Just an FYI...jakafi can reduce red blood cells and hgb. (That's why it's approved for PV). If a person is starting at the low end or at or just below the low end of the normal range, the Jakafi will likely make the person anemic or more anemic.

Mark, when I transitioned from ET to MPN my oncologist/hematologist stopped the Hydrea and started Jakafi. I knew that I was Jak2 positive long before I transitioned. My treatment has worked beautifully and as I stated I feel better than I have in years so I go with the flow and take each change as it comes.

HU is a cytotoxin (antimetabolite) that works by altering DNA activity in hematopoietic stem cells and other cells in the body that are DNA-active. Some will show a temporary decrease in JAK2 allele burden on HU, but these numbers rebound over time. While HU is an effective cytoreductive agent, it is not disease modifying in the same way the the Interferons and ruxolitinib appear to be.

To broaden the answer to your question, HU is a mutagen. It's mechanism of action can result in breaking allele strands and interfering with DNA self-repair function. HU is considered a potential carcinogen and possibly (still in debate) a leukomegen. The way my MPN specialist put it to me was "If hydroxyurea mutates TP53, your MPN is off to the races." Note that that is not an observation that all would agree with.

The issue with HU and all of the other treatment options we have for MPNs is one of informed consent. We need to understand the mechanism of action, and both the benefits and risks associated with each choice. We each need to decide on what our treatment goals will be, what our risk tolerance is, and what our treatment preferences will be. This is the only way to ensure that we actively engage in shared decision making. There are no black and white decision in treating MPNs. Each decision needs to be made on a case-by-case basis.

Wishing you all the best.

Dear Mark,

It seems like you have familial ET, given that you mentioned your mother was also diagnosed with ET. And you seem to have two somatic mutations.
I remembered about this study and maybe it could guide you towards more information towards a more accurate diagnosis:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC42...

I have hereditary thrombocytosis, which means I inherited the pathogenic gene from my father, but in your case it seems like you have familial ET. You can ask your MPN specialist what is the best treatment for cases like yours. One size does not fit all.

Best regards,
Tatiana

Familial Essential Thrombocythemia Associated with MPL W515L Mutation in Father and JAK2 V617F Mutation in Daughter

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267161/

Thanks Steve, I'm just trying to hear opinions outside the medical community. I'm trying to stay away from meds other than aspirin. My platelets are only 490, I'm very healthy but I'm 63 with jak617 and mpl515. I recently went to mpn specialist at Penn Medicine and she recommended hydroxyurea but also said it's not vital that I do so, it's up to me. Also I have no symptoms as long as I take aspirin 1 a day.