Comments
ZaxLofful t1_jcj22og wrote
I hope this pans out, but I was just reading another study that says me in is key to aging…So I wonder if this drug targeting me in will induce rapid aging.
thebestoflimes t1_jcgmar0 wrote
I'm surprised they got one of the Cancer cells to talk and reveal one of their schemes. These guys are infamously tight lipped. The question becomes how did they gain this info and will it hold up in court.
fuzzy_dunlop_221 t1_jchzbnx wrote
They bribing them cancer cell mfers
Coly1111 t1_jcgduq4 wrote
I wonder if this would help with Chronic Mylenoid leukemia.
pcream t1_jchby3w wrote
CML is generally well treated with kinase inhibitors and, as far as I know, there are no planned trials for menin inhibitors. Menin inhibitors work for NPM1 and MLL rearrangement leukemias because they both drive the cancer by overexpression of pro-growth/survival genes, such as HOX family genes. Both mutations work by epigenetically deregulating the regions around these genes, such as the HOXA locus. The inhibition of menin, a protein cofactor needed for this epigenetic deregulatory process, counteracts the abnormal expression of these genes by preventing the epigenetic changes from occurring. While there is some evidence (I found with a brief search) that HOX genes are aberrantly expressed in CML, it doesn't appear to be crucial for the leukemia to survive. So it is unlikely that a menin inhibitor would be effective, but without preclinical testing, we don't know that for sure.
noldshit t1_jchkjmi wrote
...and it will cost you everything you own to get.
staubtanz t1_jcjpewi wrote
politely remains silent in European
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drmema2 t1_jcjzhc4 wrote
my partner was treated for AML NTM mutation in a gilteritinib trial in 2017 and is still in remission thank God for this work. Ten years ago or more AML had a poor survival rate.
chrisdh79 OP t1_jcf4589 wrote
From the article: One of the papers presents results of a clinical trial in which approximately 40% of patients with acute leukemia subtypes had a complete response – a disappearance of all signs of cancer – to treatment with the drug revumenib. The other paper uncovers a molecular countermove by which leukemia cells come to sidestep the drug and reassert their growth.
The papers point to the promise of the targeted approach to acute leukemia treatment exemplified by revumenib and to the potential to extend its benefits with drugs that trip up the resistance mechanism, researchers say.
"The two genetic subtypes of acute leukemia involved in this research account for approximately 40% of all cases of acute myeloid leukemia (AML) in children and adults," says Scott Armstrong, MD, PhD, president of the Dana-Farber/Boston Children's Cancer and Blood Disorders Center and co-senior author of the paper on revumenib resistance. "They're driven by a rearrangement of the MLL1 gene or a mutation in the NPM1 gene. Both types depend on a protein called menin to sustain their growth."
The first of the new Nature studies reports on a phase I/II clinical trial of the drug revumenib, which targets menin, in 68 patients with acute leukemia that wasn't responding other therapies. The trial, dubbed the AUGMENT-101 study, found that of 60 patients who could be evaluated, 53% responded to the drug and 30% had a complete response.
"For patients with acute leukemia who have undergone several previous treatments, this is a very encouraging result," Armstrong says. "However, after the second cycle of treatment, some patients did develop resistance to revumenib."