Role of the B-cell receptor and the microenvironment in chronic lymphocytic leukemia

Despite significant progress in treatment, chronic lymphocytic leukemia (CLL) remains an incurable disease. Advances have been made to understand the molecular pathogenesis underlying CLL progression and treatment resistance. We here review the available evidences concerning the role of the B-cell r...

Full description

Saved in:
Bibliographic Details
Published inBlood cancer journal (New York) Vol. 3; no. 9; p. e149
Main Authors Oppezzo, P, Dighiero, G
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.09.2013
Springer Nature B.V
Nature Publishing Group
Subjects
631/250/1619/40/1774
631/67/1990/283/1895
631/67/327
692/420/755
Biomedical and Life Sciences
Biomedicine
Cancer Research
Hematology
Oncology
Review
microenvironment
B-cell receptor
chronic lymphocytic leukemia
Online AccessGet full text

Cover

More Information
Summary:Despite significant progress in treatment, chronic lymphocytic leukemia (CLL) remains an incurable disease. Advances have been made to understand the molecular pathogenesis underlying CLL progression and treatment resistance. We here review the available evidences concerning the role of the B-cell receptor (BCR) and the tumor microenvironment interactions in CLL pathogenesis. Antigen likely has a key role in the selection of the tumoral clone, the mutational status of immunoglobulin genes is a strong prognostic predictor and BCR signaling has been postulated to have a role for CLL trafficking and interaction with the stromal microenvironment. There is also important evidence, favoring a role for the microenvironment in CLL pathogenesis. Most, if not all, proliferative events occur in the lymph nodes and bone marrow, where leukemic cells receive through microenvironment interactions survival signals aiming to avoid apoptosis and acquire favorable tumoral growing conditions. In addition, the tumoral microenvironment appears to be the site where the acquisition of additional genetic lesions in the clone occur, which should greatly influence clinical outcome. The advent of new tyrosine kinase inhibitors which seem to be able to modulate microenvironment interactions and circumvent the p53 deletion have generated significant promise by raising the possibility that they could provide significant progress in disease treatment.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:2044-5385
2044-5385
DOI:10.1038/bcj.2013.45