Operation cure PV is not just a dream by Besremi.
Operation Cure PV: Operation cure PV is not just a... - MPN Voice
Operation Cure PV
Thanks for posting. I wonder how accessible Besremi is in UK now?
Thanks for posting! I have ET AB ( from a blood test) is 20%. Diagnosed nearly 2 years ago. I probably sound like a bit of a broken record now haha but I am wondering if people should be started earlier on interferons now to try and stop both progression of the MPN and it transforming to MF. I worry that we find out that this should be the case and we could have helped to stop or at the very least slow or stabilise progression when we have the opportunity to do so rather than wait and see. Thanks again. B
I worry about this as well. I'm on aspirin only and watch and wait.
About that, the strong science evidence is not enough for pegINF including Pegasys or Besremi as general treatment guideline specially earl stage of MPN. For PV, we are waiting about "Low PV study" result as below which should be followed one more 1 years after good interim analysis, I think.
pubmed.ncbi.nlm.nih.gov/334...
But according to more data analysis and chart of Richard T. Silver at WCM, it seem INF is first priority of MPN treatment.
Below link is for you reference.
Great new info. We've discussed the 10% AB limit in other threads. This is the first time I've seen it tied to an explicit clinical result. Maybe this will be formally published? So far much of the Heam profession remains skeptical of any clinical benefit for AB reductions.
He notes two required factors, but it's actually 3 factors required:
- Good Heam response.
-Start early after Dx
-Reduce to less than 10% AB.
Starting early has also been recommended by the Silver MPN group also.
I believe Dr Kiladjian has stated in ContiPV follow ups that younger age is also a factor. Curious why that is not repeated here, maybe these factors are more important.
The plot here I've posted elsewhere (from Besremi ContiPV) shows a steep AB decline to two years, (lower blue line) and molecular response (upper blue line) also clearly changing at 2 years. Maybe that's related to the two year significance he discussed. In this data the average AB <10% was achieved at 3-4 years.
Regarding progression I have posted recently of a study finding AB level and and progression relationship. But it doesn't discuss reduction benefit.
healthunlocked.com/mpnvoice...
As EmeraldA says, better to bet on these benefits now rather than wait to fully confirm them later.
All of this doesn't read for the other driver mutations as I believe ContiPV tracked only Jak2, reasonable since it was for PV.
In the ongoing ET/Ropeg study they will study these other mutations. Still leaves out triple neg.
clinicaltrials.gov/ct2/show...
<<Change of CALR, MPL, and JAK-2 allelic burden over time [ Time Frame: over the 12 months ] measure change of CALR, MPL, and JAK-2 allelic burden over time>>
I’m also puzzled as to why the haem community are reticent over the significance of AB reductions. Maybe they’re conservative by nature? Maybe they don’t want to get people’s hopes up? To my mind, if Interferons don’t come with the risks associated with long-term HU use, AND they’re just as effective at reducing thrombosis risk for those who need it, AND one gets a good haematological response, surely it makes sense to use a medication that has the possible added benefit of modifying the disease course - provided of course one can tolerate Pegasys or Besremi?
Hi, how to you get tested for AB limit? I've only had one BMB and I'm not interested in another unless medically necessary!
It's actually an AB "level" or simple allele burden (AB). The limits are actually 0 and 100%. But your note on limit is right for the 10% level we discussed above. Your AB level can be above or below that limit.
Agree BMB is not a fun habit. You can get your AB from blood test also. I've read that it gives ~4% lower value, Hunter said he's seen similar info. I had14% blood, 19% BMB. So you can ask your Dr at your next blood draw.
This was 10 years ago: Conclusion In this prospective phase 2 study of PV pts treated with peg-IFNα-2a after 6.4 years median follow-up, we recognized that:
1) 94% of pts were still in hematological response, including 82% CR;
2) 29% of pts could stop peg-IFNα-2a and remained in hematological response without further cytoreductive therapy after a median observation time of 28+ mos (up to 64+ mos);
3) major and sustained molecular response in %V617F was confirmed in 83% of patients, including 28% who achieved complete molecular response, while TET2 mutated clones appeared resistant to peg-IFNα-2a;
4) histological CR was also achieved in selected patients;
5) no vascular event was observed after 6.4 years median follow-up
6) no new safety concern arose with prolonged utilization of peg-IFN alpha-2a.