ArticleBlood advances2025
ATP citrate lyase is an essential player in the metabolic rewiring induced by PTEN loss during T-ALL development.
Article in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Passenger co-deletion confounds glutaminolysis signatures anchored on PTEN loss: A cautionary case for location-aware signature design.PloS one · 2026Article
- Canagliflozin synergises with serine restriction mediating anti-leukaemic effects in T-cell acute lymphoblastic leukaemia.Molecular metabolism · 2025Article
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16 authors.
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Abstract
abstractAlterations inactivating the tumor suppressor gene PTEN drive the development of solid and hematologic cancers, such as T-cell acute lymphoblastic leukemia (T-ALL), in which phosphatase and tensin homolog (PTEN) loss defines poor-prognosis patients. We investigated the metabolic rewiring induced by PTEN loss in T-ALL, aiming to identify novel metabolic vulnerabilities. We showed that the enzyme adenosine triphosphate (ATP) citrate lyase (ACLY) is strictly required for the transformation of thymic immature progenitors and the growth of human T-ALL, which remain dependent on ACLY activity even upon transformation. Although Pten-mutant mice all died within 17 weeks, the concomitant Acly deletion prevented disease initiation in 70% of the animals. In these animals, ACLY promoted B-cell lymphoma (BCL-2) epigenetic upregulation and prevented the apoptosis of premalignant double-positive thymocytes. Transcriptomic and metabolic analysis of primary T-ALL cells next translated our findings to the human pathology, showing that PTEN-altered T-ALL cells activate ACLY and are sensitive to its genetic targeting. ACLY activation thus represents a metabolic vulnerability with therapeutic potential for high-risk patients with T-ALL.
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