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Cooperation between KDM6B overexpression and TET2 deficiency in the pathogenesis of chronic myelomonocytic leukemia.

Leukemia - 1 Aug 2022

Wei Yue, Kanagal-Shamanna Rashmi, Zheng Hong, Bao Naran, Lockyer Pamela Pennington, Class Caleb A, Darbaniyan Faezeh, Lu Yue, Lin Kevin, Yang Hui, Montalban-Bravo Guillermo, Ganan-Gomez Irene, Soltysiak Kelly A, Do Kim-Anh, Colla Simona, Garcia-Manero Guillermo

Abstract excerpt

Loss-of-function TET2 mutations are recurrent somatic lesions in chronic myelomonocytic leukemia (CMML). KDM6B encodes a histone demethylase involved in innate immune regulation that is overexpressed in CMML. We conducted genomic and transcriptomic analyses in treatment naïve CMML patients and observed that the patients carrying both TET2 mutations and KDM6B overexpression constituted 18% of the cohort and 42% of...

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PMID: 35697791
DOI: 10.1038/s41375-022-01605-1

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

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