Duffy-null reference ranges for improved clinical care

RAS pathway activation is a strongly selected escape pathway in AML supports continued exploration into the mechanisms that drive this selection.This study demonstrated robust outgrowth of RAS mutant cells during gilteritinib treatment of mixed parental and NRAS Q61K mutant Molm-14 cells, however, notably found near complete suppression of all cell growth when combined with RMC-7977.Given that multiple RAS-mutant subclones can be observed in the same patient, ongoing investigation of the mutation-specific treatment response to RAS(ON) inhibitors in competitive settings will be critical for understanding the selection dynamics and potential resistance pathways. 2,3,5The activation of JAK/STAT signaling, which was observed in both solid malignancies and after RMC-7977 treatment of AML cell lines in this study, emerged as a likely mechanism that is worthy of continued evaluation. 10And lastly, if RAS(ON) inhibition proves to be the next leap in treatment for AML, what other patients might benefit from this approach?Indeed, RAS pathway mutations are found in a broad range of hematologic malignancies, including in 30% to 40% of chronic myelomonocytic leukemia and in myelodysplastic syndrome, myeloproliferative neoplasms, acute lymphoblastic leukemia, and multiple myeloma, underscoring the potential for RAS(ON) inhibitors to have meaningful therapeutic impact across diverse patient populations.