| Literature DB >> 30302202 |
John C Allen1,1, Fatima Talab2,2, Joseph R Slupsky3,3.
Abstract
B-lymphocytes are dependent on B-cell receptor (BCR) signaling for the constant maintenance of their physiological function, and in many B-cell malignancies this signaling pathway is prone to aberrant activation. This understanding has led to an ever-increasing interest in the signaling networks activated following ligation of the BCR in both normal and malignant cells, and has been critical in establishing an array of small molecule inhibitors targeting BCR-induced signaling. By dissecting how different malignancies signal through BCR, researchers are contributing to the design of more customized therapeutics which have greater efficacy and lower toxicity than previous therapies. This allows clinicians access to an array of approaches to best treat patients whose malignancies have BCR signaling as a driver of pathogenesis.Entities:
Keywords: B-cell receptor signaling; Bruton's tyrosine kinase; Mantle cell lymphoma; chronic lymphocytic leukemia; diffuse large B-cell lymphoma; follicular lymphoma; phosphoinositide 3-kinase; spleen tyrosine kinase
Year: 2016 PMID: 30302202 PMCID: PMC6171999 DOI: 10.2217/ijh-2016-0003
Source DB: PubMed Journal: Int J Hematol Oncol ISSN: 2045-1393