{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T10:16:21Z","timestamp":1781000181664,"version":"3.54.1"},"reference-count":134,"publisher":"MDPI AG","issue":"7","license":[{"start":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T00:00:00Z","timestamp":1648684800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancers"],"abstract":"<jats:p>Transforming growth factor-beta (TGFB) is a critical regulator of normal haematopoiesis. Dysregulation of the TGFB pathway is associated with numerous haematological malignancies including myelofibrosis, acute myeloid leukaemia, and lymphoid disorders. TGFB has classically been seen as a negative regulator of proliferation in haematopoiesis whilst stimulating differentiation and apoptosis, as required to maintain homeostasis. Tumours frequently develop intrinsic resistant mechanisms to homeostatic TGFB signalling to antagonise its tumour-suppressive functions. Furthermore, elevated levels of TGFB enhance pathogenesis through modulation of the immune system and tumour microenvironment. Here, we review recent advances in the understanding of TGFB signalling in B-cell malignancies with a focus on the tumour microenvironment. Malignant B-cells harbour subtype-specific alterations in TGFB signalling elements including downregulation of surface receptors, modulation of SMAD signalling proteins, as well as genetic and epigenetic aberrations. Microenvironmental TGFB generates a protumoural niche reprogramming stromal, natural killer (NK), and T-cells. Increasingly, evidence points to complex bi-directional cross-talk between cells of the microenvironment and malignant B-cells. A greater understanding of intercellular communication and the context-specific nature of TGFB signalling may provide further insight into disease pathogenesis and future therapeutic strategies.<\/jats:p>","DOI":"10.3390\/cancers14071772","type":"journal-article","created":{"date-parts":[[2022,3,31]],"date-time":"2022-03-31T21:33:03Z","timestamp":1648762383000},"page":"1772","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Transforming Growth Factor-Beta Orchestrates Tumour and Bystander Cells in B-Cell Non-Hodgkin Lymphoma"],"prefix":"10.3390","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7127-7395","authenticated-orcid":false,"given":"Matthew A.","family":"Timmins","sequence":"first","affiliation":[{"name":"Wellcome Trust\/MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AH, UK"},{"name":"Department of Haematology, Addenbrooke\u2019s Hospital, Cambridge University Hospital, Cambridge CB2 0AH, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7247-311X","authenticated-orcid":false,"given":"Ingo","family":"Ringshausen","sequence":"additional","affiliation":[{"name":"Wellcome Trust\/MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AH, UK"},{"name":"Department of Haematology, Addenbrooke\u2019s Hospital, Cambridge University Hospital, Cambridge CB2 0AH, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,3,31]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"665","DOI":"10.1038\/nrc2714","article-title":"Environment-mediated drug resistance: A major contributor to minimal residual disease","volume":"9","author":"Meads","year":"2009","journal-title":"Nat. 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