{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T06:43:47Z","timestamp":1793774627931,"version":"4.6.1"},"reference-count":69,"publisher":"American Society of Hematology","issue":"24","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,12,12]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>The US Food and Drug Administration announcement in November 2023 regarding reports of the occurrence of secondary T-cell lymphomas in patients receiving chimeric antigen receptor T cells (CAR-Ts) for B-cell malignancies resulted in widespread concern among patients, clinicians, and scientists. Little information relevant to assessing causality, most importantly whether CAR retroviral or lentiviral vector genomic insertions contribute to oncogenesis, was initially available. However, since that time, several publications have provided clinical and molecular details on 3 cases showing clonal CAR vector insertions in tumor cells but without firm evidence these insertions played any role in oncogenic transformation. In addition, several other cases have been reported without vector detected in tumor cells. In addition, epidemiologic analyses as well as institutional long-term CAR-T recipient cohort studies provide important additional information suggesting the risk of T-cell lymphomas after CAR-T therapies is extremely low. This review will provide a summary of information available to date, as well as review relevant prior research suggesting a low susceptibility of mature T cells to insertional oncogenesis and documenting the almost complete lack of T-cell transformation after natural HIV infection. Alternative factors that may predispose patients treated with CAR-Ts to secondary hematologic malignancies, including immune dysfunction and clonal hematopoiesis, are discussed, and likely play a greater role than insertional mutagenesis in secondary malignancies after CAR therapies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2024025828","type":"journal-article","created":{"date-parts":[[2024,10,11]],"date-time":"2024-10-11T16:48:32Z","timestamp":1728665312000},"page":"2473-2481","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":37,"title":["T-cell lymphomas in recipients of CAR-T cells: assessing risks and causalities"],"prefix":"10.1182","volume":"144","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0284-7235","authenticated-orcid":false,"given":"Jingqiong","family":"Hu","sequence":"first","affiliation":[{"name":"1Department of Cell Therapy, Stem Cell Center, Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7645-838X","authenticated-orcid":false,"given":"Cynthia E.","family":"Dunbar","sequence":"additional","affiliation":[{"name":"2Division of Intramural Research, Translational Stem Cell Biology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"issue":"7","key":"2024121216205685900_bib1","doi-asserted-by":"crossref","first-page":"584","DOI":"10.1056\/NEJMp2400209","article-title":"Secondary cancers after chimeric antigen receptor T-cell therapy","volume":"390","author":"Verdun","year":"2024","journal-title":"N\u00a0Engl J Med"},{"key":"2024121216205685900_bib2","unstructured":"U.S. Food and Drug Administration\n          . 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