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Targeted Medicines for MPN Treatment

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Published on July 22, 2014

Dr. Bart Scott from Seattle Cancer Care Alliance describes targeted medicines, such as ruxolitinib (Jakafi®) and the role that they play in the treatment of myeloproliferative neoplasms (MPNs). Often referred to as JAK inhibitors, Dr. Scott explains how this class of medications interrupt the JAK-Stat pathway and combat MPNs.

This event was produced in association with City of Hope and sponsored by Patient Empowerment Network through educational grants from Incyte Corporation and Geron Corporation.

 

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Transcript | Targeted Medicines for MPN Treatment

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.

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 y

Andrew Schorr:

We have one, we have the interferon we mentioned before, so that could play a role. And we have an approved, I guess we’d call targeted, medicine with a nib at the end, whatever that means. So help us understand, what is that in those treatments?

Dr. Scott:         

Okay. So Jakafi, ruxolitinib, it interferes with the JAK-STAT pathway. And I like to use that term, rather than a JAK inhibitor. Because if you use the word JAK inhibitor, it makes people think that it only works if you have the JAK2 mutation. That’s actually not correct. It’s effective whether you have the JAK2 mutation or not.

And, pre-released in Blood, and Blood is one of our major journals that we read, and we like to get our publications in there, because it’s very well read, and it’s how we communicate with other doctors about the research that we do.

But in Blood, there will be an article coming out that basically states that all of these disorders, all of the MPNs, share in common up-regulation of this JAK-STAT pathway. And for some people, it’s because of the v617 F mutation. For others, it’s because of the calreticulin mutation.

But all of you who have MPN, whether it be ET or PV or MF, or post-ET MF, or post-PV MF have in common up-regulation of this JAK-STAT pathway. What is it? It is responsible for inflammation, and it’s also responsible for stem cell productivity.

Which leads you to the problems with both numbers, high numbers, and the problem with inflammation. And, you know, just as a side note, I often say that the inflammatory component of these diseases is really underestimated. People worry about their numbers so much.

But I find that the majority of symptoms that patients experience is actually related to the pro-inflammatory state, rather than the high numbers. But what this ruxolitinib does is it basically is one area where it inhibits the JAK-STAT pathway, and that’s at the JAK2 receptor. But it works whether you have the v617F mutation or not.

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 y

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