Pankit Vachhani, MD

The field had changed going from only hydria and transplant to many options. It's exciting for me to be able to offer my patients more options and choices of therapy and I would like to hear also your thoughts on where the field is going and final closing remarks about this long discussion about the myelofibrosis and new treatments.

: Dr Komrokji we are very fortunate to now have more than one JAK inhibitor therapy in our arsenal. The important point of course is picking the right JAK inhibitor for the right patient, sequencing it, and optimizing the dose and monitoring for toxicities of these JAK inhibitors is very important. I'm personally an advocate for earlier treatment rather than later treatment and clinical trials. When I look at the future and you talked about this very nicely in just the preceding section, the future I see it as one of combination therapies, both in frontline setting as well as in second line setting. And this will be on a JAK1 or JAK1/JAK2, JAK2 inhibitor backbone. They are not going away. In fact, they will have a very central place, but additional mechanism of actions of these newer therapies that you talked about are very exciting and will if not additive or if not synergistic, maybe at least additive effects what we see hopefully. And both in myelofibrosis but also even in PV and ET. The question then that will evolve is- that will come up is how to sequence the therapies, how to combine these therapies and lead to disease modification in MPNs. And we can have a seminar in what that means, but we'll leave it for now and in terms of what disease modification means. Thank you Dr Komrokji. I found this to be very informative. I hope that our audience also found this to be very informative and enjoyable. Dr Komrokji, thank you for your insightful discussion in this section and we hope our audience found this to be of value to the treatment of MPN patients in their planning.

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Closing out their discussion on the management of myeloproliferative neoplasms, Rami S. Komrokji, MD, and Pankit Vachhani, MD, look toward the future treatment paradigm. 

Myeloproliferative Neoplasms: Future Directions in Care 

: Now we talked about a wide variety of JAK inhibitors and how to manage, which one to pick, the verse events. Dr Komrokji to discuss some of the novel therapies which are on the horizon for myelofibrosis? And this is a big area. If you can take us through some of these JAK inhibitors as well as non-JAK inhibitors therapies like for example navitoclax. There are many. Would you take us through these?

Absolutely. You and I could talk about those for hours. I will try to make it brief hitting some of the highlights for our audience. Maybe we can think of them first other JAK2 inhibitors. Momelotinib which hopefully is on the horizon for approval soon. Momelotinib is a JAK1, JAK2 inhibitor that also have activity against active and receptor or the ACV are that interferes with the hepcidin and could have an anemia response. As you alluded, there's some recent data showing that pacritinib also could affect that receptor. Momelotinib was already tested in simplify 1 and 2 studies but eventually try to highlight is the momentum study that was recently presented. They took patients for a second line after talks of failure that had splenomegaly and anemia. The momentum study showed that momelotinib was superior to danazol. It achieved spleen response, total symptom improvement and probably more importantly for our area that there were like patients that became transfusion independent, hemoglobin increased. In terms of toxicity, it was in general well tolerated. Originally, there were concerns about neuropathy with the momelotinib. In the momentum study, those were not seen. Momelotinib hopefully based on the momentum study is going to get approved and be available for our patients soon. Probably based on the momentum study, it's going to be as a second line for patients particularly with anemia, but I'm sure we're going to see more clinical trials really figuring out the role of momelotinib in MPN patients. Another JAK inhibitor is NS-018 or Ilginatinib. That's an early phase and it's been looked at in patients after other JAK2 failure. Another area is this combination therapy. We're going to have 4 JAK2 inhibitors, but there are efforts to improve still on that by a combination therapy and studies have either looked upfront or in patients that have suboptimal response. And I'm probably going to highlight 2 or 3 of those only given limitation of time. First is Pelabresib. This is the BET inhibitor. It's tested in a study called the Manifest. There are different arms. I think, you know, to highlight probably the up front arm or in patients that have suboptimal response that the addition of pelabresib to ruxolitinib has been demonstrating encouraging activity upfront almost approaching 60%, spleen volume reduction more than 35% or more, well iterated treatment, anemia response as well. And also, in the suboptimal certain responses seen. This is moving now into a phase 3 trial up front. We have the study, it's open. We are accruing patients to that. Navitoclax is a second generation venetoclax, but it's affects the BSL XL that is more important in patients with MPN. Again, similar study looked at patients with sub optimal response. Just published recently in the JCO 30 some patients where there were 20 to 30% responses. Again, some cytopenia response, maybe some change in the fibrosis. Encouraging data in a small-scale study. That also has moved now to a phase 3 up front randomizing patient with navitoclax. Parsaclisib is a PI3 Kinase inhibitor. They had presented data and updating them at Soho. It's also been looked in patients that have sub optimal response to ruxolitinib. It does have activity or returned the activity in patients with low platelets. The activity seems to be a little bit more modest than what's observed with the navitoclax or parsaclisib add on, but we have to see particularly now after failure of upfront combinations, maybe this drug will have role later on. Finally, do we have any options after all JAK2 inhibitor fails? This is obviously an area of unmet need. The group from MD Anderson and our group published that failure in the era before the other JAK2 inhibitor, the survival for those patients is 14 months. There are some studies on going there. Imetelstat a telomerase inhibitor that's been tested in MDS and myelofibrosis had been tested in myelofibrosis originally, you know, particularly in the patients after JAK2 failure. Although the responses were modest, there was a signal of survival advantage where the patients treated with imetelstat had a median overall survival approaching 30 months compared to historical of 15 month or so. Now there is ongoing phase 3 and patients post JAK2 failure with imetelstat which is the only study with overall survival endpoint in patients with myelofibrosis. There are other agents. You've taken the lead on the the MDM2 inhibitor. You just recently published data showing activity. It's been tested in- MDM inhibitors as you alluded have been tested in but they're also tested in myelofibrosis and there is a notion that they could alter the natural history or change fibrosis in the bone marrow as you recently published. The anti-SLAM7 antibody elotuzumab also had been looked at. Other several agents, I tend to think of them in those categories. Other novel JAK2 inhibitors. Momelotinib is the frontrunner for approval. Combination strategies navitoclax collaborative are the frontrunner post JAK2 failure is there. It's an exciting time that we have options on clinical trial to offer our patients more than the standard of care as well.

Key opinion leaders provide a comprehensive review of agents under investigation, alone or in combination, in patients with myelofibrosis. 

Novel Therapies Being Investigated in Myelofibrosis 

 Dr Komrokji, these 3 JAK inhibitors which are available right now for use, my question to you is, how do you use and sequence these drugs in particular in frontline space? How do you use them and do some symptoms play a role or what features guide your decision making?

Absolutely. Obviously, it's a good thing to have more than one option. I try to keep things simple in my mind. As we mentioned, the first step I risk assess the patients. If they're on the higher risk, potentially eligible for transplant, I bring that discussion and may refer them to my colleagues in the transplant to have that discussion and then decide, do they need a treatment or not. And obviously that's based mostly on symptoms, and the symptoms as we said could be either constitutional, cytopenia or a combination. If patients are just cytopenic, anemic from both cytopenic with no splenomegaly and constitutional symptoms so far we don't have much role for the JAK2 inhibitors. Maybe as you did with the pacritinib and momelotinib, down the road they may have some role there but currently active patients' cytopenia’s would worsen with those treatments and we unfortunately that's an area of unmet need. We use you ASA, [acetaminophen] danazol medications with some limited success. That could be an area of different topic. But most of the patients do have constitutional symptoms and splenomegaly. Plus, minus cytopenia that may dictate your choice. If patients are symptomatic, those are the patient’s candidates for JAK2 inhibitors and the NCCN [National Comprehensive Cancer Network] guidelines are very reasonable. For patients that we call proliferative, and they don't have profound cytopenia, I think ruxolitinib is still going to be our backbone treatment up front for many of those patients. It has in almost a decade data, people have used it, they might know how to manage the toxicity and its pretty effective treatment. Obviously, you expect some anemia and cytopenia with it, those are just for that. But it has been our main treatment and it's effective and its role is going to continue in patients with proliferative disease. Fedratinib is listed in that setting as an option. Obviously, you know, with probably less data and people being used to ruxolitinib, rarely fedratinib as a first line would offer advantage over ruxolitinib because it's probably for the same proliferative group. Now the NCCN guidelines currently incorporated, you know, what you discussed with the data with pucritinib in their guidelines saying that if patients have thrombocytopenia platelets less than 50 by the package insert- as you mentioned, the study was even below less than 100, that pacritinib is going to be the first choice up front. And the reason for that, although ruxolitinib has been used in settings of platelets 50 and above, many times it's hard to get to a meaningful dose that will lead to reduction in discipline in that setting because of the cytopenia’s. Pacritinib is now an upfront choice for patients with thrombocytopenia. Ruxolitinib fedratinib for the proliferative. Maybe ruxolitinib still is going to be the main pacritinib for patients with thrombocytopenia. In the second line, I think all of those could be an option and as you mentioned, we have some data on activity sequencing those JAK2 inhibitors. Fedratinib could be a second line after ruxolitinib failure in patients that are proliferative. Pacritinib in the NCCN guidelines is listed as second line regardless of the platelet counts as we mentioned. So that's how I think of it, but obviously all those agents have their unique safety profile and need monitoring and maybe you can highlight how do you do that in your practice. How do you monitor those patients? What are the adverse events you look at and do you add other agents and probably like when do you make the shift? That's probably an area of debate now. Maybe you can tell us a little bit more how you do it.

: On anyone who goes on a JAK inhibitor therapy, any of the 3 that we talked about before, I like to get labs and by that I mean CPC even a CMP ideally on a 2 to 4 week basis at least initially when I'm beginning the JAK inhibitor therapy. Subsequently that it could be every maybe every month to maybe even every 3 or 4 month basis to monitor mostly for cytopenia’s but even otherwise. I do like to make sure that I have a good assessment of the spleen and baseline and subsequently. If I can do that with my physical examination skills then and that's great. But if I'm not comfortable or I'm not sure, then I do make sure to get an ultrasound or a CT scan at least and baseline then subsequently it would depend on the scenario. And the third piece over here is symptom burden assessment, which I do at baseline using one of the forms. For example, we can access that from the NCCN guidelines and subsequent to that I use it on an as required basis when I feel that maybe that the disease course is changing. You brought it up, Dr Komrokji about what counts as a first line JAK inhibitor failure or ruxolitinib failure. This has been an area where we have had a few different struggles in terms of understanding what exactly constitutes that. Many of us would agree that if we just don't see a response with the JAK inhibitor after we begin, that would be counted as a failure. But an additional area might be a scenario where for example, a patient achieved a nice spleen response and subsequently lost that response or progress to an accelerated phase or a blast phase, meaning more than 10 to 20% plus. That would be an area where the first line treatment has failed. Yet another area would be ruxolitinib treatment or the JAK inhibitor treatment leading to adverse events or toxicities which are just unacceptable to the patient at least after 4 weeks of treatment. Primarily, this comes up in the form of cytopenia’s like anemia or thrombocytopenia. The presence of symptoms to some extent even on JAK inhibitor therapy is to be expected, but if some symptoms go away and the new emergence of let's say very specific MF related symptoms like night sweats may also be reflective of a failure scenario. Now, the way I think about adding, changing, or sequencing therapy all in addition to everything that Dr Komrokji mentioned is that if I have a patient on let's say ruxolitinib my frontline JAK inhibitor therapy of choice in the vast majority of our patients and if the primary issue is anemia only, then I try to incorporate an anemia directed therapy there that could be an edit reporting stimulating agent. Maybe in those with a high equal level that might be danazol or sometimes one of these medications or very occasionally steroids. These agencies, additive agents don't have a substantial improvement IM in terms of the hemoglobin improvement, but they do have 1 to 2 grams, occasionally more of hemoglobin improvement or at least stabilization in many patients. If the primary concern is thrombocytopenia and this is much in agreement with what Dr Komrokji said that if we cannot even sustain our patients on a stable dose of let's say ruxolitinib 10 mg twice a day, then there my choice too would be pacritinib. But we want to make sure that if we are using drugs, we should at least use ruxolitinib 10 mg twice daily. That would be the idea. As Dr Komrokji mentioned pacritinib can be used even in those who have platelets more than 50,000 and this would be a point especially true in second line scenario. Fedratinib is an agent which too can be used in second line setting and I would tend to use it only in those who were very proliferative features after ruxolitinib. Let's not forget clinical trials. These are the backbones at many places, and if possible, clinical trial enrollment would be great. We talked about cytopenia’s as being one of the major adverse events that we should keep in mind and that is true. Platelet counts initially increase but subsequently decrease in the 4 to 12 week time period after starting a JAK inhibitor therapy and this is especially true for ruxolitinib. Knowing that is of help. Hemoglobin levels may decrease by 1.5 grams to 2 grams per deciliter, but subsequently they stabilize and improve at a baseline that's just below where the patients had started in the first few weeks after you begin. Knowing these and supporting the cytopenia’s is very important with some of the addictive drugs like you mentioned or maybe even with appropriate dose reductions as and when required. The second set of adverse events that comes up frequently is nausea, vomiting or diarrhea. The GI adverse events and these are primarily seen with fedratinib or pacritinib which happen to be FLT3 inhibitors as well. An important point is to use prophylactic drugs, antiemetics or antidiarrheal agents like Imodium. I tend to send my patients home on these medications so that they have it ready whenever it this happens. And usually, these adverse events happen early on in the course. And then there are the rarer adverse events, but certainly the ones which are being seen for example like viral reactivation, shingles and so on and so forth. I try to make sure that my patients have had vaccination to that. Don't usually use acyclovir as a prophylactic drug, but should that episode of shingles for example happen, I try to keep my patients on a suppressive antiviral therapy subsequent to that.

Focusing on real-world management of myelofibrosis, experts share insight on how they would select and sequence therapies within the current paradigm.

Practical Use of Targeted Therapy in Patients With Myelofibrosis 

: We are excited and fortunate that we finally have more than one JAK2 inhibitor approved for patients, particularly with the constitution symptoms splenomegaly. As it stands now, we have three JAK2 inhibitors, and hopefully in the coming future, fourth will be approved as well. We have ruxolitinib, that has been our back corner for treatment. We have fedratinib and we have pacritinib. Will you highlight the mechanism of action, the clinical trials behind those three JAK2 inhibitors that led to their approval.

: Ruxolitinib was FDA approved in 2011, more than 10 years ago. The approval came through the results primarily of the COMFORT-1 and COMFORT-2 studies. It's a JAK1, JAK2 inhibitor as we spoke. And in COMFORT-1, the patients were randomized against placebo, and it was a double blinded study. In COMFORT-2 the patients were randomized against- from ruxolitinib versus best available therapy. Largely speaking, very comparable clinical trials. The primary endpoint was 35% spleen volume reduction from baseline to 24 weeks in COMFORT-1 or 48 weeks in COMFORT-2. Numerous secondary endpoints including symptom burden reduction in COMFORT-1 for example, survival endpoints as well. And a whole host of other endpoints as well. Now, what's important to note, and we have seen these results and talked about before, but this is remarkable that in COMFORT-1 the spleen volume reduction of 35% more occurred in 41.9% of patients as compared to 0.7% in placebo. For COMFORT-2 it was 28% versus 0%. A clear advantage in the favor of ruxolitinib there. Similarly, the symptom burden reduction occurred far more in patients who were on ruxolitinib compared to the standard arms of placebo or best available therapy. But over the years, as we have followed the patients more with long term follow from both COMFORT-1 and COMFORT-2, what we have realized is that things go way beyond just the spleen volume reduction or symptom burden improvement. That is now overall survival data, it's well published and well documented at this point, which for example has shown that when you pull comfort 1 and comfort 2 patients, the survival for patients who were initially randomized to ruxolitinib was 5.3 years as compared to the control arm patients who had survival of 3.8 years. And that's rather remarkable given that the patients who were in the control arms had deep option and did crossover to ruxolitinib 6 months later. Despite that, a survival advantage in favor of ruxolitinib. The second one is fedratinib. That's a JAK2 inhibitor and a FLT3 inhibitor. It was studied in the Jakarta of one phase 3 study where patients were randomized to fedratinib 500 mg daily or 400 mg daily or Placebo and as a note that the dose that was FDA approved which we can use now is fedratinib 400 mg daily. When you look at the results of that cohort, the spleen volume reduction rate was 36%, and similarly the symptom burden reduction of 50% or more was also 36%. In terms of Jakarta 2, which is the phase 2 single arm open label study, multicenter study in patients who had previously been on ruxolitinib, the spleen volume reduction rates and symptom burden reduction rates were around 30% roughly speaking, suggesting that it is an option for use even in patients who have previous been on ruxolitinib. Now it is a FLT3 inhibitor as well and GI adverse events are seen in patients who go on fedratinib. Pacritinib, which is the third FDA approved drug in Myelofibrosis as a JAK inhibitor, that is a JAK2 and IRAK1 inhibitor. The drug was FDA approved on February 28th, 2022 mainly based on the results of Persist-2 study, but it has been studied previously in Persist-1 and also the dose finding part 2 or 3 study not to mention the ongoing Pacifica study as well. This Persist-2 study randomized patients to pacritinib 400 mg daily. That's not the dose that's FDA approved or 200 mg twice daily, just the FDA approved dose versus best available therapy on. And whether you take the intent to treat population or focus more so on the population that has platelets less than 50,000, i.e. that site which is where the drug is actually approved in 2022, the spleen volume reduction as well as the symptom burden reduction favored pacritinib as opposed to past available therapy. For example, for spleen volume, the rate was almost 30% whereas in best available therapy on it was 3%. That's the third JAK inhibitor that we have available right now. The Pacifica study, which is ongoing, it is a study for patients with platelet counts of 50,000 or less and JAK inhibitor naive patients. The results are expected in a few years from now. Very recently though we have seen that pacritinib also happens to have inhibitory activity against ACVR1. ACVR1 inhibition is thought to be the primary or one of the main mechanisms through which momelotinib maybe has hemoglobin improvements or hemoglobin stabilization data. Now we are seeing data in favor of pacritinib being a very potent, only more potent than the other JAK inhibitors. Pacritinib has a ACVR1 and maybe there is partly the reason if not all as to why some patients at least in Persist-2 saw hemoglobin improvements of 1 gram per deciliter or 2 grams per deciliter or even transfusion independence achievement at various time points or in rolling phases. This space will be very interesting to see in how cytopenias play out anemia will be very interesting to see. The fourth point that I do want to mention is the concept of early treatment. What does early treatment mean? This is a topic which can mean different things to different people. Early treatment could mean that you just diagnosed a patient with high risk disease or it could mean someone with low clinical risk disease like what Dr Komrokji was mentioning. Lower risk MF by one after a stratification schema or it could mean a disease that's in the pre-fibrotic phase, so not yet MF fully or something a scenario where the MF is there but has a low disease burden. We call early disease by different names as we just spoke about, but maybe treating early has an advantage. We have seen data for ruxolitinib whereby treating earlier rather than later, meaning earlier in the diagnosis process right after diagnosis may have better outcomes. We have seen this data. Patients with lesser splenomegaly behave and have better outcomes as well and down the line it may even allow for potentially halting the clonal evolution, maybe allow us for adding additional therapeutics and stop cytopenia’s from development and truly lead to disease modification down the line.

A review of the treatment armamentarium for patients with myelofibrosis in the context of clinical trial data supporting use of these agents. 

Treatment Paradigm for Myelofibrosis 

: We'll switch gears and talk about myelofibrosis. There are different words like primary myelofibrosis, secondary myelofibrosis. Now more so in the lexicon, we are hearing about proliferative myelofibrosis and then cytopenic or myeloproliferative depleted myelofibrosis. Dr Komrojki, can you take us through some of these words and what they mean, how you differentiate between these categories? And then what risk stratifications tool do you use in your practice?

As we said, myelofibrosis obviously is the most symptomatic disease out of the myeloproliferative neoplasms and unfortunately the one that impacts overall survival for patients the most. Obviously, we use terms primary and secondary, deferring if this is de novo myelofibrosis or secondary coming from polycythemia vera or essential thrombocythemia. As you know 10 to 15% of the patients roughly with ET or PV will end as myelofibrosis. There are some slight differences in the outcome, the mutation landscape between primary and secondary. Obviously, not to confuse sometimes we say reactive fibrosis in the bone marrow from other diseases as we mentioned earlier. But primary and secondary is term used to a de novo myelofibrosis or a myelofibrosis secondary is post ET or post PV myelofibrosis, which probably is better term than even secondary. And as you alluded, we revealed the underlying biology of the disease, confirming clinical observations for many years that those patients have different presentation with myelofibrosis. You have those patients that are predominantly proliferative, have high wide count, splenomegaly constitutional symptoms. Or you have that group that are cytopenic, present namely with cytopenia. There are some patients that technically don't have splenomegaly or constitutional symptoms. And the most difficult in my practice historically had been the patients that have a combination. They have slenomegaly that they need treatment, but then yet have profound cytopenia that limit some of the historical options we use for those patients. Now we use this term of cytopenic and proliferative myelofibrosis describing that. And it turns out that there are some differences in the landscape or the genomic landscape of those diseases. For example, patients with cytopenic myelofibrosis have lower JAK2 allele burden, they tend to be more primary. They have more enrichment with splicing mutations, like MDS. Proliferative myelofibrosis tends to have higher allele burden of JAK2, less of the splicing mutations, more of some signaling mutations. Now, as we mentioned, once we establish the diagnosis, the theme in all myeloproliferative diseases, like any oncology disease is the next step is risk stratification. Because that's your prognostic tool and that's sometimes how we tailor the treatment. In myeloid diseases in general, that's a tool also we are using, are we going to send those patients to transplant or not. And it gets complicated in myelofibrosis because there are several models. There are clinical models, now genomic models, hybrid models. You would have heard terms like international prognostic scoring system, IPSS, dynamic IPSS, IPSS plus, GIPPS, MIPSS, those are molecular mutations. The idea obviously that you are weighing on alarm score from certain factors. Most of those models will account for presence of constitutional symptoms, leukocytosis, circulating blasts, and importantly, anemia and thrombocytopenia and transfusion dependency are probably in all those models counted for as poor prognostic factors. The molecular models are enhanced by presence of mutations. Calreticulin is favorable, for example. Complex karyotype, bad cytogenetics are incorporated. Certain mutations like SXL1, SRSF2, IDH1, IDH2, UTF, the Q157, a hotspot are counted as bad prognostic mutations. Obviously, nobody expects a busy practitioner to memorize those models. The MIPSS70 is available online, can be easily calculated. Would give you a risk for the patient and the category and the estimate. But I would say the idea is obviously you are weighing some clinical variables, molecular variables. And the end, you put the patients into probably 2 major buckets, a lower risk, or a higher risk, or lower intermediate and higher. The intermediate and higher, we always are going to be asking obviously about the role of allogeneic stem cell transplant. But then in the rest of the patients, we are going to be asking about treatment, what options do we have.

Shifting their attention to myelofibrosis, Rami S. Komrokji, MD, and Pankit Vachhani, MD, define differences between various subsets of disease.

Identifying the Categories of Myelofibrosis

What are some of the other strategies or the ongoing studies with the rusfertide®, the PTG-300 that has been- is in development in for patients with polycythemia vera.

 Yes, many options. In polycythemia vera. And rusfertide® or PTG-300, this is a non-cytoreductive drug, which is a hepcidin mimetic. In other words, it plays a role and works on the iron homeostasis. Recently we have seen results from the 2 phase 2 trials of rusfertide®, REVIVE and PACIFIC, which were done in patients who had excessive erythrocytosis despite therapeutic phlebotomies plus minus cytoreductive agents. And what was seen in these two trials was that rusfertide or PTG-300 virtually eliminated the need and brought the hematocrit levels down rather robustly and fast, in both the studies. It did not have any major concerning grade 3 or 4 adverse events. The ones which were there were mostly grade 1 or grade 2. Additionally, what we have also seen very recently is that when rusfertide® is held, the improvements are reversed. The therapeutic phlebotomy requirement increases, hematocrit increases, serum ferritin drops, but re-initiating rusfertide normalizes these hematologic parameters. What that suggests is that rusfertide® may be a good drug for decreasing the therapeutic phlebotomy requirements, keeping hematocrit under control. It is not a cytoreductive drug, it won't have an effect on the white blood count or even platelet counts, but it will help with the iron homeostasis. And hopefully the phase 3 trials will establish a role down the line. But in addition to that, there are many other drugs under investigation in various phases. We have seen in some results and talked about MDM2 inhibitors, which work through the P53 pathway for example. Idasanutlin® and navtemadlin® are 2 of those drugs. There are the JAK2 Keller vaccine developments. For PV of course, the JAK2 vaccine component would be the- of most importance. There are LST1 inhibitors, which are in the development process. And if I may, I would bring up and say that givinostat® or givinostat® and HDAC inhibitor, which selectively targets the JAK2 V617F cell growth also seems to be demonstrating very good efficacy and safety in multiple studies with polycythemia vera. Things to look out for, and I'm sure the field will get exciting over there down the line.

Before closing out their review of polycythemia vera management, expert hematologist-oncologists highlight novel therapies in the pipeline. 

Pankit Vachhani, MD | Authors

Articles

Myeloproliferative Neoplasms: Future Directions in Care

Novel Therapies Being Investigated in Myelofibrosis

Practical Use of Targeted Therapy in Patients With Myelofibrosis

Treatment Paradigm for Myelofibrosis

Identifying the Categories of Myelofibrosis

Novel Therapies Being Investigated in Polycythemia Vera