Tag Archive for: MD Anderson cancer center

The Importance of the FLT3 Mutation in AML

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The Importance of the FLT3 Mutation In AML from Patient Empowerment Network on Vimeo.

What do acute myeloid leukemia (AML) patients need to  know about FLT3 mutation? Dr. Naval Daver from the University of Texas MD Anderson Cancer Center discusses considerations about the mutation. Learn about the incidence of the FLT3 mutation, risk of relapse, and treatment options.

[ACT]IVATION TIP from Dr. Daver: “ it is very important to know the status of the FLT3 the mutation, both in diagnosis to see if one would benefit by the addition of the FLT3 inhibitor to the frontline induction chemo as well as in relapse because this would open up the option for FLT3  inhibitor targeted therapies, which would probably have the best chance of response and long-term outcomes.“ 

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Transcript: 

Art:

Dr. Daver, for AML with a FLT3 mutation, what have we learned, and what is currently being investigated?

Dr. Naval Daver:

AML with the FLT3 mutation is very important from both prognostic and from therapy perspective, prognostically, this is considered to be one of the high-risk mutations, it’s also one of the most frequent mutations in AML in, seen in about 30 to 35 percent of younger and about 15 to 20 percent of older patients with AML, and these patients often have very prolific disease, elevated white count leukocytosis. And without the addition of FLT3 inhibitors, there is a high risk of relapse and a short overall survival. 

Over the last 15 years, a number of targeted therapies called the FLT3 inhibitors have emerged, these started with the first-generation FLT3 inhibitors drugs, such as lestaurtinib and sorafenib (Nexavar), now we have the second-generation FLT3 inhibitors, this includes drugs like gilteritinib (Xospata), quizartinib, and crenolanib which are more potent, specific, and better tolerated.

The first study that showed that the incorporation of FLT3 inhibitors improves outcome was a study called RATIFY Study, this is a frontline study looking at newly diagnosed FLT3 mutated younger patients where we added the FLT3 inhibitor midostaurin (Rydapt or Tauritmo), which is the first-generation FLT3 inhibitor to the standard induction chemo versus a placebo, added to standard induction chemo, induction chemo being standard of care to that time and this showed that in the addition of FLT3 inhibitor to induction chemo did improve remission rates and overall survival as compared to induction, and led to the approval of the FLT3 inhibitor midostaurin in the frontline setting. 

Since then, two other FLT3 inhibitors, second-generation potent FLT3 inhibitors drugs called gilteritinib, and lestaurtinib have also been evaluated. Gilteritinib, in a relapsed setting where single-agent gilteritinib, has given 50 to 60 percent response rates and has been extremely well-tolerated and much better than any other salvage treatment in the FLT3 space that we have ever seen, and in the frontline setting quizartinib and second-generation inhibitor also very recently, just a few months ago, there was data showing the combination of his art with intensive chemotherapy improved survival as compared to intensive chemotherapy alone. 

And so we think we are…they will be a third for the inhibitor to get approved, so there’s been a lot of progress overall in the three space, and there are other newer FLT3 inhibitors also in early clinical investigation that we think could eventually be as part or even better, the activation point related to this question is that, for the inhibitors have dramatically improved outcomes, both in the frontline setting when added to traditional backbone intensive chemotherapy as well as potentially lower intensity therapy, as well as in the relapsed refractory setting, and it is very important to know the status of the FLT3 the mutation, both in diagnosis to see if one would benefit by the addition of the FLT3 inhibitor to the frontline induction chemo as well as in relapse because this would open up the option for FLT3  inhibitor targeted therapies, which would probably have the best chance of response and long-term outcomes. 

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What Different AML Subtypes Are More Prevalent in Certain Demographics?

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What Different AML Subtypes Are More Prevalent in Certain Demographics? from Patient Empowerment Network on Vimeo.

Are some acute myeloid leukemia (AML) subtypes more common in some demographic groups? Dr. Naval Daver from the University of Texas MD Anderson Cancer Center discusses different forms of AML. Learn about the extent of knowledge about AML subtype demographics.

[ACT]IVATION TIP from Dr. Daver: “Patients, when they transformed what we call secondary AML or MDS, seemed to have a higher predilection for certain high-risk communications such as TP53, and these are best treated with ongoing frontline clinical trials at large academic centers.“

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Transcript: 

Art:

Dr. Daver, what are the different subtypes of AML, are various subtypes more prevalent in certain demographics?

Dr. Naval Daver:

The main way we have classified AML has actually been changing, so when we talk about subtypes  there are actually two different classification systems like WHO and the ICC or ELM classification system. Traditionally, we have been using the ELM for prognostic classification of AML, this divides patients into three major buckets, what we call a favorable intermediate and adverse, and these are based on the underlying chromosome cytogenetics abnormalities and molecular or next-generation sequencing profile of the patients.

In general, in AML there has actually been limited data and publications regarding the demographic distribution, whether it’s regional or racial or cultural, one of the things that we do know, for example, in acute lymphoblastic leukemia is that in the Hispanic population, there seems to be higher frequency of things like FLT3-positive ALL. 

But in the AML population, there actually does not seem to be, at least based on published data, huge differences in the molecular or cytogenetic presentation. We have seen some data from different countries that there may be a difference in the prevalence of communications across different regions. For example, in Japan, we do see that the incidence of FLT3 and NPM1 appears to be lower than what has been reported in the United States.

Also, we see in Europe and United States, the incidence of these mutations with FLT3, NPM1 is similar, and then we are seeing in some of the larger academic centers in the U.S., there is an enrichment of referral of patients with TP53, which is very adverse and most difficult to treat mutation, and a lot of that we think is because patients with solid tumors and with other hematological malignancies are surviving longer with the CAR-T therapies, immunotherapies, and because it is over time, they have a risk of developing second AML, which is enriched for TP53 mutation, so we do see over the last two decades that from TP53, which used to be about 5 percent to 10 percent, is now up to 20 percent to 25 percent of AML and growing in proportion because it’s better survival and solid tumors and lymphomas.  

The activation tip related to this question is that in general, they don’t review discrepancies based on geography and race, and region in the molecular cytogenetics. However, we do see differences in patients who have received prior chemotherapy, radiation therapy, AML therapy for other solid tumors and lymphoma.

These patients, when they transformed what we call secondary AML or MDS, seemed to have a higher predilection for certain high-risk communications such as TP53, and these are best treated with ongoing frontline clinical trials at large academic centers. 

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AML Treatment Approaches Expand for Older and High-Risk Patients

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AML Treatment Approaches Expand for Older and High-Risk Patients from Patient Empowerment Network on Vimeo.

How have acute myeloid leukemia (AML) treatment approaches expanded for older and high-risk patients? Dr. Naval Daver from the University of Texas MD Anderson Cancer Center shares insight about additional treatment options. Learn about the potential for long-term cures for these patient groups. 

[ACT]IVATION TIP from Dr. Daver: “There is a dramatic progress, especially in the treatment of older unfit AML with the approval of the azacitidine-venetoclax combination.”

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Transcript: 

Art: 

Dr. Daver, for older and high-risk AML patients, how are the treatment approaches expanding?

Dr. Naval Daver: 

In older and high-risk AML, the major approval has been the combination of azacitidine (Onureg or Vidaza) and venetoclax (Venclexta), which is a BCL-2 inhibitor, the regimen was evaluated in a large Phase III study called the VIALE study, where we looked at the standard of care for the last two decades for older unfit AML, which azacitidine alone versus the combination of azacitidine and venetoclax and this combination showed a three times higher remission rate, 75 versus 28 percent overall remission rate as well as an improvement in overall survival and long-term survivors.

So this has led to great progress with now remission rates of 75 percent achievable in older unfit AML and many of them being durable at three years with ongoing follow-up, so this has really opened the door for us to be able to treat patients up to 75, 80, 85 years of age with effective therapy given the three parts of these to achieve remission, which is usually associated with freedom from transfusion improvement, quality of life, improved energy, less time in the hospital, less infections.

The other progress now is coming from the use of targeted therapies as well in these populations, and even though the HMA venetoclax or azacitidine combination is doing very well.

We now have data, in fact, from the ASH 2022 December meeting that at three years, about 25 percent or so I would still remain alive with azacitidine was even or 8 percent, now it’s 25 percent. But, of course, we want to do much better than that, and so this is where we are incorporating the targeted therapies, the FLT3 inhibitors, the IDH1, IDH2 inhibitors, menin inhibitors, and immunotherapies onto the backbone of azacitidine-venetoclax, which we hope will further improve that long-term survival cure from 25 to hopefully 50 to 60 percent and beyond.

So a lot of progress, you know, going from less than 10 percent, a 30 percent survival, long-term, and I think in the next few years, even up to 50 percent with some of these new combinations. The activation tip related to this question is that there is a dramatic progress, especially in the treatment of older unfit AML with the approval of the azacitidine-venetoclax combination.

This regimen is now giving high remission rates, which approximate remission rates that are seen with traditional intensive chemotherapy without the mucositis and toxicities and better volatility, and we are now working to further improve the remission and the durability of this dominant of initial.

 …potentially adding targeted therapy such as FLT3 inhibitors, IDH1, IDH2 menin inhibitors, and we think that potentially in the next decade, we could be achieving long-term cures in a large proportion of older unfit AML, which was something one could just dream of a decade ago. 

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What Promising AML Treatments Are Available for Newly Diagnosed Patients?

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What Promising AML Treatments Are Available for Newly Diagnosed Patients? from Patient Empowerment Network on Vimeo.

What do newly diagnosed acute myeloid leukemia (AML) patients have for promising treatment options? Dr. Naval Daver from the University of Texas MD Anderson Cancer Center discusses progress in available treatments. Learn about therapies determined by key factors.

[ACT]IVATION TIP from Dr. Daver: “It’s very important to really consider all the available treatment options and if needed to seek consultation with an expert or academic center to get the most up-to-date treatments available for AML.“

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Transcript: 

Art:

Dr. Daver, for newly diagnosed AML patients, what are the latest and most promising available therapies?

Dr. Daver:

For newly diagnosed AML at this time, the most promising agents include targeted therapies and BCL-2 inhibitor treatments, these are non-chemotherapeutic drugs, and we’ve seen great progress in the application of these as well as recent FDA approvals.

So one of these is an agent called venetoclax (Venclexta), which is a BCL-2 inhibitor and venetoclax in combination with hypomethylating agents such as azacitidine (Onureg or Vidaza) has shown a response to close to 75 percent. 

And the nice thing is that this regimen can be given and patients who are older than 70, 75 years of age, and even those who are having comorbidities are not fit for traditional intensive chemotherapy with similar response rates, so this has been approved in the last couple of years for the frontline treatment of AML, and we’ve been using this combination of venetoclax and azacitidine quite frequently with high efficacy in this patient population, the other new agents that have shown breakthroughs in AML are the targeted therapies, these include FLT3 inhibitors that target the FLT3 mutation and these have shown good activity, but the single agents with gilteritinib (Xospata) being approved in the relapsed refractory setting as a single agent where gilteritinib showed a response rate of about 50 percent as a single oral targeted therapy in relapsed FLT3-mutated AML, which is actually better than the response rate with high-dose combination more where the response rate is only about 25 to 30 percent.

So, gilteritinib is now approved, and it’s now moving and being evaluated in frontline setting other FLT3 inhibitors like lestaurtinib (CEP-701), actually just recently completed frontline studies showing improved outcome when lestaurtinib added to intensive chemo versus just intensive chemo in FLT3 in AML. And we hope and think there’s a good chance lestaurtinib will be approved in the near future.

And also IDH inhibitors have been approved both in the relapsed setting, frontline setting, and now we even have a third group of targeted therapy is called the menin inhibitors, they target MLL rearrangement and NPM1 mutations, which are seen in about 15 percent to 20 percent of the AML, so there’s been a lot of progress.

All of this in the last seven years, six, seven years with multiple targeted therapies, with multiple inhibitor-based treatments, showing progress in AML and then also recently, the concept of maintenance therapy, this is something we used for the last couple of decades in a acute lymphoblastic leukemia and multiple myeloma and in lymphoma.

But we had not had clear data in AML, but the recent study using oral formulation of a azacitidine in CC486 has shown the maintenance in patients who complete an induction consolidation and could not go to allogeneic stem cell transplant for one reason or the other was important and improve both overall survival and relapse-free survival, and so this is the first time now we have an FDA-approved and standard use of maintenance therapy after the traditional induction consolidation, so even changing the general paradigm of AML therapy.

So a lot has changed in the last seven to eight years in the treatment of acute myeloid leukemia, and this is very exciting.

And the activation tip related, this question is that there are multiple new targeted and low intensity therapeutic options available for patients with acute myeloid leukemia, and in our institution, in my opinion, even older patients are eligible for some form of therapy or the other…very few patients, if any, today, are being sent to hospitals or palliative care without treatment.

So it’s very important to really consider all the available treatment options and if needed to seek consultation with an expert or academic center to get the most up-to-date treatments available for AML. 

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[ACT]IVATED AML Resource Guide

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Myeloma Treatment & Research Updates From 2022 ASCO and EHA Meetings

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Myeloma Treatment & Research Updates From 2022 ASCO and EHA Meetings from Patient Empowerment Network on Vimeo.

Myeloma specialist and researcher Dr. Krina Patel discusses highlights from the recent American Society of Clinical Oncology (ASCO) annual meeting and the European Hematology Association (EHA) 2022 Congress. Dr. Patel shares promising research updates related to approaches including: stem cell transplant, CAR T-cell therapy, and bispecifics.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

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How Does Immunotherapy Treat Myeloma?

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Transcript:

Katherine:   

Dr. Patel, cancer researchers recently came together at the annual ASCO and EHA meetings. Are there any highlights from the meetings that myeloma patients should know about?

Dr. Patel:    

Yeah, so we had some amazing trials that were presented at both. And I got to actually go to Chicago for the ASCO meeting, and I’ll say we actually had a plenary session that was presented for myeloma. That doesn’t happen as often as we like. So, basically that was a study presented by Dana-Farber and all of the different groups around the U.S. that did a transplant study. And basically, they’re looking at patients who got induction therapy when they’re newly diagnosed with transplant versus they didn’t get transplant upfront. And it’s called the DETERMINATION study, and it was to determine should everybody be getting a stem cell transplant.

Katherine:  

Right.

Dr. Patel:   

And this is a trial that’s been going on for over 10 years; that’s why it was so highly anticipated. And basically, the biggest thing that we saw was what we call progression-free survival; so, the time that the myeloma hibernates is what I call it, for PFS. Basically, patients who got transplant upfront, it was 21 months longer that it stayed hibernating than if you didn’t get transplant upfront. So, that’s the trial, that’s what it was looking at, and that’s all they could really say about it. The good news is, even patients who didn’t get transplant upfront but then got transplant in second remission tended to have a really good, long progression-free survival or hibernation in that second remission.

So, it still tells us that right now, a transplant is still important for the majority of our myeloma patients. And basically, that’s sort of what that trial showed.

Now, the difference is we do different types of upfront therapies, and we have new things like CAR T and bispecifics that are coming up earlier. So, we’ll see in the future if it still holds up. But as of right now, it still holds up for transplant. The other big studies, of course, were some of our bispecific studies that use different antigens. So, antigens are the flags that are on the myeloma that we make these receptors for CAR T, so they can find the myeloma, or bispecifics go after that.

And basically, there are other antigens. BCMA, B-cell maturation antigen, is the big one that we use for everything right now. But now, we found even more antigens, which is fantastic.

So, we have something called FcHR5. We have something called GPRC5D. It’s like alphabet number soup, basically. But what’s really exciting is that these new antigens give us a different way of getting to that myeloma, especially if someone has already had a BCMA therapy and they’ve relapsed on that. Well, now we have even new ways to get to that myeloma cell. So, I think that’s some really, really exciting data.

And then, I’ll say the other big one was one of the CAR Ts, Cilta-Cel was something that they presented.

Again, this was two years after the last patient had gotten treated on the trial. And so far, they still have about 71 percent of patients that are still in remission two years after. So, that is huge.

Katherine:                  

Wow.

Dr. Patel:  

We’ve never seen that in relapsed refractory patients before, so we’re really, really excited to kind of have gotten that data to say, “Okay, we found a brand-new way of treating myeloma.” And it really is changing how we’re looking at even earlier lines of therapy now.

Katherine:   

Such promising news. That’s great.

What Are the Side Effects of Myeloma Immunotherapy?

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What Are the Side Effects of Myeloma Immunotherapy? from Patient Empowerment Network on Vimeo.

Myeloma specialist and researcher Dr. Krina Patel discusses the common side effects of immunotherapy and reviews tools that may be used to prevent complications.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

How Does Immunotherapy Treat Myeloma?

 What Is Myeloma CAR T-Cell Therapy?

 Myeloma Treatment & Research Updates From 2022 ASCO and EHA Meetings

Transcript:

Katherine:   

Are there other side effects that patients should know about and side effects that they might experience?

Dr. Patel:  

Yeah, so neurotoxicity is one that we don’t see as much as we see in lymphoma patients, which is again great but sometimes people can get something called ICANS, which is a type of neurotoxicity in the first 30 days after CAR T.

And basically, it can be as bad as seizures, but thankfully we don’t see that very often, or I haven’t seen it at all. But it can cause confusion. It can cause people to be extra sleepy. So, we have different treatments that we give to turn that around. Longer term, really, the big side effects are the counts being low. So, what we call cytopenias. So, white count, hemoglobin, platelets.

And so, that is something we see quite often in our patients who have had a lot of therapy for myeloma already, and then are getting something like CAR T.

So, a lot of my patients will still need transfusions even a month or two or three after, and we’re giving GCSF to help their white count come back up, et cetera.

Katherine:    

What’s that?

Dr. Patel: 

So, G-CSF is basically a growth factor that helps your neutrophil; so, a different type of white blood cell – come back up, which helps fight against bacterial infections.

So, it’s the same medicine for anyone who’s had a stem cell transplant. It’s the same medicine you get to get your stem cells into your blood but it’s at a lower dose. But again, it’s to avoid infections, to help present bacterial infections. The other one is infections can also be caused because of low IgG levels or what we call immunoglobulins; these are our antibodies that we have.

And the good news is, when CAR Ts or bispecifics or some of these immune therapies work really well, they’ll kill as many myeloma cells as we possibly can.

But they also kill good cells. So, they kill good plasma cells that make us antibodies and good B cells that make us antibodies. So, when that happens, people’s IgG levels will go down and that puts you at risk for infection too. So, we actually aggressively give people IVIG to help prevent those infections.

Immunotherapy: Which Myeloma Patients Is It Right For?

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Immunotherapy: Which Myeloma Patients Is It Right For? from Patient Empowerment Network on Vimeo.

Dr. Krina Patel, a myeloma specialist and researcher, explains how newer therapies, such as CAR T-cell therapy, are being used in myeloma and which patients these treatments are most appropriate for.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

How Does Immunotherapy Treat Myeloma?

 What Are the Side Effects of Myeloma Immunotherapy?

 Myeloma Treatment & Research Updates From 2022 ASCO and EHA Meetings

Transcript:

Katherine:   

Now, in reference to immunotherapy and CAR T-cell therapy, who are these types of treatments right for?

Dr. Patel:    

So, I think it’s really exciting that we finally are getting standard of care therapies for all these new immune therapies. So, our first CAR T for myeloma got approved a little over a year ago. Our second CAR T got approved just a couple of months ago, and we’re hoping our first bispecific will be approved in just a couple months.

Our fingers crossed. On the clinical trials, I will say our patients who had a good performance status, meaning they’re able to do everything else normally life-wise, those are the patients that got onto those clinical trials; and the reason is safety-wise.

So, T cells when we use them to kill myeloma, they release cytokines or enzymes, you can say, that are inside the T cells and that’s what they use to communicate with other immune cells to come help them kill.

Those are the same cytokines that make people feel really ill when they have the flu, for instance. So, as our immune system tries to fight infections when people get fevers, they feel chills, they feel just fatigued and tired, it’s those same kind of cytokines that, even when you try to kill the myeloma with T cells, people can get that same type of symptoms.

And really, the main, fevers and things like that, we can take care of. But when patients’ blood pressure drops or if their oxygen levels drop really low, that’s where we can run into some trouble. Now, the good news is, in myeloma, most of these new therapies don’t cause really bad CRS [Cytokine Release Syndrome] or really bad neurotoxicity that we can sometimes see. And so, thankfully most patients are okay, but really it’s making sure that none of our patients have bad toxicity. So, most of our myeloma patients, I will say, are eligible for these therapies. However, if someone has really bad heart disease or really bad lung disease, those are patients that maybe these are not the right therapies for.

What Is Myeloma CAR T-Cell Therapy?

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What Is Myeloma CAR T-Cell Therapy? from Patient Empowerment Network on Vimeo.

How does CAR (chimeric antigen receptor) T-cell therapy work to fight myeloma? Dr. Krina Patel, a myeloma specialist and researcher, explains how this novel therapy uses your immune system to treat the disease.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

How Does Immunotherapy Treat Myeloma?

 Immunotherapy: Which Myeloma Patients Is It Right For?

 Myeloma Treatment & Research Updates From 2022 ASCO and EHA Meetings

Transcript:

Katherine:   

What is CAR T-cell therapy?

Dr. Patel:    

So, CAR-T cells are sort of a biologic immune therapy where we are able to take T cells, a type of lymphocyte which help us, normally. All of us have them in our blood.

They come from our bone marrow, go into our blood, and they sort of go around in the blood and look for bad things, pathogens. So, infections, even cancer cells, our T cells help get rid of all of those bad things that we’re not supposed to have. And they each have a receptor. And so, T cells have this night vision, and they’re made for a specific type of pathogen out there that we aren’t supposed to have that can hurt us.

And so, what we can is to either take your own T cells out, or sometimes with something called allo CAR-T use a normal donor’s T cells. And when we take them, we basically can put a new receptor in there, a new night vision; and so, now they are trained to go after something that’s specific on the myeloma instead of a bacteria or a virus or anything. And basically, we grow those cells, and then we give those cells back to our patient after a low dose of chemotherapy, just so these T cells can go in, find the myeloma, use that night vision to find that myeloma wherever it is, kill, and then it actually causes other immune cells in your system to come there and start helping to kill as well.

And then, they start coming back down again. And so, really, it’s a novel way of using your own immune system, or somebody else’s, but to actually enhance both by the target to get that myeloma precisely as well as making more of them so that there’s enough to go around and kill all the cells that we possibly can.

How Does Immunotherapy Treat Myeloma?

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How Does Immunotherapy Treat Myeloma? from Patient Empowerment Network on Vimeo.

Immunotherapy harnesses one’s own immune system to fight cancer. Dr. Krina Patel, a myeloma specialist and researcher, explains how this therapy changing the treatment landscape for myeloma.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

What Is Myeloma CAR T-Cell Therapy?

 Immunotherapy: Which Myeloma Patients Is It Right For?

 What Are the Side Effects of Myeloma Immunotherapy?

Transcript:

Katherine:   

We’ve been hearing a lot recently about immunotherapy. Would you tell us what it is and how it works to treat myeloma?

Dr. Patel:       

Yeah, so I think immunotherapy is sort of where everything is  really changing the way we look at myeloma. So, I’ll date myself a little bit, but 15 years ago when I was a first-year fellow most people thought that immunotherapy wouldn’t necessarily work for myeloma. So, in all cancer care we have surgery possibly in myeloma.

We don’t use it as much, but if someone has a bone lesion that we need to do we might do some surgery there. We use radiation sometimes if we really need, for painful lesions or something that might be at risk for fracture. And we use chemotherapy all the time for treatment.

Immunotherapy is actually different types of medications. Some are proteins. Some are biologics that we can talk about it. But really, they harness your immune cells, all the other white blood cells that are in your bone marrow and in your blood, to actually go after the myeloma themselves. And so, there’s different ways we can do that. And, again, 15 years ago most people said, “No, we’re not going to be able to use immune therapy for myeloma because plasma cells,” which are myeloma cells, “are a white blood cell. So, their sisters, brothers, cousins, whatever you want to call those other white blood cells, how do we turn those into the enemy, or how do we make myeloma the enemy?”

And so, it took a long time for us to figure it out, but really, it’s about using your immune cells to kill that myeloma.

Myeloma Induction and Consolidation Therapy Defined

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Myeloma Induction and Consolidation Therapy Defined from Patient Empowerment Network on Vimeo.

Myeloma expert, Dr. Krina Patel, defines the role and purpose of induction therapy and consolidation therapy in myeloma care.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

Expert Advice for Newly Diagnosed Myeloma Patients

 The Role of a Myeloma Specialist on Your Care Team

 Relapsed and Refractory Myeloma Defined

Transcript:

Katherine:    

What is induction therapy?

Dr. Patel:      

So, induction therapy is usually referred for newly diagnosed patients who have never had therapy before and we are now trying to give something to knock that myeloma down. A diagnosis usually is when we have the most myeloma for somebody because they really didn’t know necessarily that they had myeloma before. And our goal is to knock that myeloma down, so it doesn’t cause any more clinical problems.

Katherine:  

What is consolidation therapy?

Dr. Patel:     

So, consolidation means that we’ve knocked that myeloma down now and we’re trying to keep it down, or there’s a little bit of myeloma left that maybe that initial induction therapy didn’t kill; that we try to kind of sweep it all up with the consolidation. So, usually the best example that I can give of consolidation therapy is high-dose melphalan (Alkeran) with stem cell rescuer or what we call autologous stem cell transplant. That, for patients who are in some type of response; then we do that transplant to really kill as many myeloma cells as possible. And then, we do maintenance.

The other part of consolidation therapy is, sometimes after transplant for some of our high-risk patients, or for patients that still have some myeloma even after stem cell transplant, we might give them three or four drugs again to knock the rest of that myeloma down for a little while. Sometimes we do four cycles or so. So, that’s another consolidation strategy.

Katherine:   

How long is a cycle?

Dr. Patel:      

So, each therapy is different but most of our different myeloma therapies cycles are either three or four weeks.

Relapsed and Refractory Myeloma Defined

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Relapsed and Refractory Myeloma Defined from Patient Empowerment Network on Vimeo.

Myeloma expert Dr. Krina Patel reviews the difference between relapsed and refractory myeloma and how these distinctions may impact care and treatment.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

Expert Advice for Newly Diagnosed Myeloma Patients

 The Role of a Myeloma Specialist on Your Care Team

 Myeloma Induction and Consolidation Therapy Defined

Transcript:

Katherine:  

Dr. Patel, could you define what relapsed myeloma is?

Dr. Patel:     

Yes, so as of today, for the majority of our patients we can’t cure myeloma to the point where we treat it, and it’s gone forever, right? I’m hoping one day we get there. And we’re getting better, but we’re not there yet. However, myeloma’s very, very treatable. So, what relapsed means is that, once you’ve had initial therapy after you’ve been diagnosed, our goal is to get that myeloma to as low as possible level so that it hibernates as long as possible. But eventually, that myeloma’s going to start waking back up. So, when it does, that’s called a relapse. That now, the proteins are coming up, the myeloma cells are growing and we need to do something to knock it back down again. So, that’s relapsed disease.

Katherine:

How is that different from refractory myeloma?

Dr. Patel:

That’s a great question. We talk about relapsed refractory all the time for myeloma. So, refractory actually means that your myeloma started waking up while on a certain medication. So, if you were on no medicines and then your myeloma came up, that’s considered relapsed. That’s not refractory. However, biggest example I can give you is when patients are on maintenance therapy after stem cell transplant, for instance. When they’re all on maintenance and their myeloma starts coming up while on maintenance, then they are considered refractory to that drug; so, if it’s lenalidomide (Revlimid), if it’s bortezomib (Velcade), whichever one it is.

So, any time the myeloma’s coming up while on active treatment, you become refractory. So, we talk about triple refractory or penta-refractory, and what that really means is how many drugs is your myeloma refractory to.

So, if you’re refractory to a proteasome inhibitor plus an immunomodulatory drug plus a CD38 antibody, right – I can give you examples of all of those, but basically different categories –then you’re considered triple refractory. And the more refractory it is, the harder it is to treat and the more novel therapies we need.

Katherine:

So, if a patient is taking three or four different drugs, how can you pin it down to know which drug or all of them are causing the refractory myeloma?

Dr. Patel:

So, it would be all of them. Let’s say, salvage therapy. You’re on three different medications or four different medications, usually three. We would say, if the myeloma’s coming up while you’re on all of them, you’re technically refractory to now all those medications.

Katherine:

All of those. Okay, all right.

The Role of a Myeloma Specialist on Your Care Team

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The Role of a Myeloma Specialist on Your Care Team from Patient Empowerment Network on Vimeo.

Why should you seek a consultation with a myeloma expert? Dr. Krina Patel discusses the important roles a specialist can play in your myeloma care, even from a distance.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

Expert Advice for Newly Diagnosed Myeloma Patients

 Relapsed and Refractory Myeloma Defined

 Myeloma Induction and Consolidation Therapy Defined

Transcript:

Katherine:  

You mentioned the healthcare team. Dr. Patel. How does a myeloma specialist fit into that care team?

Dr. Patel:

So, I will say, as a myeloma specialist, I probably have three different ways that I am involved in different patient’s care. So, I have patients who are from Houston, where I’m at, that come to MD Anderson for their treatment. So, I see them on a regular basis if they’re on treatment, or I’m following them to make sure their disease is stable, what’s going on. So, I see them regularly, and I’m their main doctor for their cancer. And then, I have patients who are maybe a little bit farther away, and I see them as part of the team.

So, they have their own oncologist in their community that they’re seeing and they come see me either virtually or in person every few months, or if something’s happening; if their myeloma’s returning or they’re having toxicity, then they reach out to me so I can talk about different ways we can change therapy. And then, the third really is for second opinions where patients don’t necessarily  want to come see me all the time but they might want to be on a clinical trial that we might have at MD Anderson. So, they come just for that trial and then they go back to their doctors again. So, we sort of do whatever works best for the patient.

Expert Advice for Newly Diagnosed Myeloma Patients

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Expert Advice for Newly Diagnosed Myeloma Patients from Patient Empowerment Network on Vimeo.

Myeloma expert and researcher Dr. Krina Patel shares key advice for patients newly diagnosed with myeloma, encouraging patients to take an active role in their care.

Dr. Krina Patel is an Associate Professor in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center in Houston, Texas. Dr. Patel is involved in research and cares for patients with multiple myeloma. Learn more about Dr. Patel, here.

Related Resources:

The Role of a Myeloma Specialist on Your Care Team

 Relapsed and Refractory Myeloma Defined

 Myeloma Induction and Consolidation Therapy Defined

Transcript:

Katherine:  

Myeloma can be a complex diagnosis. What are three key pieces of advice for patients who has just been diagnosed with myeloma?

Dr. Patel: 

I think any diagnosis of cancer, of course, is really hard, but multiple myeloma is so rare in the sense that people don’t know about it; that sometimes it’s the first time they’ve heard of it, when they’re diagnosed. And so, I think the biggest thing about more rare diseases in general, the best advice I could give is getting a myeloma specialist as part of your team. That doesn’t mean they have to treat you, but having them as part of your team. And we can talk about that in more detail. But the second part is really learning as much as you can and not necessarily all on the Internet.

Not everything on the Internet is correct. But really asking questions to your doctors, your nurse practitioners, your nurses, they all have different perspectives that asking questions for all of them is really worthwhile to kind of understand what you’re going through and what’s to be expected. And then, the last piece. I think with multiple myeloma patients, there are so many amazing patient support systems, especially after COVID but even before COVID, in terms of different groups that are sponsored by patients where you can listen when people come to give talks, et cetera. I think those are all phenomenal resources for patients.

Katherine: 

What do you think the role is of the patient in their own care?

Dr. Patel:     

So, gone are the days of paternalistic medicine, especially in the U.S. My job is not to tell you what to do, but my job is to really give you options as to what is the best possible therapy for you at that time. And really, your job is, as a patient, to make sure that they tell me all the information that’s important for them. So, for instance, if they can’t come to chemo every week because they just don’t have a ride or they have some other medical problems that maybe I didn’t know about, those types of things. We just have to have that open communication, so we can come to that best next therapy together with those decisions.

An Overview of Current DLBCL Treatment Approaches

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An Overview of Current DLBCL Treatment Approaches from Patient Empowerment Network on Vimeo.

What do diffuse large B-cell lymphoma (DLBCL) patients need to know about current treatment approaches? Expert Dr. Loretta Nastoupil provides an overview and gives an update about ongoing research comparing two treatment regimens.

Dr. Loretta Nastoupil is Director of the Lymphoma Outcomes Database in the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center. Learn more about Dr. Nastoupil, here.

See More From The Pro-Active DLBCL Patient Toolkit

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An Expert Review of DLBCL Research and Treatment Advances

 Diffuse Large B-Cell Lymphoma (DLBCL) Treatment and Research News

Diffuse Large B-Cell Lymphoma (DLBCL) Treatment and Research News

 How Is Diffuse Large B-Cell Lymphoma (DLBCL) Treated

How Is Diffuse Large B-Cell Lymphoma (DLBCL) Treated?

 

Transcript:

Katherine:

Dr. Nastoupil, now that we’ve discussed factors that go into the treatment choices, can you walk us through the currently available DLBCL treatment approaches and who they might be right for?

Dr. Nastoupil:

Absolutely. So, again, this is changing, and that’s good news. So, up until recently, R-CHOP or rituximab in combination with CHOP, which is an acronym for four different drugs, cyclophosphamide, doxorubicin, vincristine, and prednisone, has been our standard.

Again, what would potentially challenge that is the POLARIX study where we exchange vincristine for polatuzumab. We don’t know the results of that study yet. All we know is that it met its primary endpoint, meaning it met what it set out to do in terms of improving upon some of the outcomes achieved with R-CHOP.

We need to see the details to know if that means now every newly diagnosed diffuse large B-cell lymphoma patient will be offered the polatuzumab in combination with R-CHP study or whether or not there will still be some patients appropriate for R-CHOP.

But that is generally our first approach. Whether you get six cycles or a shortened course plus/minus radiation depends on your state. Once patients have completed therapy, generally, then we pursue what’s called surveillance.

So, we’re monitoring for any signs that the lymphoma has recurred or has not gone away. That’s a controversial topic in terms of how to conduct surveillance and one that I suspect will change over time. But for most patients, if the lymphoma is going to recur, it generally recurs within the first two years.

So, assessing patients either in the form of a CT scan, a PET CT, or a physical exam with labs every four to six months for the first two years is what most practices will pursue. I’m not saying that there is no chance that you would relapse beyond two years. It’s just that the majority of patients, at least 90 percent, if the lymphoma comes back, it usually does so within two years.

And the relapses that occur beyond two years are less predictable. They could happen at three years. They could happen at 10 years, as it’s hard to know how to do surveillance beyond two years.

If the lymphoma recurs, the first thing we need to do is biopsy it because there are many things that can mimic lymphoma on a scan – infection, inflammation, other tumor types. So, if there is ever a question about whether or not the lymphoma has recurred, I generally advise for all patients they undergo a biopsy to ensure that we know what we’re treating.

Depending on when the lymphoma recurs, if it happens within 12 months, this is another area that we are shifting our practice. In the past, for all patients who had relapsed large cell lymphoma, we would pursue what we call salvage or second-line chemotherapy. So, we mix up the chemo. We keep, generally, the rituximab, but we alter the chemotherapy agents. We wouldn’t give CHOP again.

And then we give a shortened course where we give two to three cycles. We repeat the scan. And for patients who’ve achieved what we call chemo-sensitive disease – so, that’s generally a complete response on scan – we would then move forward with high-dose therapy and an autologous stem cell transplant. So, essentially giving different but more intense chemo and rescuing patients from that maneuver with their own stem cells that will go back to the bone marrow and start making white blood cells, red cells, and platelets again.

What has shifted in the last six months is we now know that CAR T-cell therapy is superior to that approach, at least with two CAR Ts for patients whose lymphoma came back within 12 months. Again, we’re eagerly awaiting the full results of those randomized studies. But three trials were conducted. Two of the three suggest CAR T is better than second chemo and transplant for those patients who relapse within 12 months.

So, currently, we think that you’ll have a CHOP-like therapy with plus rituximab frontline. If you progress within 12 months, you potentially would be a candidate for CAR T-cell therapy. If the CAR T-cell therapy fails, which is true for about half of patients. Or if you’re deemed to not be a candidate for CAR T, we have several other new options that didn’t exist a year ago, including targeted or non-chemotherapy options.

So, there are at least four options in that setting now that are therapies that target the lymphoma cells, either by targeting CD19, which is another surface marker, augmenting that either with an antibody drug conjugate, such as loncastuximab tesirine (Lonca), or with an immune therapy, such as lenalidomide (Revlimid) and tafasitamab. Polatuzumab (Polivy) is available in that third line or later space combined with bendamustine (Treanda) and rituximab (Rituxan). There’s an oral agent called Selinexor (Xpovio).

So, a lot of that is not to burden patients with information but to let them know they’ve got lots of options. And many of these can be sequenced. So, if we can’t achieve cure with R-CHOP and/or CAR T, there are still very good outcomes in that third line or later space.