{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T18:21:57Z","timestamp":1778610117963,"version":"3.51.4"},"reference-count":13,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2023,8,3]],"date-time":"2023-08-03T00:00:00Z","timestamp":1691020800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Hematological Oncology"],"published-print":{"date-parts":[[2023,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:italic>TNFRSF13B<\/jats:italic>\n                    mutations are widely associated with common variable immunodeficiency.\n                    <jats:italic>TNFRSF13B<\/jats:italic>\n                    was recently counted among relevant genes associated with childhood\u2010onset of hematological malignancies; nonetheless, its role in acute myeloid leukemia (AML) remains unexplored. We report the study of a family with two cases of AML, sharing a germline\n                    <jats:italic>TNFRSF13B<\/jats:italic>\n                    mutation favoring the formation of a more stable complex with its ligand TNFSF13: a positive regulator of AML\u2010initiating cells. Our data turn the spotlight onto the\n                    <jats:italic>TNFRSF13B<\/jats:italic>\n                    role in AML onset, inserting a new fragment into the complex scenario of a hereditary predisposition to myeloid neoplasms.\n                  <\/jats:p>","DOI":"10.1002\/hon.3212","type":"journal-article","created":{"date-parts":[[2023,8,3]],"date-time":"2023-08-03T06:49:13Z","timestamp":1691045353000},"page":"942-946","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["<i>TNFRSF13B<\/i>\n                    gene mutation in familial acute myeloid leukemia: A new piece in the complex scenario of hereditary predisposition?"],"prefix":"10.1002","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2509-6200","authenticated-orcid":false,"given":"Cosimo","family":"Cumbo","sequence":"first","affiliation":[{"name":"Hematology and Stem Cell Transplantation Unit Department of Precision and 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