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@newsen.bsky.socialOct 5, 2026, 2:24 PM

Pillar Biosciences Unveils Advanced oncoReveal® Myeloid v2 Panel for Enhanced Detection of FLT3-ITDs #United_States #Natick #Pillar_Biosciences #oncoReveal #FLT3-ITD

@cancers-mdpi.bsky.socialSep 9, 2026, 8:35 AM

🎯Editor's Choice!
Management of Acute Myeloid #Leukemia: A Review
🧑‍⚕️by Chetan Jeurkar, Lana King et al. from @jeffersonuniv.bsky.social
📊 Cited 7 times
Full text➡️ www.mdpi.com/2072-6694/18...
#ALL #FLT3 #TP53

Figure 1. Schematic representation of the major molecular pathways driving leukemogenesis and targeted therapies in acute myeloid leukemia (AML). Black arrows indicate stimulation, red lines with stop bars indicate inhibition. (Left) In NPM1-mutated and KMT2A-rearranged AML, formation of the menin–KMT2A transcriptional complex leads to aberrant activation of HOX and MEIS1 genes, sustaining leukemic proliferation and differentiation arrest. Small-molecule menin inhibitors (e.g., revumenib, ziftomenib) disrupt this interaction and suppress oncogenic transcription. (Middle) In FLT3-mutated AML, internal tandem duplication (ITD) or tyrosine-kinase domain (TKD) mutations result in constitutive activation of FLT3 and downstream PI3K, RAS, and JAK signaling pathways, driving proliferation and survival. Targeted agents including type 1 inhibitors (midostaurin, gilteritinib) and type 2 inhibitors (quizartinib) block these pathways. (Right) In IDH-mutated AML, formation of the onco-metabolite 2-hydroxyglutarate (2HG) induces DNA hypermethylation and dependence on BCL2 survival related to cytochrome C oxidase inhibition, leading to AML.