Published on January 30, 2018
What do genetic mutations reveal about prognosis in MPN patients? Dedicated experts, Dr. Abdulraheem Yacoub from the University of Kansas Medical Center and Dr. Srdan Verstovsek from The University of Texas MD Anderson Cancer Center, help patients understand the JAK2 mutation and the risk and prognostic significance it has for MPNs. Watch now to learn more about the JAK2 mutation.
Produced in partnership with The University of Texas MD Anderson Cancer Center. We thank Incyte for their support.
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Transcript | How Does the JAK2 Mutation Impact Prognosis in MPNs?
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 you.
Hi, I’m Ranisa. And I’m recently diagnosed with ET, JAK2 positive. And so, I’m just trying to learn all of this. But I’m wondering how does the JAK2-positive diagnosis affect my condition and my long-term prognosis?
Beth Kart Probert:
And so, Dr. Yacoub, did you want to address that?
So, JAK2 mutation is one of the markers that present in essential thrombocytosis in about 60 percent of patients. We have tried, over the years, to try to predict if that’s of prognostic value, meaning do patients with JAK2 positive do better or worse compared to JAK2 negative? But really, there is not such an impact that this would actually matter, whether positive or negative. We, actually, believe that everybody with ET has a dysfunction in the JAK-STAT pathway, at one level, whether we find a mutation for it or not. But there is a dysfunction in that pathway, which is also in the disease picture. So, this dysfunction, the JAK-STAT pathway is what is causing the ET.
We can try to predict your best by being young, not having had a clot, which predicts a low risk versus older age or history of clotting predicting a worse risk. And that risk is predominantly based on whether you’re going to have a clot down the road or not. So, we still—that’s really the science we have right now in terms of advising you about long term, or advising any ET patient about long-term risk with their disease.
Probably, the question is also related to the progression, which is rare. That’s why we focus on thrombosis and what was explained is very good explanation on the thrombotic risk. Progression is rare. And we don’t have evidence that one mutation over the other leads to increased risk of progression. But it’s rare. And so, let’s focus on more imminent problem.
And that is thrombotic risk. And when you’re healthy had young, that would be a low risk regardless of the mutation status.
And statistically speak, low-risk patients with ET have really the general outlook as normal young people without ET in terms of if you take everybody, all comers because even healthy people come down with things. But I think, when you average everybody on the healthy population and the patient with low-risk ET, you, actually, do head to head equally well as if you didn’t have this. So that’s when I compare all of those low-risk ET patients to the general population. If you compare the same individual with or without ET, I rather you didn’t have it. But it still is, in the big scheme of things, you would do equally well to your peers, basically, as long as you continue to have low-risk ET.