Importance of Crosstalk Between Chronic Lymphocytic Leukemia Cells and the Stromal Microenvironment: Direct Contact, Soluble Factors, and Extracellular Vesicles.

chronic lymphocytic leukemia extracellular vesicles mesenchymal stromal cells microenvironment prognostic factor

Journal

Frontiers in oncology
ISSN: 2234-943X
Titre abrégé: Front Oncol
Pays: Switzerland
ID NLM: 101568867

Informations de publication

Date de publication:
2020
Historique:
received: 15 04 2020
accepted: 06 07 2020
entrez: 25 9 2020
pubmed: 26 9 2020
medline: 26 9 2020
Statut: epublish

Résumé

Chronic lymphocytic leukemia (CLL) is caused by the accumulation of malignant B cells due to a defect in apoptosis and the presence of small population of proliferating cells principally in the lymph nodes. The abnormal survival of CLL B cells is explained by a plethora of supportive stimuli produced by the surrounding cells of the microenvironment, including follicular dendritic cells (FDCs), and mesenchymal stromal cells (MSCs). This crosstalk between malignant cells and normal cells can take place directly by cell-to-cell contact (assisted by adhesion molecules such as VLA-4 or CD100), indirectly by soluble factors (chemokines such as CXCL12, CXCL13, or CCL2) interacting with their receptors or by the exchange of material (protein, microRNAs or long non-coding RNAs) via extracellular vesicles. These different communication methods lead to different activation pathways (including BCR and NFκB pathways), gene expression modifications (chemokines, antiapoptotic protein increase, prognostic biomarkers), chemotaxis, homing in lymphoid tissues and survival of leukemic cells. In addition, these interactions are bidirectional, and CLL cells can manipulate the normal surrounding stromal cells in different ways to establish a supportive microenvironment. Here, we review this complex crosstalk between CLL cells and stromal cells, focusing on the different types of interactions, activated pathways, treatment strategies to disrupt this bidirectional communication, and the prognostic impact of these induced modifications.

Identifiants

pubmed: 32974152
doi: 10.3389/fonc.2020.01422
pmc: PMC7466743
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

1422

Informations de copyright

Copyright © 2020 Dubois, Crompot, Meuleman, Bron, Lagneaux and Stamatopoulos.

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Auteurs

Nathan Dubois (N)

Laboratory of Clinical Cell Therapy, ULB-Research Cancer Center (U-CRC), Jules Bordet Institute, Université Libre de Bruxelles (ULB), Brussels, Belgium.

Emerence Crompot (E)

Laboratory of Clinical Cell Therapy, ULB-Research Cancer Center (U-CRC), Jules Bordet Institute, Université Libre de Bruxelles (ULB), Brussels, Belgium.

Nathalie Meuleman (N)

Laboratory of Clinical Cell Therapy, ULB-Research Cancer Center (U-CRC), Jules Bordet Institute, Université Libre de Bruxelles (ULB), Brussels, Belgium.
Department of Hematology, Jules Bordet Institute, Brussels, Belgium.

Dominique Bron (D)

Laboratory of Clinical Cell Therapy, ULB-Research Cancer Center (U-CRC), Jules Bordet Institute, Université Libre de Bruxelles (ULB), Brussels, Belgium.
Department of Hematology, Jules Bordet Institute, Brussels, Belgium.

Laurence Lagneaux (L)

Laboratory of Clinical Cell Therapy, ULB-Research Cancer Center (U-CRC), Jules Bordet Institute, Université Libre de Bruxelles (ULB), Brussels, Belgium.

Basile Stamatopoulos (B)

Laboratory of Clinical Cell Therapy, ULB-Research Cancer Center (U-CRC), Jules Bordet Institute, Université Libre de Bruxelles (ULB), Brussels, Belgium.

Classifications MeSH