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Article

ASAH1-mediated sphingolipid metabolic reprogramming in venetoclax resistance of AML: beyond the monocytic phenotypes.

BMC cancer - 22 Nov 2025

Zhao Lei, Xiang Xinrong, Zhong Ailing, Yu Hongbin, Yang Jinjun, Chen Mengran, Ding Hong, Yang Chenlu, Wu Yu

Abstract excerpt

BACKGROUND: Venetoclax (VEN) in combination with hypomethylating agents has emerged as a pivotal therapy for elderly acute myeloid leukemia (AML) patients ineligible for intensive chemotherapy. However, monocytic AML exhibit greater resistance to VEN-based regimens compared to non-monocytic AML. Identifying exploitable vulnerabilities will mitigate resistance and relapse. METHODS: We conducted a comprehensive...

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Topics

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Share to Antineoplastic Agents
Share to Bridged Bicyclo Compounds, Heterocyclic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Leukemia, Myeloid, Acute

Share to Monocytes

Share to Sphingolipids

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Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 41275169
DOI: 10.1186/s12885-025-15272-9
PMCID: PMC12781537

Genes

ASAH1
CD14
ITGAX
SPHK1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

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ASAH1-mediated sphingolipid metabolic reprogramming in venetoclax resistance of AML: beyond the monocytic phenotypes.PMID 41275169Read ↗

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