"Inventors at Stanford's Porteus lab have developed a CRISPR-based method in hematopoietic stem cells (HSCs) to deactivate the JAK2 mutation most frequently altered in polycythemia vera"
Nothing new except you may have read recent news of UK clinical approval for this tech category to actually cure sickle cell.
This proof-of-use should help smooth the path as the Stanford guys proceed for curing Jak2. It still requires SCT, but uses our own cells to take care of the rejection problem.
A similar cure for autoimmune diseases (my top concern these days) is not in sight.
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EPguy
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Step by step the science moves on-very heartening too, yesterday at Living with MPNs day to hear of the steady flow of new ieas and approaches in the pipeline.
Would deactivating the JAK2 solve the problem of ET though for those who have the JAK2 variation? It seems like ET isn't so straightforward. Be lovely if it did though.
It is a good question since triple neg ET has no operative levels of Jak2 nor other drivers and still ET happens. Even PV has very rare Jak2 negatives.
Likely in the future when these procedures are available to remove Jak2 allele we'll find out which other mutations or conditions remain troublesome.
Notably CALR ET is ahead, with clinical trials beginning already.
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