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Transforming Growth Factor-Beta Orchestrates Tumour and Bystander Cells in B-Cell Non-Hodgkin Lymphoma

Wellcome Trust/MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AH, UK
Department of Haematology, Addenbrooke’s Hospital, Cambridge University Hospital, Cambridge CB2 0AH, UK
Author to whom correspondence should be addressed.
Academic Editor: Franck Verrecchia
Cancers 2022, 14(7), 1772;
Received: 14 March 2022 / Accepted: 23 March 2022 / Published: 31 March 2022
(This article belongs to the Special Issue Feature Paper from Journal Reviewers)
Transforming growth factor-beta (TGFB) is a ubiquitously expressed cytokine involved in numerous functions in both normal and cancer cells. Here, we review, for the first time, the evidence of how B-cell lymphoma cells respond to TGFB and utilise TGFB to modulate surrounding cells in the microenvironment. We highlight recent data supporting the bi-directional signalling between B-cell lymphoma cells and their microenvironment. Targeting TGFB signalling in B-cell lymphoma may provide a future therapeutic strategy but further research is required to understand how lymphoma cells interact in different microenvironmental contexts.
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. View Full-Text
Keywords: TGFB; B-cell lymphoma; microenvironment TGFB; B-cell lymphoma; microenvironment
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MDPI and ACS Style

Timmins, M.A.; Ringshausen, I. Transforming Growth Factor-Beta Orchestrates Tumour and Bystander Cells in B-Cell Non-Hodgkin Lymphoma. Cancers 2022, 14, 1772.

AMA Style

Timmins MA, Ringshausen I. Transforming Growth Factor-Beta Orchestrates Tumour and Bystander Cells in B-Cell Non-Hodgkin Lymphoma. Cancers. 2022; 14(7):1772.

Chicago/Turabian Style

Timmins, Matthew A., and Ingo Ringshausen. 2022. "Transforming Growth Factor-Beta Orchestrates Tumour and Bystander Cells in B-Cell Non-Hodgkin Lymphoma" Cancers 14, no. 7: 1772.

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