into cancer cells at some point over their lifespans.

They can go anywhere in the body that the blood goes to—you can find them in the bone marrow, lymph nodes, liver, and spleen, and in the blood, because it’s leukemia.

You can make a CLL diagnosis when there’s a certain number of these leukemic white blood cells or CLL cells in the blood. You can diagnose it with a blood test, and the most common way these days that people come to be diagnosed with CLL is when their white blood count appears too high and then goes through blood tests.

Many people diagnosed have no symptoms whatsoever and are sometimes somewhat confused about going to the cancer hospital to meet with me.

When thinking about CLL, it’s also important to realize that this is the most prevalent adult leukemia, meaning more adults live with CLL than any other type of leukemia.

People with CLL can expect to live a very long time, including their natural lifespan, and not everyone needs treatment. Because of that, it’s imperative to think about how well people are going to live with their CLL.

Categories and Stages of CLL

Unlike solid tumors like breast cancer or lung cancer, where the staging is based on how far it’s spread in the body, and if it’s left the site where it developed, which could mean the patient is in big trouble, we stage these blood cancers differently. Since they go over where the blood goes, which is everywhere, we can’t use the same basis.

In the United States, the most common staging for CLL is called Rai Staging. It was developed by Dr. Rai, a very nice man if you ever get the chance to meet him.

Rai Staging
  • Stage 0: CLL cells are in the blood
  • Stage 1: CLL cells are in large lymph nodes
  • Stage 2: An enlarged liver or spleen from CLL
  • Stages3 & 4: CLL cells are on the bone marrow that has caused people to have low hemoglobin, be anemic, or have a low platelet count from the CLL
How is CLL staged?

It’s staged simply by physical exam and looking at blood counts, and many people don’t need a bone marrow biopsy for staging. Some people need it to know why people’s blood counts are low, but it’s not always necessary.

The other part was the main forms of CLL and if there’s a slow-growing or a fast-growing type.

Everybody’s a little bit different. You’ll see some people diagnosed with CLL, and they’ve had it longer than I’ve been a doctor, and they’re doing fine with it. Their white count is the same as it has been for the last couple of decades.

But there are people whose CLL isn’t moving very fast at all. Then, some were diagnosed 18 months ago, and their white count has gone from 15 to 200 over that time.

Tests for CLL

The course of the disease can be quite different in many cases, and there are some tests that we can do to help better estimate if it’s going to be a slower or faster-growing CLL.

IgHV mutational status

One of those tests is called IgHV mutational status, or immunoglobulin heavy chain gene mutational status, where unmutated usually means a faster-growing, higher risk CLL.

I’d like to think of mutated as a special, low-risk slow-growing CLL, and that’s mutating your immunoglobulin as a normal process in B cells. This just says whether or not the CLL cells did that before they turned into leukemia cells. 

FISH test for CLL

Some other tests that can help include FISH panel testing, which is just a fancy way to look at chromosomes in the CLL cells, not like the ones you pass onto your kid.

Things like deletion of the short arm of chromosome 17 or deletion of 17p can mean that we’d expect the CLL to be faster-growing, and deletion of 13q, which is part of the 13th chromosome, predicts slow-growing.

We can use a combination of these factors to guess how someone’s CLL will do.

Of course, sometimes we’re surprised. Sometimes, it looks like it will be slow-growing and it’s not, or people with some high-risk features really have an extended course but their CLL isn’t causing them any issues.

CLL in layman’s terms

One thing that really helps people that’s not necessarily fancy is knowing how to look at your own blood counts.

People get these complete blood counts all the time, and you’ll see your white blood cell (WBC) count, hemoglobin, platelets, and then below that, you’ll see a differential that tells you what type of white blood cells those are.

You always want to look at the lymphocyte count, because the CLL cells are counted under lymphocytes.

The other testing is something you do just on the leukemia cells.

It’s always very important to ask if this testing is done and what the results are so that you can know more about your CLL.

It helps you predict how much trouble you might have from the CLL in the future, the time before needing treatment, help in selecting a better course of treatment, how many treatments you might need in your lifespan, or if, at some point, a clinical trial might be appropriate for you.

The major ones are the IgHV and CLL FISH panel, which stands for fluorescence in situ hybridization. It is a chromosome analysis where they look at all the chromosomes because people with three or more changes in their chromosomes actually predict a higher risk of CLL.

They can expect to have more treatment and more difficulty with it in their lifetime. People with normal karyotype, like normal chromosomes, actually expect to have less difficulty. 

»MORE: Hear from CLL specialist, Dr. Jacqueline Barrientos

Standard CLL Treatment

Shifting Away from Chemotherapy

First, it’s important to realize that the median age that people are diagnosed with CLL is in the mid-60s or almost 70. There’s a lot of older people who might have other health conditions.

It’s always important to think about what other health conditions someone has when planning treatment.

It has been a goal in the field of CLL medicine for a long time to make sure that some treatments are appropriate even for older people in their 80’s or even 90’s with other health conditions.

But here, I’m going to talk about more of the chemotherapy for younger, fit people because I think it’ll be easier to understand in that setting.

We’ve always had some chemotherapies that could lower the white count or improve symptoms. But the mark was moved on how long people are living with CLL or survival by combinations of chemotherapies with an antibody medication called rituximab.

Fludarabine, cyclophosphamide, rituximab (FCR)

The last several decades before my time working in CLL were spent developing a regimen called FCR (fludarabine, cyclophosphamide, and rituximab). Rituximab is the antibody and the other two are chemotherapies.

Bendamustine and rituximab

There’s a similar regimen you can use in people who might be slightly less able to tolerate chemotherapy called bendamustine and rituximab. These are highly effective chemotherapies that could be given to most reasonably healthy people and can control the CLL for years.

Targeted Therapy

ibrutinib and venetoclax

It’s important to know that as a first treatment, our new targeted agents, like ibrutinib and venetoclax-based treatments, were compared to these chemotherapies and had longer progression-free survival. This is a measure of how long people are alive without their leukemia returning.

We have found that these targeted agents were actually better than these chemotherapies.

That means people lived longer without their CLL coming back after they took the non-chemotherapy targeted agents. Also, they have a different group of side effects that are generally better than chemotherapy.

»MORE: Read more about ibrutinib and other patient experiences

Choosing between Chemotherapy and Targeted Therapy

Some people choose to get chemotherapy because it’s different from these targeted agents, or they might have a health condition that makes the targeted agents inappropriate.

These days, the vast majority of CLL patients should be receiving treatment with a targeted agent and not with chemotherapy.

It’s very uncommon that you’d have to use chemotherapy to treat CLL. The one exception to that is young fit patients. IgHV mutated people and don’t have a high-risk feature such as deletion 17p can have 10 years or more of being alive with no detectable leukemia after getting FCR.

A group of younger people fit for chemotherapy treatment are those mutated and don’t have deletion 17p, called a TP53 mutation. But they might choose to get FCR because it might actually cure them.

I don’t know what else to call 10 years of being alive without detectable leukemia. We don’t usually say CLL is curable, but this is the one case where it might be.

However, there’s a lot of risks to doing FCR, like getting a different type of leukemia called acute myeloid leukemia (AML). That happens down the road due to bone marrow damage from FCR.

That is the one case where it could be very important to offer chemotherapy, especially to young healthy people that might want to do a treatment course of about six months and then potentially never need treatment again in their lifespan.

It’s not a guarantee that they’ll never have leukemia come back, but that is the one case where it’s important to think about it. But for the vast majority of other people, targeted agents are safer and more effective.

How long have the targeted agents been in use

The BTK inhibitors were developed in the last decade, and venetoclax shortly on the heels of that. When things are through phase III studies, that’s when they start being prescribed more commonly.

We—the academic centers—get to use all these drugs and people that come see us here might benefit from taking them as a participant in a clinical trial.

I’ve seen many people who did really well doing a research study to get a newer drug that later became approved. This becomes more widely available and used by general practice, hematologists, oncologists after phase III studies.

Continuous novel agent therapy vs. time-limited

For previously treated or relapsed refractory CLL once, it’s been about five years. In 2018, we had those randomized phase III studies comparing ibrutinib regimens to FCR or BR reported that ibrutinib had a longer progression-free survival, which is, again, being alive without leukemia. That really put those in very widespread use.

There is some resistance to it just because you have to take the pills for a long time. You take them indefinitely until either leukemia comes back while you’re taking them, you develop a side effect and have to stop taking them, or you have some other health condition that you have to stop.

In younger patients, compared to FCR, ibrutinib even had a survival advantage, meaning you’re more likely to be alive if you took the pills instead of FCR.

When you explain to them that, yes, it is not the first choice, most people decide that that’s better than something that has a shorter progression-free survival or doesn’t work as well.

Most people are more comfortable taking pills long term when they find out that it works better than chemotherapy.

In both people who have taken a treatment before or selecting a first treatment, there are two major standard of care options outside of a clinical trial.

Although I think participating in clinical trials is always something to consider if you can do it. I’ve seen a lot of people benefit from that. You won’t get a placebo without knowing that’s an option. From where I work, we have zero CLL trials with a placebo.

Treatment for relapsed/refractory (R/R) CLL

The two standard options are both highly effective. If patients haven’t taken either class of drugs, they’re both excellent, and you can pick based on preferences and side effects.

BTK inhibitors

There are BTK inhibitors, which are pills that target a protein called BTK. This blocks a cell signaling pathway called B cell receptor signaling. This makes the CLL cells not behave like CLL cells and die off over time.

The two main BTK inhibitors that are approved for CLL are ibrutinib and acalabrutinib. Ibrutinib is a once-daily pill. Acalabrutinib is more selective and targets pure things that ibrutinib does. It is a twice-daily pill. 

Ibrutinib and acalabrutinib are both excellent options. They’re usually given by themselves, although they can be given with an antibody medication in some cases.

Venetoclax

The other option is another oral targeted agent called venetoclax. It inhibits a protein called Bcl-2, which is an anti-cell death protein. If you block an anti-cell death protein, that’s like a double negative, and it kills the CLL cells really fast.

The problem with this drug is that it has to be started slowly so people can be monitored. It can work so quickly that it can cause tumor lysis syndrome. It is usually given with an antibody and requires monitoring. 

Venetoclax treatments are given in a shorter duration. If people are taking it as a first treatment, you give it with an antibody called obinutuzumab and take it for one year. If you’re giving it after people have already gotten treatment, you usually give it with an antibody called rituximab, and you take it for two years.

It’s whether or not they’ve taken treatment before it determines whether or not you take venetoclax for one or two years.

Venetoclax vs. BTK inhibitors

Venetoclax is like a time-limited treatment versus BTK inhibitors, which you take indefinitely till they stop working or you develop side effects and have to quit.

Some people have very strong feelings about if they want to take something and just get it done and stop, or if they’re just fine adding another pill to their pillbox. They don’t want to bother with antibody infusions. They just want to take some pills and go back to working or golfing or whatever it is they want to do.

Both are usually tolerable for the majority of patients. The ones who take long-term, obviously, for some patients have more chronic side effects.

Targeted Therapy Side Effects

Both these treatments are so effective, if you’ve never taken venetoclax or BTK inhibitors before, you can really pick based on your preference for treatment duration, and what side effects may or may not matter for your other health conditions.

btk inhibitors side effects

The main side effects of BTK inhibitors are:

  • Bleeding
  • Bruising
  • Cardiovascular side effects
  • Increase in blood pressure – high blood pressure can increase the risk for things like heart attacks and strokes. Overall, it can decrease cardiovascular health.
  • Abnormal heart rhythm called atrial fibrillation, or a-fib. A-fib is usually not life-threatening but is very irritating to deal with.

In addition, it can sometimes cause:

  • Joint aches or pains
  • Inflammatory arthritis
  • Diarrhea
  • Heartburn
  • Rashes – those usually go away or are less of a problem

Most people find the side effects from the BTK inhibitors tolerable, so they still go about their life with these things.

But for someone that has atrial fibrillation or is taking several blood pressure medications already, this might not be the best idea. People with bleeding disorders or who need warfarin anticoagulation don’t want to take this class of drugs if they have options.

Venetoclax side effects

Venetoclax, on the other hand, can cause tumor lysis syndrome at the start.  All the CLL cells die so quickly it releases toxins into the blood. That’s treatable, but if you don’t watch out, it can be life-threatening or fatal.

You actually have to start the dose low and increase it slowly. People take a low dose, and over five weeks, they increase the dose every week to get to the full dose of venetoclax, which is 400 milligrams. They have to come for at least two days in a row for blood tests or monitor tumor lysis syndrome every time.

»MORE: Cancer patients share their treatment side effects

With this monitoring scheme, it’s very safe, and people developing tumor lysis syndrome can get that treated usually with medications. Things seem to go very well for people, but it’s a lot of hassle to do that.

To protect people from tumor lysis syndrome, they have to stay hydrated. People who have heart failure, take diuretics or have kidney impairment, which could make tumor lysis syndrome more common and more dangerous, might not want to go this path just because that’s a greater risk to their health.

Once people are at the target or treatment dose of venetoclax, it actually seems to have fewer chronic side effects than the BTK inhibitors. Some of them include diarrhea, lower neutrophil count or neutropenia (neutrophils are infection-fighting cells).

People can sit down and look at their health conditions. If they have severe kidney impairment, they probably want to take a BTK inhibitor. If they have abnormal heart rhythm problems, they would want to take the Venetoclax.

It’s a decision you make together with your treating physician.

I sometimes see patients considering their options for first treatment who ask me right off the bat, “Which one should I do?”

I say, “I don’t know, we just met. I need to ask you some things about you, and then I can tell you what you might want.”

I think these are really important, and the discussion is very similar for people picking a treatment that has taken before but never taken either of these classes of drugs before.

»MORE:Learn more about the process of clinical trials from one program director

Clinical Trials

Triple Therapy (Ibrutinib, Venetoclax, Obinutuzumab)

We always like to make treatment safer and better for our patients. So we had a study combining the BTK inhibitor ibrutinib, venetoclax, and an antibody, obinutuzumab, as a treatment for one year.  It’s ongoing in follow-up, but everyone in this study has completed treatment.

When you give more drugs together, you get more side effects. It’s not a surprise, but the nice thing about this is it’s one year, and now we’re seeing how long people remain in remission at the end of that one year of treatment.

So far, we’re at about three years of follow-up, and it looks very good.

We’ve treated people with both relapsed/refractory CLL and people taking this as a first treatment. Several other studies are going on for BTK inhibitor and venetoclax combinations. We expect the response rates to be very high, but we are excited to know how long people remain in remission with this.

We hope to learn with longer follow-up who might most benefit from this combination and who’s going to stay in remission longer than with other things.

I’m just super excited that we really move the mark and get regimens into the standard of care in CLL and are able to do a randomized phase III trial, where you sign people to treatment in your treatment.

Again, there’s no placebo here, and usually, you know which one you’re getting to, after you randomize. You don’t know when you sign up, but you know before you get treated.

There are two ongoing studies, one through the Eastern Cooperative Oncology Group, or ECoG, and one through the Alliance. Those are both US Oncology Cooperative groups that do studies conducted on hundreds of sites across the US. They are both randomizing patients to ibrutinib and obinutuzumab.

You take the antibody for a limited time, but the ibrutinib indefinitely, and then the three-drug combination, ibrutinib, venetoclax and obinutuzumab given for a fixed duration. You don’t take it forever, and they’re looking at progression-free survival.

One study is for younger individuals, one’s for older individuals. They have a few small differences, but that’s mainly what they’re looking at.

»MORE:Read more on FDA approvals of clinical trials

I am excited to see over the next several years how that turns out, and I’ve also treated several people in that study who were really excited to participate in it.

You have to emotionally think it’s okay to be randomized, but a lot of people thought it was fun. They were like, “Oh, great, I’m going to get one of two great things, and I don’t have to pick.” 

Metrics for these studies

When you pick a new standard, you compare standard treatment, which in this case is ibrutinib and obinutuzumab, to an investigational treatment, which is that three-drug combination.

The main goal is to determine progression-free survival: how long people are alive without leukemia and if one’s longer or shorter than the other. That’s a measure of how effective these things are.

Some studies use the overall response rate, but these drugs are so effective that they don’t really work out CLL because everyone responds to these things, which is great, by the way.

Then, when we look at the patients in the study who had high-risk features, low-risk features. Then we see how our high-risk patients did compared to high-risk patients with the other treatment. 

For ibrutinib, some people have their leukemia come back while they’re still taking it.

Determining resistance to treatment

We have some neat studies going on at our institution and some other institutions across the country, looking at how we can identify who’s developing resistance to ibrutinib before they actually get sick.

We can look at mutations in BTK, which is the protein that binds at the drug binding target. Once people develop mutations in BTK, in particular spurts, we know that the drug will stop working.

We’ve offered them clinical trials to add a second drug like venetoclax to reduce this resistance and see if we can keep the leukemia from relapsing and be healthy for longer.

The CLL Community is looking at adding a second drug to people who are on ibrutinib and doing well. Remember, I said that ibrutinib, and actually, acalabrutinib II, which is the other BTK inhibitor, changed the way the CLL cells work and behave, but it doesn’t actually kill them off.

Lots of people still have CLL floating around, which is why we think they need to keep taking those drugs. We’re wondering if people can have another drug added to it to just knock out those residual leukemia cells. That way, they can be in off-treatment remission. If you do that, then they won’t be on it long enough to get resistance ideally.

Importance of clinical trials

It’s always good to know what your standard options are, and what your clinical trial options are.

For people who haven’t taken BTK inhibitors or venetoclax, those are good standard options. For people who are resistant to both those, usually clinical trials are your best option.

You always want to know what drug is being studied, how the study is going, who’s been in it, and what your doctor expects from the study.

Misconceptions about clinical trials and “placebos”

In cancer trials, you would know there was a placebo because you have to sign a consent saying there’s a placebo. But it’s usually considered unethical to give people who need cancer treatment a placebo.

It will explain if it’s randomized and what are the treatments that you would be getting. A lot of studies, especially the ones we have, are studying very new treatments. Sometimes they’re studying the dose of the drug.

You should know exactly what drugs you’re getting. It can feel really weird but you should consider your options.

With the state of cancer research these days, we actually have a very good feeling that these drugs are going to help patients before we give them to patients. Many of them have been studied obviously in the lab using CLL cells; cell lines have been studied in animal models of CLL.

We don’t start trials with new drugs until we’re fairly confident that it will help people. I’ve seen many patients benefit from drugs that they wouldn’t be able to get just because they’re not yet approved.

If anyone’s considering it and unsure if they have someone they know in the CLL community or peer support for someone that’s been in a clinical trial, it’s always good to talk with people who have done it just because the individual benefit to doing something like that can be significant.

People always tell me, “Oh, I feel like I’m your guinea pig.” I’m like, “Oh, you should be so lucky to be my Guinea pig, you know what that thing’s lifestyle is?” I was like, “My personal guinea pig is not an experimental animal. It’s my pet, has a super nice lifestyle. People would love to be my guinea pig.” 

But really, people aren’t guinea pigs as much as you think. If you’re considering a research study, make sure you get to ask all the questions about what the drug is and why being in this study might benefit you or others, and your doctor should be able to answer those questions for you.

Up and Coming New Treatments

CAR T cell therapy

CAR T-cell is exciting. It’s still investigational for CLL, but I’ve seen it help a subset of patients, especially those that are resistant to these drugs I’ve been talking about. It can be very powerful for select people, but it is a hassle to do, and it is still investigational.

For people who have very good, other treatment choices, it’s usually not something we run to as a first treatment or even a second treatment. But it can be great for people that need that.

Reversible BTK inhibitors

The things that I’m excited about are some drugs that are hopefully going to move up to benefit more patients. We’re always trying to make treatment safer, more effective.

There’s reversible BTK inhibitors. Ibrutinib and acalabrutinib bind BTK at the same site and bind it irreversibly, meaning forever.

Reversible BTK inhibitors bind at different sites than the two approved ones and bind and unbind BTK, which seems to limit some of the side effects.

Also, for some reason, these drugs can work in people who are resistant to the BTK inhibitors, which you expect ’cause they bind to it at a different site but can work in people resistant to BTK inhibitors and Venetoclax. They seem to be very well tolerated.

A reversible BTK inhibitor such as LOXO-305 (pirtobrutinib) is now under study. LOXO-305 is the one that’s the furthest in development, and they just gave it a direct name.

It’s just exciting when I go to professional meetings to see what new types of drugs are being developed in CLL or things like cyclin-dependent kinase inhibitors that are coming back into play. These drugs, either alone or in combination, are likely to benefit patients.

Again, we keep moving the mark more and more towards safe, highly effective treatment, and it just keeps getting better.

New drugs with new mechanisms, drugs with the same mechanism but in a different way—these are the way we move the mark in CLL.

It seems to have fewer side effects, not no side effects. Anyone that tells you there’s are no side effects is lying. You never get anything for free or don’t do anything. But, that, and also because the mechanism is different from the irreversible BTK inhibitors, it can be used in resistance.

If someone takes ibrutnib until their leukemia comes back while they’re taking it, taking acalabrutinib isn’t going to work because they have the same mechanism. But taking a drug that binds the same protein but with a different way of doing it can work after your resistance.

This allows people to take two BTK inhibitors before moving on to a drug like Venetoclax or other treatment options. They’re just really effective, especially in people with really resistant CLL. It’s not just that there are fewer side effects, but also they seem to work great, which is awesome.

Treatments for Hairy Cell Leukemia (HCL)

Hairy cell leukemia vs. chronic lymphocytic leukemia

I love talking about hairy cell leukemia, which is another chronic B-cell leukemia. It also has very long survival rates, but it has some different features than CLL.

Unlike CLL, it’s very rare. It’s not very common to have people diagnosed with hairy cell leukemia.

HCL Treatments
Purine analogue chemotherapy

Over the last couple of decades, purine analogue chemotherapy was developed for hairy cell, and it’s actually spectacularly effective for the majority of patients.

People can take a single course of purine analogues and be in remission for decades sometimes. But there’s a group of hairy cell leukemia patients who don’t get decades of remission from purine analogues, or aren’t able to take them for other reasons such as side effects.

New drugs (cladribine, pentostatin, vemurafenib)

The hairy cell community has been working on new drugs for this group of hairy cell leukemia patients who aren’t expected to benefit from purine analogues like cladribine or pentostatin.

There are a couple of drugs in this area that are available and FDA-approved for people. But vemurafenib, which is not approved for hairy cell leukemia, has been very well studied. It can be used in people with hairy cell leukemia with a BRAF mutation which is found in the majority of people with classic hairy cell leukemia.

But there’s still a need for new drugs for this group of patients as those drugs don’t cover everybody.

We have actually conducted a phase two study of ibrutinib. It’s been FDA-approved for four different cancers. We’ve studied it in hairy cell leukemia, in a group of patients who aren’t expected to benefit from purine analogues.

People who have been previously treated or people with a variant of hairy cell leukemia have been found to have a very long progression-free survival. Around 73% of people are alive for three years without their leukemia returning. 

The response rates don’t look quite as high, but that’s probably the response criteria we were using. You can really see how many people benefited by looking at progression-free survival.

It’s definitely a really important treatment option for people with this rare leukemia that aren’t expected to benefit from therapies like Purine analogues.

I think we published those results in a journal called Blood recently so that other doctors could find them and think about using that for their patients with a hairy cell that might need something beyond purine analogues.

Prognosis and findings so far

The prognosis for hairy cell, in general, is quite good. Most people can expect to finish their natural life span. Some people die of infection and rarely will someone die of leukemia. 

Before purine analogues, survival was actually expected to be a couple of years, and not a couple of decades. When people don’t benefit from purine analogues, usually, they take more treatments, and their lifespan can be shortened by this. It’s still possible depending on what treatments you get to live for years.

It’s not like people had a very, very short survival, but certainly not the decades you’d expect from people that really get a lot of benefit from purine analogues, and other treatments like vemurafenib which is usually given for a fixed duration. Their relapse-free survival, or roughly how long it is before the leukemia returns in the majority of patients, is less than two years.

With this ibrutnib study, people are still alive without their leukemia returning for three years. Almost three-quarters of them are really quite good.

The study has been open since 2013. Some people have been in it a really long time, and I look forward to continuing to see how it benefits those patients. Some people are obviously quite sick and had taken 8 or 10 treatments before being in the study and probably wouldn’t be doing very well if they hadn’t been in a research study.

It’s also a nice example of how participating in a clinical trial can benefit people, because folks with hairy cell leukemia would not have had access to this if they didn’t decide to be in a research study.


More Medical Expert interviews


Dr. Christopher Weight, M.D.



Role: Center Director Urologic Oncology
Focus: Urological oncology, including kidney, prostate, bladder cancers
Provider: Cleveland Clinic
...
Dr. Babis Andreadis of UCSF shares his approach with patients, the importance of patient self-advocacy, whether to ask for a second opinion, and more on shared treatment decision-making. ...

Doug Blayney, MD



Oncologist: Specializing in breast cancer | HER2, Estrogen+, Triple Negative, Lumpectomy vs. Mastectomy
Experience: 30+ years
Institution: Stanford Medical
...

Dr. Kenneth Biehl, M.D.



Role: Radiation oncologist
Focus: Specializing in radiation therapy treatment for all cancers | Brachytherapy, External Beam Radiation Treatment, IMRT
Provider: Salinas Valley Memorial Health
...

James Berenson, MD



Oncologist: Specializing in myeloma and other blood and bone disorders
Experience: 35+ years
Institution: Berenson Cancer Center
...

Jacqueline Barrientos, MD



Role: Hematologist, researcher
Focus: Chronic lymphocytic leukemia (CLL), lymphoma, 17p Deletion (Ibrutinib, Acalabrutinib, Venetoclax), IgHV mutation
Provider: Northwell Health (NYC)
...

Dr. D. Ross Camidge, M.D., Ph.D.



Role: Thoracic oncologist, Director of the Thoracic Oncology Clinical Research Programs
Focus: Lung cancer, small cell (Immunotherapy), EGFR (Osimertinib), ALK (Alectinib), ROS1 (Crizotinib), BRAF (Dabrafenib & Trametinib), NTRK
Provider: Univ. of Colorado
...

Edmund Tai, M.D.



Role: General oncologist, hematologist
Focus: Specialist in treating Chinese-speaking patients
Provider: Sutter Health (Bay Area, CA)
...

Irene Ghobrial, MD



Role: Clinical investigator and professor of hematological oncology
Focus: Multiple myeloma, Waldenström’s Macroglobulinemia, early screening, clinical trials
Provider:Dana-Farber Cancer Institute (Boston)
...

Tim Fenske, MD, MS



Role: Hematologist-Oncologist
Focus: chronic lymphocytic leukemia (CLL) & leukemia and lymphoma | CAR T, targeted therapy
Provider: Medical College of Wisconsin
...

David Miklos, MD



Date: Jan. 2021
Focus: Who benefits from CAR T, ZUMA-2 clinical trial, Stanford's CAR 22 Work
Provider: Stanford Medical
...

Kimmie Ng, MD, MPH



Role: Gastrointestinal oncologist
Focus: Young-onset colorectal cancer, microbiome
Provider: Dana-Farber Cancer Institute (Boston)
...

Farrukh Awan, MD



Role:Hematologist-oncologist, associate professor
Focus:Leukemias, Lymphomas, BMT
Institution:UT Southwestern
...
Mark Lewis, MD, is not just an oncologist, he's a cancer survivor, himself. This gives him a unique perspective as both physician and patient. Hear more about his thoughts on second opinions and importance of self-advocacy. ...

Kerry Rogers, MD



Role: Hematologist, researcher
Focus: Chronic lymphocytic leukemia (CLL), Hairy Cell Leukemia (HCL)
Institution: OSUCCC-The James
...

Nina Shah, MD



Role: Hematologist-oncologist, researcher
Focus: Multiple Myeloma
Institution: University of California, San Francisco (UCSF)
...

Rafael Fonseca, MD



Role: Interim executive director, hematologist-oncologist
Focus: Multiple myeloma, new drug development
Institution: Mayo Clinic
...

William Wierda, MD, PhD



Role: Hematologist, Med. Dir., Dept of Leukemia
Focus: Chronic lymphocytic leukemia (CLL), other leukemias
Provider: MD Anderson
...

Latest on CLL Treatment (2022)



Featuring: Nicole Lamanna, MD; William Wierda, MD, Ph.D 
Hosted by: Michele Nadeem-Baker
Topics: Pirtobrutinib, new oral combinations, venetoclax updates, CAR T
...

David Miklos, MD, Ph.D



Role: Hematologist, researcher
Focus: How MCL treatments have improved, importance of clinical trials
Provider: Stanford Medical Center
...
transplant patient in hospital

David Miklos, MD, Ph.D



Role: Hematologist, researcher
Focus: Role of allogeneic BMT, response to graft versus host disease (GVHD)
Provider: Stanford Medical Center
...

CAR T Cell Therapy in Myeloma



Dr. Fonseca shares his insights on emerging T-cell therapies for multiple myeloma, describing the role T-cells play in our bodies and then focusing on chimeric antigen receptor (CAR) T-cell therapy and bispecific T-cell engagers.
...

How Do Clinical Trials Work?



In this episode, Dr. Fonseca details the process of clinical trials, as well as how patients and families can better understand what goes on during each of the main parts of the study.
...

Joseph Mikhael, MD



Role: Dir. Myeloma Research, CMO at International Myeloma Foundation (IMF)
Focus: Multiple myeloma
Provider: TGen/City of Hope
...

Ruben Mesa, MD



Role: Executive Director, Mays Cancer Center; Prof. of Medicine
Focus: Myeloproliferative neoplasms (MPN)
Institution: UT Health San Antonio MD Anderson
...

Srdan Verstovsek, MD, PhD



Role: Director, Clinical Research Center for MPNs at MD Anderson; Section Chief, MPNs; Prof., Dept. of Leukemia
Focus: Myeloproliferative neoplasms (MPN)
Institution: MD Anderson
...
Favorite0