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Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms
B-cell non-Hodgkin lymphoma (B-NHL) evolution and treatment are complicated by a high prevalence of relapses primarily due to the ability of malignant B cells to interact with tumor-supportive lymph node (LN) and bone marrow (BM) microenvironments. In particular, progressive alterations of BM stroma...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8694563/ https://www.ncbi.nlm.nih.gov/pubmed/34956214 http://dx.doi.org/10.3389/fimmu.2021.784691 |
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author | Dumontet, Erwan Mancini, Stéphane J. C. Tarte, Karin |
author_facet | Dumontet, Erwan Mancini, Stéphane J. C. Tarte, Karin |
author_sort | Dumontet, Erwan |
collection | PubMed |
description | B-cell non-Hodgkin lymphoma (B-NHL) evolution and treatment are complicated by a high prevalence of relapses primarily due to the ability of malignant B cells to interact with tumor-supportive lymph node (LN) and bone marrow (BM) microenvironments. In particular, progressive alterations of BM stromal cells sustain the survival, proliferation, and drug resistance of tumor B cells during diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and chronic lymphocytic leukemia (CLL). The current review describes how the crosstalk between BM stromal cells and lymphoma tumor cells triggers the establishment of the tumor supportive niche. DLBCL, FL, and CLL display distinct patterns of BM involvement, but in each case tumor-infiltrating stromal cells, corresponding to cancer-associated fibroblasts, exhibit specific phenotypic and functional features promoting the recruitment, adhesion, and survival of tumor cells. Tumor cell-derived extracellular vesicles have been recently proposed as playing a central role in triggering initial induction of tumor-supportive niches, notably within the BM. Finally, the disruption of the BM stroma reprogramming emerges as a promising therapeutic option in B-cell lymphomas. Targeting the crosstalk between BM stromal cells and malignant B cells, either through the inhibition of stroma-derived B-cell growth factors or through the mobilization of clonal B cells outside their supportive BM niche, should in particular be further evaluated as a way to avoid relapses by abrogating resistance niches. |
format | Online Article Text |
id | pubmed-8694563 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86945632021-12-23 Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms Dumontet, Erwan Mancini, Stéphane J. C. Tarte, Karin Front Immunol Immunology B-cell non-Hodgkin lymphoma (B-NHL) evolution and treatment are complicated by a high prevalence of relapses primarily due to the ability of malignant B cells to interact with tumor-supportive lymph node (LN) and bone marrow (BM) microenvironments. In particular, progressive alterations of BM stromal cells sustain the survival, proliferation, and drug resistance of tumor B cells during diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and chronic lymphocytic leukemia (CLL). The current review describes how the crosstalk between BM stromal cells and lymphoma tumor cells triggers the establishment of the tumor supportive niche. DLBCL, FL, and CLL display distinct patterns of BM involvement, but in each case tumor-infiltrating stromal cells, corresponding to cancer-associated fibroblasts, exhibit specific phenotypic and functional features promoting the recruitment, adhesion, and survival of tumor cells. Tumor cell-derived extracellular vesicles have been recently proposed as playing a central role in triggering initial induction of tumor-supportive niches, notably within the BM. Finally, the disruption of the BM stroma reprogramming emerges as a promising therapeutic option in B-cell lymphomas. Targeting the crosstalk between BM stromal cells and malignant B cells, either through the inhibition of stroma-derived B-cell growth factors or through the mobilization of clonal B cells outside their supportive BM niche, should in particular be further evaluated as a way to avoid relapses by abrogating resistance niches. Frontiers Media S.A. 2021-12-08 /pmc/articles/PMC8694563/ /pubmed/34956214 http://dx.doi.org/10.3389/fimmu.2021.784691 Text en Copyright © 2021 Dumontet, Mancini and Tarte https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Dumontet, Erwan Mancini, Stéphane J. C. Tarte, Karin Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms |
title | Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms |
title_full | Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms |
title_fullStr | Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms |
title_full_unstemmed | Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms |
title_short | Bone Marrow Lymphoid Niche Adaptation to Mature B Cell Neoplasms |
title_sort | bone marrow lymphoid niche adaptation to mature b cell neoplasms |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8694563/ https://www.ncbi.nlm.nih.gov/pubmed/34956214 http://dx.doi.org/10.3389/fimmu.2021.784691 |
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