Some have been curious about the prospects of the potential ATO-INF therapy I posted recently at:
healthunlocked.com/mpnvoice...
MPN Research just released an update for the latest on INF including this very issue.
I've looked at the report and this is my summary of some notable items.
--ATO-INF <<These results have led to the planning of IFN and arsenic based clinical trial approaches for MPN patients.>> So unspecified experts are on top of this exciting new finding. We can hope to see a recruitment notice some time in the future.
--There are studies for INF on Double mutant MPN, but it seems they are just getting started digging deeper into the subject.
--JAK2 vs CALR with INF <<It was learned that the JAK2V617F mutation sensitizes IFN pathway signaling much better than CALR mutations>> The use of plural in mutation(s) suggest both common types of CALR are included.
Jak2 responds better to INF than Calr. Having CHR (complete blood response) with Jak 2 indicates a molecular response (MR) vs less MR without CHR, while CALR responds minimally to INF for any HR. So best allele response to INF has both of: Jak2 and CHR. No info yet on CALR against ATO/INF.
--Combining INF with type 1 Jak 2 inhibitor (ie Rux) may be helpful. But this has been studied and it seems they are more excited by the new ATO combo in my opinion, note the term "mildly" here: <<the combination of a JAK2 specific inhibitor with IFN mildly increases IFN target gene expression in vitro>>
--INF works better for homozygous compared to a heterozygous JAK2V617F. Homozy is with both copies of the gene pair being mutant. I had a fairly complete BMB but this was not studied in my case and I suspect is not often done, any comments here are welcome. I've also read that homozy can have worse prognosis, unrelated to INF.
<<We are closer to optimizing IFN treatment strategies based on a patient’s specific driver mutation, allele burden and overall genomic profile.>>