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Editorial
. 2025 Feb 13;145(7):658-660.
doi: 10.1182/blood.2024027671.

Heme fuels venetoclax resistance in multiple myeloma

Affiliations
Editorial

Heme fuels venetoclax resistance in multiple myeloma

Mariateresa Fulciniti. Blood. .
No abstract available

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Conflict of interest statement

Conflict-of-interest disclosure: The author declares no competing financial interests.

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References

    1. Nair R, Vu AH, Freer AK, et al. Heme promotes venetoclax resistance in multiple myeloma through MEK-ERK signaling and purine biosynthesis. Blood. 2025;145(7):732–747. - PubMed
    1. Bajpai R, Sharma A, Achreja A, et al. Electron transport chain activity is a predictor and target for venetoclax sensitivity in multiple myeloma. Nat Commun. 2020;11(1):1228. - PMC - PubMed
    1. Lin KH, Xie A, Rutter JC, et al. Systematic dissection of the metabolic-apoptotic interface in AML reveals heme biosynthesis to be a regulator of drug sensitivity. Cell Metabol. 2019;29(5):1217–1231.e7. - PMC - PubMed
    1. Guièze R, Liu VM, Rosebrock D, et al. Mitochondrial reprogramming underlies resistance to BCL-2 inhibition in lymphoid malignancies. Cancer Cell. 2019;36(4):369–384.e13. - PMC - PubMed
    1. Bajpai R, Matulis SM, Wei C, et al. Targeting glutamine metabolism in multiple myeloma enhances BIM binding to BCL-2 eliciting synthetic lethality to venetoclax. Oncogene. 2016;35(30):3955–3964. - PMC - PubMed

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