Choosing Treatment for Polycythemia Vera (PV)

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Topics include: Treatments

MPN expert Dr. Srdan Verstovsek from The University of Texas MD Anderson Cancer Center explains how doctors assess patients with polycthemia vera (PV) and determine the best treatment for each individual. He explains driver mutations associated with MPNs and how various treatments work to treat the condition. Dr. Verstovsek believes that the most important thing to consider when choosing a therapy is the patient's quality of life. 

This town meeting was sponsored by the Patient Empowerment Network, which received an educational grant from Incyte Corporation. It was produced by Patient Power in partnership with The University of Texas MD Anderson Cancer Center. 

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Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you. 

Andrew Schorr:

Dr. Verstovsek, let me ask you about stratifying within PV. The drug that I take for myelofibrosis is now also approved for some patients in PV. How do you decide who gets what in PV; who has sort of more aggressive PV? How do you do that? 

Dr. Verstovsek: 

The two basic factors in assessing thrombosis risk in polycythemia vera are age and history of blood clot. Some say that perhaps there are other factors but not fully fledged established as such, like elevation in white cell count or, what Dr. Bose mentioned at the beginning, how many cells in blood do have a particular mutation that would indicate how many cells are affected by the disease in the blood or in bone marrow. 

These are some novel factors that perhaps sometimes come to a discussion about assessing risk for thrombosis, but basically it’s age over 60 or 65 and a history of blood clotting. So patients that have either one are at the risk of having a blood clot for the first time or have another one. In this condition, then, the patient with polycythemia vera, in addition to taking low-dose aspirin as a pill, we offer one of the other medications.

Guidelines suggest that hydroxyurea (Hydea), a chemotherapy by mouth, or interferon, which is injectable biological product under the skin can be offered to the patients as a first choice. Now, the pill is obviously easier to take, but it is a chemotherapy, and we don't like to offer this to younger people, like in 30s or 40s, because you never know what happens if a patient takes it for 45 to 50 years. Is there any subtle difference in the risk of getting some other kind of cancer, for example, a skin cancer or so?

So in younger people, we like interferon. Interferon, because it’s a little bit more challenging in causing some side effect; flulike symptoms, autoimmune problems and such, it is perhaps harder to provide to older folks. So that’s how we choose usually what to give in a frontline setting as a first choice. 

You can always try one. And if it doesn’t work, try the other one. Now, the medication that you mentioned that is a new development in the field, that is ruxolitinib (Jakafi). It’s another pill that is approved in patients that do not do well on hydroxyurea, like a second choice, second line. And it goes along with our understanding of what is the disease all about biologically. What was mentioned before is that the JAK mutation, for example, which is just one of the mutations think about we find in these diseases, is present in patients with ET, PV and myelofibrosis. 

There are other mutations that are present in these conditions; some of you may know calreticulin mutation, MPL mutation and many others can be identified in patients’ samples. But we know that underlying biological problem in everybody is super active signal inside the bone marrow cells. We call this JAK stat pathway. It’s a pathway of proteins inside the bone marrow cells that makes cells grow.

Now why? In some patients it presents with too many platelets; another patients it presents with PV with too many red blood cells and platelets. Or a third patient, it presents with anemia in big spleen, like myelofibrosis; we don’t really understand that very well. It’s a combination of multiple mutations, probably, in each individual that leaves a different clinical scenario. But every single patient has the JAK stat pathway proteins inside the cell in bone marrow; super high and makes cells grow. 

And the ruxolitinib inhibits that, inhibits JAK stat pathway. It’s a JAK inhibitor that makes cells grow less. So in PV, you would lower the red blood cells, lower the platelets, lower the white cells and improve the symptoms. And I can’t tell you enough that it’s not only about control of the symptoms in any—control of the blood cells in any of these conditions. It is about the complete person. We look heavily and importantly on the quality of life to improve the life quality for the rest of the time of the patients that live with the disease forever.

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you. 

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Page last updated on July 17, 2017