Targeting ACSF2 overcomes Ara-C resistance in acute myeloid leukemia via the cholesterol metabolism-ERK signaling axis.
Blocking a specific protein restores chemotherapy sensitivity in treatment-resistant leukemia, opening a potential path forward for patients who've exhausted standard options.
ACSF2 inhibition restores cytarabine (Ara-C) sensitivity in resistant AML via impaired cholesterol esterification, mitochondrial ROS, and suppressed ERK signaling; SREBF1 inhibitor fatostatin synergizes with Ara-C against resistant AML in vitro and in vivo. This record was retained from the prior triage attempt for PubMed pipeline handoff.
What the study was
- Study design
- experimental (mechanistic, in vitro + in vivo)
- Category
- hematologic_malignancies
- Maturity
- Exploratory
- Journal
- Leukemia
Why it surfaced
Novel metabolic target (ACSF2) in R/R AML—one of the most important unmet needs in hematology; published in Leukemia (top-tier journal); strong mechanistic study with in vivo validation. Directly relevant to AML cornerstone therapy resistance.
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