How can you elevate your overall myelofibrosis care and treatment? Dr. Naveen Pemmaraju discusses the importance of engaging in myelofibrosis care decisions with your healthcare team, shares advice for setting treatment goals, and reviews factors that may impact therapy options. Dr. Pemmaraju also provides tips and resources for self-advocacy, including coping with emotional health.
Dr. Naveen Pemmaraju is Director of the Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN) Program and Professor in the Department of Leukemia at The University of Texas MD Anderson Cancer Center. Learn more about Dr. Pemmaraju.
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Transcript:
Katherine Banwell:
Hello and welcome. I’m your host, Katherine Banwell. Today’s webinar is part of the Patient Empowerment Network’s Elevate Series to help myelofibrosis patients and care partners feel well-informed when making treatment decisions with their healthcare team. On today’s program, an expert will join us to share advice for accessing better overall care.
Before we get into the discussion, please remember that this program is not a substitute for seeking medical advice. Please refer to your healthcare team about what might be best for you. Well, let’s meet our guest today. Joining us is Dr. Naveen Pemmaraju. Dr. Pemmaraju, it’s good to see you again. Welcome. Would you please introduce yourself?
Dr. Naveen Pemmaraju:
Oh, thanks, Katherine, and to Jamie and the team. I’m Dr. Naveen Pemmaraju, a Professor of Leukemia at MD Anderson Cancer Center in Houston, Texas. I also serve as the director for our rare disease program focusing on BPDCN and, of course, MPNs. Also, I want to mention, I have another hat, which is executive director for MD Anderson Cancer Network for Cancer Medicine. Thanks, Katherine.
Katherine Banwell:
Well, thank you so much for taking the time out of your day to join us. I’d like to start by discussing your role as a researcher. You’re on the front lines for advancements in the myelofibrosis field. What led you here, and why is it important to you?
Dr. Naveen Pemmaraju:
Well, I think it’s an important question to start with and one that we need to evaluate and dynamically reevaluate over time. I think really for me, two major themes, Katherine, that brought me to this point. One is the absolute desire to be there for patients who don’t have a voice. So, that means giving voice to the voiceless. It’s something I’ve always been good at ever since I was a youth, which is advocating for those who may not be able to or cannot advocate for themselves.
So, this is the rare disease thread. A lot of my colleagues were going into lung cancer, breast cancer, and colon cancer, very important. We need folks there. However, those were common diseases, largely elucidated. I was always drawn to the more difficult-to-treat diseases, esoteric, and rare, and I think that’s one component, which is the patient voice.
The second aspect is scientific interest. Again, in the more common tumor types and diseases, there’s a lot already known. So, many of the researchers and research being done is either derivative from that knowledge, Katherine, a or kind of secondary. I wanted to put my efforts and my team’s efforts and frankly, my life effort into trying to figure out new science, new pathways, new breakthroughs, new ideas, and new concepts. I find that in the rare disease space, that’s where I can do that. So, both from the humanistic patient aspect and the science aspect.
Katherine Banwell:
Well, it sounds like it’s a challenge to you as well.
Dr. Naveen Pemmaraju:
I think that’s a great point. So, while it’s intellectually satisfying and very important to pursue this, and I love my patients, the clinic, and my team, you make a really good point. Every day when I wake up, it is the challenge that really drives you, which is to try to improve not only the lives of our patients but the quality of life.
Try to improve the education barriers, which are many, and then the access barriers, not only here in the U.S., but all over the world. Social media has helped that, democratization of information, and platforms like yours right now to get the message out there to folks who need it the most. However, you make a good point. We have a lot of challenges and a lot of barriers, and that motivates me to get up in the morning every day.
Katherine Banwell:
When it comes to choosing therapy, Dr. Pemmaraju, it’s important to work with your healthcare team to identify what is going to work best for you. So, as a clinician, how do you define shared decision-making?
Dr. Naveen Pemmaraju:
Very important. So, shared decision-making to me means a partnership. It means a journey that the patient and the providing team are about to embark on. It’s a very different approach than a one-way, I tell you, you do this. Instead, I see it as a bi-directional exchange of ideas.
Each visit, each EPIC in-basket or EMR communication, each touch with the healthcare system, the pharmacist, the PA, nurse, whoever is dealing with the patient, I think that’s the key.
So, a bi-directional exchange of ideas, what’s important to you as the patient? What’s important to the caregiver? What are the worries? What are the barriers? Designing a treatment system around that, a treatment paradigm and approach. Discussing risks, benefits, side effects, toxicities, alternatives, and then a constant dynamic reevaluation throughout. That’s what I pictured. It has to be a journey and a partnership.
Katherine Banwell:
Well, part of making care decisions is setting goals and I think you’ve just alluded to that. What are treatment goals for myelofibrosis, and how are they determined?
Dr. Naveen Pemmaraju:
That’s a great question. Myelofibrosis treatment goals are changing in real-time. I would say as of this recording, 2024, the main three things that I want patients to think about and the caregivers.
Number one is a stem-cell transplant eligible or not? It used to be based on age and comorbidities, but there are other factors. So, are we going to stem cell transplants or not? That determines a lot of the journey. Two is a clinical trial or not. So, are we doing the standard of care therapy, often one pill at a time, or clinical trial, either an IV drug, a pill, or combinations? Then three is that dynamic assessment that we talked about, which is what are the goals of care? Often our patients with myelofibrosis have decreased quality of life, enlarged organs, fatigue, cachexia, and malnutrition.
These are the central components. A lot of times they’re due to the myelofibrosis itself. So, the treatments may improve that. A lot of times it’s the other comorbidities, other health issues. So, working with the PCP, the primary care provider, and the local team. In my case, many of my patients are referrals, as you know, the local MD team. I think these are the three components, transplant eligibility or not, clinical trial versus standard of care.
Then once we’ve made a treatment decision, minding toxicities and quality of life.
Katherine Banwell:
Right, okay. So, you’ve touched upon the factors that are considered when choosing therapy for myelofibrosis. Let’s talk about test results. What sort of tests should be done following a myelofibrosis diagnosis?
Dr. Naveen Pemmaraju:
Well, I think this is something that’s an active area of evolution. I think the good news is I can give you a few standard items. I think most, if not all, of our patients, will require a bone marrow biopsy to be done at baseline and possibly even later on to assess the status of the therapy. Now, in some cases, that may not be available or accessible due to patient preference or comorbidities.
However, a bone marrow biopsy is a way to look inside and see how the bone marrow tissues are doing. Outside of that, for the blood tests, the two most critical sets are what we call a CBC and a CMP. So, CBC complete blood count. This is where you get your hemoglobin, platelets, and white blood cell count, very important to know at baseline and dynamically.
Then the complete metabolic profile is very important, Katherine because we need to know how the potassium, kidney function, and liver function are doing. Then finally, I would also say you’ll see your provider add in other blood tests over time, depending on the particular case. Thyroid testing if it’s needed in the case of fatigue, just to name one example. So, I think these are the main categories.
I think what’s also interesting over time is that this is an issue with us as well in the MPN clinic. You end up seeing your MPN provider and team so much that it’s easy to forget and lose sight of the primary care items too. So, this is a good time to remind folks to stay in touch with their MPN team, the provider, and their caregiver, whether it’s colonoscopies, mammogram, or prostate. I remember over the COVID pandemic time, especially, a lot of that was either sacrificed, forgotten, or on purpose put aside. So, let’s remind people in 2024 to remember to have that partnership as well.
Katherine Banwell:
How does molecular testing affect treatment options and prognosis?
Dr. Naveen Pemmaraju:
Right, yeah, I haven’t mentioned that yet because that’s something that we’re trying to layer into. I do find that to be the standard of care now in the treatment of myelofibrosis. What you’re asking about is very important. So, outside of the normal labs in bone marrow morphology, seeing what it looks like under the microscope, we’re starting to add three or four items. One is called cytogenetics, that’s chromosomes. You’re born with 46, so 23 from mother, 23 from father, for example, 46 total.
Even though most people are not born with an MPN per se, those chromosomes can change and become abnormal over time. So, we want to know that, and that can help us tell low versus high versus intermediate risk. Two is the molecular test you ask about. Most people have heard of JAK2, that’s the most common out of myelofibrosis, maybe 50 percent to 60 percent of cases, JAK2V617F. However, did you know there’s also CALR, which is the second most common molecular mutation, and then MPL.
Those three are the big three driver mutations. They make up roughly about 90 percent of our cases, 10% being so-called triple-negative. So, you’re negative for all three. When you do deeper sequencing, which is available now clinically, and we check that here, you will find almost always, some other mutation, ASXL1, EZH2, SRSF2, etc. It becomes an alphabet soup very quickly. However, I think basically you should know that there’s JAK2, CALR-MPL, the big three driver mutations, and additional molecular mutations.
So, therefore we and others believe you should check these as standard. Finally, there’s also flow cytometry. Just want to give a shout-out to that. Most people haven’t heard of that. When you send your bone marrow for testing, in addition to the pathologist looking under the microscope with the human eyes, there’s also a test that does side scatter of light called flow cytometry. That helps to look at a deeper level, maybe the thousandth, maybe even down to the millionth level, what these cancer cells do.
Katherine Banwell:
What sorts of questions should patients be asking about test results?
Dr. Naveen Pemmaraju:
I think the number one and number two questions that I advocate for patients or on programs like this, I think the one question that may help a lot is this question of when you hear all the data and ask the question, “Hey, is there any other questions I should be asking that I’m missing?” It’s an interesting question, right? It’s almost a meta, right, kind of a situation. However, when you ask that, every time I’ve been asked in the clinic, it makes me pause and say, “Now that you mentioned it, X, Y, and Z.”
So, I think it’s a good one to ask either your physician or whoever healthcare provider is in the room, again, nurse, or PA. It’s an interesting one, right? It kind of makes someone maybe even put themselves in your shoes. So, I like it as a device to make people pause in a busy clinic. Yeah, the second question that I think is a good one is to say, “While things are going well right now, I wanted to ask you, doc, what are some things that could happen in the next six months, one year, or two years, adverse events or abnormal things, and is there something I can do to plan for it?”
Again, it may be somewhat of a theoretical question. The doctor may say, “Okay, right now things are going well,” but it kind of makes people think about contingency plans, and alternative things. Well, now that you mention it, there is this one side effect of this drug. I don’t know, I think those are two kinds of go-to questions that I want people to be equipped with.
Katherine Banwell:
Yeah, that’s great advice. I’d like to add that if you, the viewer, are interested in learning more about myelofibrosis testing and treatment, PEN has a number of resources available to you. You can find these at powerfulpatients.org/MPN or by scanning the QR code on your screen.
So, once all testing is complete and the patient has an accurate diagnosis, they’ll work with their doctor then on a treatment approach. You’ve touched on this a little bit, but
What are the types of treatment available for people with myelofibrosis?
Dr. Naveen Pemmaraju:
Yeah, thanks, Katherine. We’ll keep it general and standard of care. As you mentioned at the top, I’ll reiterate, that none of these are intended to be specific instructions for specific folks. However, in general, for the category of patients with myelofibrosis, in general, there’s not many treatments, unfortunately. As of 2024, we have only four standard JAK inhibitors. So, that’s this pathway we’re talking about, JAK-STAT. Interestingly, you don’t have to be JAK2V617F mutated. These are for the whole pathway.
So, all patients with myelofibrosis, are intermediate to high risk. The first one, Katherine, is ruxolitinib (Jakafi), which has been around for more than a decade, and first in class JAK inhibitor. The second drug is fedratinib (Inrebic). The third is pacritinib (Vonjo), approved only in 2020 for those patients with less than platelets of 50. Then the myelofibrosis drug, momelotinib (Ojjaara), just approved not even a year ago, in September of 2023 for myelofibrosis with anemia. So, those four are considered as called JAK inhibitors.
They are really the only targeted therapy class of drugs specifically approved in the MF space. Outside of that, there’s older and other drugs that me and others have used, if you will, so-called off-label or historical use, hydroxyurea (Hydrea), interferon products such as pegylated interferon. Hypomethylators such as azacitidine (Vidaza) and decitabine (Dacogen), particularly in more advanced cases. Some of those drugs are borrowed from MDS and AML and have been around for decades.
Then of course, finally, clinical trials. We really recommend folks, if they have the ability and feasibility, clinical trials, even in the first diagnosis setting. So, untreated, first therapy. These clinical trials, Katherine, are based on three factors. One is JAK inhibitor plus another agent. So, that’s kind of like a combination trial. Two is add-on agents. So, you’re already on the JAK inhibitor for a while, maybe it’s starting to not work. Then you add in a third agent.
Then three is a completely novel agent beyond the JAK-STAT pathway. Then maybe we can even add a fourth one now as this is evolving in real-time, which is anemia-targeting drugs. Many of our patients have either transfusion-dependent or bad anemia. Some of the drugs that are being developed are specifically aimed at them.
Katherine Banwell:
There are a couple of new and emerging treatments as well, right? What are those?
Dr. Naveen Pemmaraju:
Yeah, so right. So, I’m proud to report to the viewers that just now in real time, just in the last year, really we have had several major developments. Now these are not yet FDA-approved agents. They’re experimental investigational agents, but they’ve reached what’s called Phase II or Phase III testing which are the later stages of testing. I’d like to highlight four or five of those.
These are mostly in the combination space. So, this is a JAK inhibitor plus the new agent. One is called navitoclax. That’s a BCLXL inhibitor, not yet FDA-approved for any indication. However, this has been shown to have activity in the Phase I and II trials, either as a single agent or in combination.
Now that’s reached Phase III testing. The second one is the pelabresib agent, which is a bromodomain or BET inhibitor. A third, if you can believe it, it’s selinexor (Xpovio), which is an XPO1 inhibitor. Also, a fourth really now entering into Phase III trials is the MDM2 inhibitor navtemadlin. You have these four drugs, which are either completing or starting Phase III, which is the most advanced testing.
That means they’re randomized trials, usually international trials, many hundreds of patients. It’s an amazing effort that’s unprecedented. By the way, these are being tested in the frontline setting before patients have ever had a JAK inhibitor in combination with. Beyond that, Katherine, there’s many, many trials with novel agents by themselves. So, imetelstat (Rytelo) comes to mind, which is a telomerase inhibitor, for example, which is also in Phase III testing in the relapse setting. So, you’ve already had a JAK inhibitor, it didn’t work out for you. Interestingly in that trial, the overall survival is the primary endpoint rather than spleen and symptoms, which marks the first time we’ve ever seen that.
It also marks the understanding that these chronic diseases, chronic myelofibrosis can then turn into a more advanced acute in the relapse setting. So, that’s just a sample of some of the ones that are now entering the late stages of trials, many more in Phase I and II. In a good way, there’s a new trial opening once a week.
Katherine Banwell:
That’s exciting news. So, the symptoms of myelofibrosis as well as the side effects of certain medications can vary greatly among patients.
Dr. Naveen Pemmaraju:
Yeah.
Katherine Banwell:
Why is it critical for patients to share any issues they may be having with their care team?
Dr. Naveen Pemmaraju:
Yeah, exactly what you said. So, those two concepts are tied. Since the disease is so rare and it’s so heterogeneous, not just patient to patient, but within the same patient over the journey of years, that is the reason. So, because of that, that’s why one has to communicate every single thing to the healthcare team. It’s interesting. Something that the patient may not believe is serious, the caregiver sometimes knows, right, team?
So, sometimes the person who’s your loved one or caregiver, “Oh, you know, that’s not-quite-right.” Sometimes the patient knows obviously, and then sometimes the healthcare team may say, “You know, that’s not-quite-right.” I think the not-quite-right thing is the key because that is what supersedes or at least precedes lab testing, X-rays, imaging, and bone marrows, it has to be some provocation. So, what I try to tell people is you know your body best. So, you want to be in touch with yourself, with your body, and anything that isn’t right, don’t be the final judge on that.
Push it up the chain, let your caregiver know, let your doctors know, let your team know, and let them help you decide. Sometimes it may be nothing, that’s fine. Sometimes it may be something. Sometimes it may be something outside of your MPN. That’s another key theme, I think, I mentioned here a couple of times. Anemia is a good example. So, lowering of the hemoglobin. It’s exactly what you just asked me. So, in addition to looking to see if it’s the disease progression itself, okay, fine.
However, could it also be drug toxicities, as you mentioned? So, the JAK inhibitor may be causing the anemia or whatever. Then the third bucket is, could it be anemia of regular life stuff, iron deficiency anemia. Could it be a colon cancer or a polyp that’s hiding there? Could it be vitamin B12 deficiency, hemolysis, immune, or something destroying the red blood cells, etc., etc.? So, you make an awesome point, which is all of that can be alleviated or the ball can be started rolling, if you will, by mentioning it. So, the key is no shame, no silence, and mention everything.
Katherine Banwell:
No silly questions.
Dr. Naveen Pemmaraju:
No silly questions, that’s right.
Katherine Banwell:
Right. I’d like to get to a few audience questions that we received prior to the program.
Dr. Naveen Pemmaraju:
Sure.
Katherine Banwell:
Cliff wrote in with this question. “Can you explain the dynamic international prognostic scoring system or DIPSS?” Thank goodness there’s an acronym for that.
Dr. Naveen Pemmaraju:
Yeah, no, it’s a great question, scoring systems, right?
Katherine Banwell:
Yeah, and Cliff wants to know how he can ask his doctor about it.
Katherine Banwell:
Right, so the easiest way to talk about it, the good news is everything we’ve been talking about is incorporated in the scoring system. So, said in another way, we’ve been talking about it subjectively, the scoring systems try to make the subject objective. So, quick history, these started in 2009 with the IPSS, International Prognostic Scoring System. The concept there were a thousand patients in Europe and basically trying to observe the natural history of the progression of myelofibrosis. This was just before, just as the JAK inhibitor era was starting. What we found is that the four groups nicely separate.
So, the lowest of the low-risk group potentially can be measured in decades for overall survival. Intermediate one, intermediate two, and high risk, again, all separated by overall survival and AML leukemia transformation risk. Now, that’s evolved over time as the questioner is asking for more sophisticated scoring systems. So, that’s all you need to know. So, DIPSS Plus just means Dynamic International Prognostic Scoring System.
Then there’s DIPSS plus, and can you believe it? There’s even the MIPSS now, the Molecular International Prognostic Scoring System. All right. So, at least there’s a rhyme and reason there. I think each iteration is telling you that we are dynamically understanding more about the disease. Two, the IPSS, the original one, was meant to be only at diagnosis, and the DIPSS by definition, dynamic scoring, is any time during the course of the disease, that’s interesting. Then three, they’re incorporating new factors each time.
So, from the time of the IPSS to the DIPSS and now the MIPSS, you’re incorporating all these factors that we couldn’t before. Cytogenetics, molecular findings, anemia, transfusion, burn, thrombocytopenia, etc. So, that’s basically it. You can ask your doctor. I mean, basically, in the course of what we do in the non-clinical trial standard of care, even if somebody doesn’t hand stop and calculate these risk scores, we’re talking about the same thing, right? The subjective or the objective matchup.
However, of interest to the patients, there are calculators that are available, you know, obviously rather than doing it in isolation in your house. Yes, it is better, I agree to do it with your doctor, with your provider team, and see what it means for you. The goal of these is twofold. In clinical trials to help stratify patients so you can understand who’s high risk versus lower. However, in the standard of care, sure it may help with transplant decisions, referrals for clinical trials, etc.
Katherine Banwell:
Okay. All right, this next question comes from Joel. “I understand that mutational testing should be done at diagnosis. Is there a point where there would be a need to repeat this test?”
Dr. Naveen Pemmaraju:
Oh, that’s an awesome question. So, we were mentioning that earlier. I do believe and I advocate that all patients should have molecular testing, particularly now as it’s more available widely before it wasn’t. Again, we level set what we’re talking about. In myelofibrosis, three common driver mutations, JAK2, CALR, MPL makes up about 90 percent.
Then in addition to that, there’s the triple-negative, and you usually find an additional mutation. Then on top of these big three, it’s common to have co-mutations, ASXL1, etc. What we found in this MIPSS score that we just mentioned ties into that. We found now that for the first time, we can incorporate these molecular findings to prognosticate for the patients. That’s why it’s important to check them. So, to this question by Joel, yes, if you have access and availability, not only checking it at baseline but later on at a provoking event.
So, at the time of relapse, progression, going onto a clinical trial, just to name three of several. I think it’s a good idea to recheck the molecular status. The problem and barriers are what you would expect, cost, expense, access, availability, justification, etc., etc. So, it’s not a mandatory part of the field, especially in the standard of care, non-research aspect. However, if we can get to the point where we can do that, it would be nice and helpful because these mutations change, they’re dynamic.
You can have negative for mutation at baseline, positive, and even vice versa, depending on therapies. Are you goimg to go for a transplant? Are you going to go to a clinical trial? Are you changing therapy? It would be nice to know.
Katherine Banwell:
Right. All right, here’s one more from Diana. “Can diet play a role in either manifesting the disease and or helping with healing? Also, how important is exercise to the healing?”
Dr. Naveen Pemmaraju:
I give a lot of credit to this area, to my colleagues, Ruben Mesa, Dr. Angela Fleischman, and Dr. Robyn Scherber. A lot of data that’s come out of these groups, which has shown two major findings in our MPN patients of potential clinical significance. One is as the questioner is asking about diet. It is true that we’re, several studies are pointing towards the anti-inflammatory Mediterranean diet as a potential benefit to our patients with MPN. Lots of different ideas there when they measure cytokines.
These abnormal protein signatures that are in MPN patients can cause fatigue and some of the bad quality of life can be dramatically improved in some cases by following a strict Mediterranean diet over weeks and months. So, that’s something important. People should check it out. Obviously, diets have to be addressed with each patient and each provider because sometimes a diet may work for someone and not for you because of comorbidities, vitamin deficiencies, electrolytes, etc.
Then the second aspect, if I may include in this question, is also the concept of yoga/meditation. Dr. Ruben Mesa and others have shown, the same thing, that you can have a potential downregulation of some of these abnormal cytokines. However, the caveat is it must be done right with a guided trainer in a real program over a certain period of time. What I think both of these non-pharmacological interventions tell us is that there are things beyond medicines and pills that may really help our patients in some aspect of the disease.
Well, if that aspect is fatigue, night sweats, headaches, I think that’s a really important thing. So, let’s say together on this program that these data sets are evolving, they’re interesting, they’re intriguing. For some people, it may be an easy incorporation. Frankly, some people may already be doing these things, but as you ask nicely, let’s include in the discussion non-pharmacologic as we heavily investigate the pharmacologic as well. We’re all open to that. Let’s see the data, and the data is evolving.
Katherine Banwell:
Yeah, absolutely. Well, those were all great questions from our viewers. We ask that you continue to send them to question@powerfulpatients.org, and we will work to get them answered on future programs. I’d like to turn back to self-advocacy for a moment, Dr. Pemmaraju. Managing the worry associated with a diagnosis or concerns about the future, and we did touch upon that earlier, it can lead to anxiety and fear. Why is it important for patients to share any worries they may be having with their care team?
Dr. Naveen Pemmaraju:
Well, I love this question. It really wraps up everything we’re talking about here. I believe that part of the journey for the patient does include mental and psychological safety. So, it’s very difficult to make major life decisions when one is not feeling mentally, or psychologically safe. So, that’s what you’re hitting on here. Anxiety, fear, and worry, of course, are a natural and important part of the patient journey with any cancer, much less a rare cancer and blood cancer on top of that. However, sometimes in some patients, it can become so paralyzing, so overtaking, and overwhelming that it may prevent the ability of the patient to receive information, process it, and then make a decision back. Yes, we want people to have caregivers, and power of attorney, all those things are essential, but we also want people to have their own agency in aegis.
So, I would approach this from three aspects. I really love this question because I don’t think we were addressing it head-on 10 or 15 years ago. One aspect is the disease itself. These MPNs, systemic mastocytosis, eosinophilia, myelofibrosis, PV, ET, all of these MPNs can secrete these cytokines and granules that can mess up the patient’s mindset, even just profound fatigue leading to a slowing down of the neurological process. So, I think underlying control of the disease is something that can affect this. Number two is the side effects from some of these medicines. Interferon is a great example, a wonderful class of drugs that’s been around for decades, treated for solid and liquid tumors, but it has a known side effect of causing brain fog. Some of these issues can even cause depression and anxiety in some people. So, education, mitigation, following these things with dose reduction, that’s an important part.
A third aspect, Katherine, is actually looking with a counselor and a therapist on the spectrum of this. So, normal, adjustment disorder, depression, for example. What we’ve had as a breakthrough at our center has been the supportive palliative care team. They’ve been phenomenal. So, this is a group of doctors who’s kind of one-third internist, one-third oncologist, and one-third psychiatry support.
So, rather than the usual consults that we used to do either to psychiatry or to social work case managers, there is this burgeoning field of supportive care medicine which has revolutionized the care, I think, particularly for solid tumor patients and now hopefully for our blood cancer patients. So, I’m able to refer patients for a variety of reasons. There’s a fatigue clinic for overwhelming fatigue. There is obviously depression, and anxiety support, either with medications, talk therapy, or both. Smoking secession for folks who are still smoking and maybe either withdrawing or quitting is causing stress.
So, it’s a really cool science and if your center has that, that’s something to inquire about. Then lastly, as we mentioned, a nice running theme today, Katherine, is looking for other medical stuff outside of the MPN. I mentioned thyroid earlier. Remember, you have a thyroid abnormality that can cause fatigue, depression, and anxiety, right? So, what’s your TSH thyroid function, and vitamin deficiencies?
Screening for your other well-person screening exams, looking for solid tumors, looking for other conditions that may be mimicking the MPN, or mimicking one of your other aspects. So, again, it comes down to partnership with the primary care team and looking at that. So, I think those are some of the aspects that I want to mention, but it’s such an important part of the journey. I really have to mention that as well.
Katherine Banwell:
Financial concerns may weigh heavy on patients and families. While everyone’s situation is different, do you have advice for where patients can turn for financial support?
Dr. Naveen Pemmaraju:
I think this is going to be the next great revolution. Just like I mentioned, the psychiatry, mood, and quality of life realm, I think this will be the next one of the next decade. I think largely it has been not even overlooked, just misunderstood. I’m an academic. I’ve been an academic my whole life, so I’ve never practiced in a private practice. So, some of these issues are quite difficult and foreign for many of us academic doctors.
In the community setting, there’s a whole set of pressures. Then of course, as you mentioned, there is a whole theme of the pharmaceutical companies helping. In the case of the JAK inhibitors, many of them have patient assistance programs, which have been vital to our patients. So, I think that financial toxicity, that’s what you’re asking about, right, is going to be the next era, the next realm, has been severely underlooked at, really misunderstood.
You know, I think at the academic centers, you know, obviously we have access to financial counselors, business office, those folks are invaluable. I see them as an essential part of our team, particularly on patients who are trying to get on clinical trials, etc. I think in the community aspect where many of our patients are treated, I think there’s going to be a challenge. So, we have to work with insurance companies, pharmaceuticals, local clinics.
For patients who don’t have healthcare insurance, try to get them insurance, county systems, cache safety net systems. However, I think you hit on it. I think this will be a new vital sign. It’ll be a new toxicity. It’ll be a new aspect when we consider new drug approvals, and financial toxicity.
Katherine Banwell:
As we close the program, Dr. Pemmaraju, what would you like to leave the audience with? Why are you hopeful about the future of myelofibrosis care and treatment?
Dr. Naveen Pemmaraju:
You know, I am hopeful. I am very hopeful. I think the two biggest things that I’m excited about for our patients and their caregivers are one, the burgeoning clinical trial portfolio that we have all over the world.
Very excited to see the interconnections from Asia, Europe, North and South America. We’re trying to make inroads into Africa and Australia as well. So, a true worldwide effort for MPNs, particularly myelofibrosis and clinical trials. So, stay tuned for that. I think that’s an exciting aspect. So, not just the existence of them, but the interconnectivity, communication, improvement, and availability. I think the second aspect that I’m super excited about is the democratization of information.
Honestly, 10 years ago, it was kind of difficult to find out information about these diseases, not 100 years ago, just 10 years ago. I really attribute social media and the interconnectivity of folks on these platforms to getting information out there. I would put this type of a platform as well in that same conversation, which is newsflash, nobody’s reading books anymore. Okay, there I said it.
However, people do have time for a quick two or three-minute blurb while they’re in the coffee line. So, if they can watch a snippet of an interview like this. They can get an email blast about a community town hall. They can get a paragraph on the new drug that just came out. People can take in information in small amounts so I think we have to meet folks, Katherine, where they are.
We cannot expect people to go to the library and open up a dusty book. I mean, that was in my generation 30 years ago. So, people are on their phones, let’s meet them on their phones. They’re online let’s meet them there. If you’re going to have an in-person town hall, make it high-yield, make it worth somebody’s time and energy and effort frankly, to leave their house to come. Finally, let’s make things affordable from an educational standpoint, if not free, to get the information to the people who need it the most. I’m hopeful about that. I think social media and online platforms have helped us with that.
Katherine Banwell:
Yeah. Well, that’s great advice, Dr. Pemmaraju. I want to thank you for joining us today. It’s been a pleasure speaking with you.
Dr. Naveen Pemmaraju:
Thank you so much, Katherine, to the team. I love doing these with you, and thanks for doing this good work.
Katherine Banwell:
Thank you to all of our collaborators. To learn more about myelofibrosis and to access tools to help you become a proactive patient, visit powerfulpatients.org. I’m Katherine Banwell. Thanks for being with us today.
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