{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,7]],"date-time":"2026-11-07T02:54:04Z","timestamp":1794020044483,"version":"4.8.0"},"reference-count":48,"publisher":"American Society of Hematology","issue":"7","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,2,17]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Adult T-cell leukemia\/lymphoma (ATL) is an aggressive neoplasm immunophenotypically resembling regulatory T cells, associated with human T-cell leukemia virus type-1. Here, we performed whole-genome sequencing (WGS) of 150 ATL cases to reveal the overarching landscape of genetic alterations in ATL. We discovered frequent (33%) loss-of-function alterations preferentially targeting the CIC long isoform, which were overlooked by previous exome-centric studies of various cancer types. Long but not short isoform\u2013specific inactivation of Cic selectively increased CD4+CD25+Foxp3+ T cells in\u00a0vivo. We also found recurrent (13%) 3\u2032-truncations of REL, which induce transcriptional upregulation and generate gain-of-function proteins. More importantly, REL truncations are also common in diffuse large B-cell lymphoma, especially in germinal center B-cell\u2013like subtype (12%). In the non-coding genome, we identified recurrent mutations in regulatory elements, particularly splice sites, of several driver genes. In addition, we characterized the different mutational processes operative in clustered hypermutation sites within and outside immunoglobulin\/T-cell receptor genes and identified the mutational enrichment at the binding sites of host and viral transcription factors, suggesting their activities in ATL. By combining the analyses for coding and noncoding mutations, structural variations, and copy number alterations, we discovered 56 recurrently altered driver genes, including 11 novel ones. Finally, ATL cases were classified into 2 molecular groups with distinct clinical and genetic characteristics based on the driver alteration profile. Our findings not only help to improve diagnostic and therapeutic strategies in ATL, but also provide insights into T-cell biology and have implications for genome-wide cancer driver discovery.<\/jats:p>","DOI":"10.1182\/blood.2021013568","type":"journal-article","created":{"date-parts":[[2021,10,25]],"date-time":"2021-10-25T20:06:14Z","timestamp":1635192374000},"page":"967-982","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":98,"title":["Whole-genome landscape of adult T-cell leukemia\/lymphoma"],"prefix":"10.1182","volume":"139","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1158-5131","authenticated-orcid":false,"given":"Yasunori","family":"Kogure","sequence":"first","affiliation":[{"name":"Division of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0100-1710","authenticated-orcid":false,"given":"Takuro","family":"Kameda","sequence":"additional","affiliation":[{"name":"Division of Hematology, Diabetes, and Endocrinology, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0605-1226","authenticated-orcid":false,"given":"Junji","family":"Koya","sequence":"additional","affiliation":[{"name":"Division of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5935-0385","authenticated-orcid":false,"given":"Makoto","family":"Yoshimitsu","sequence":"additional","affiliation":[{"name":"Department of Hematology and Rheumatology, Kagoshima University Hospital, Kagoshima, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6682-2451","authenticated-orcid":false,"given":"Kisato","family":"Nosaka","sequence":"additional","affiliation":[{"name":"Department of Hematology, Rheumatology, and Infectious Disease, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7939-2080","authenticated-orcid":false,"given":"Jun-ichirou","family":"Yasunaga","sequence":"additional","affiliation":[{"name":"Department of Hematology, Rheumatology, and Infectious Disease, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2954-5691","authenticated-orcid":false,"given":"Yoshitaka","family":"Imaizumi","sequence":"additional","affiliation":[{"name":"Department of Hematology, Atomic Bomb Disease and Hibakusha Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4030-4653","authenticated-orcid":false,"given":"Mizuki","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2686-9604","authenticated-orcid":false,"given":"Yuki","family":"Saito","sequence":"additional","affiliation":[{"name":"Division of Molecular Oncology, National Cancer Center Research Institute, Tokyo, Japan;"},{"name":"Department of Gastroenterology, Keio University School of Medicine, Tokyo, Japan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuta","family":"Ito","sequence":"additional","affiliation":[{"name":"Division of Molecular Oncology, National Cancer Center Research Institute, 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