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To identify the molecular driver of LCT, we collected tumor samples from 133 MF patients and performed whole-transcriptome sequencing on 49 advanced-stage MF patients, followed by integrated copy number inference and genomic hybridization. Tumors with LCT showed unique transcriptional programs and enriched expressions of genes at chr7q. Paternally expressed gene 10 (PEG10), an imprinted gene at 7q21.3, was ectopically expressed in malignant T\u00a0cells from LCT, driven by 7q21.3 amplification. Mechanistically, aberrant PEG10 expression increased cell size, promoted cell proliferation, and conferred treatment resistance by a PEG10\/KLF2\/NF-\u03baB axis in in\u00a0vitro and in\u00a0vivo models. Pharmacologically targeting PEG10 reversed the phenotypes of proliferation and treatment resistance in LCT. Our findings reveal new molecular mechanisms underlying LCT and suggest that PEG10 inhibition may serve as a promising therapeutic approach in late-stage aggressive T-cell lymphoma.<\/jats:p>","DOI":"10.1182\/blood.2021012091","type":"journal-article","created":{"date-parts":[[2021,9,28]],"date-time":"2021-09-28T21:35:28Z","timestamp":1632864928000},"page":"554-571","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":24,"title":["PEG10 amplification at 7q21.3 potentiates large-cell transformation in cutaneous T-cell lymphoma"],"prefix":"10.1182","volume":"139","author":[{"given":"Fengjie","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Dermatology and Venereology, Peking University First Hospital, Beijing 100034, China;"},{"name":"Beijing Key Laboratory of Molecular Diagnosis on Dermatoses, Beijing 100034, China;"},{"name":"National Clinical Research Center for Skin and Immune Diseases, Beijing 100034, 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