|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|5509238||1538505||2017||13 صفحه PDF||سفارش دهید||دانلود رایگان|
- GPCRs regulate B cell migration, proliferation, apoptosis, development and function.
- Mutation, fusion and copy number alterations of GPCRs occur in B cell malignancies.
- B cell lymphoma subtypes contain unique GPCR expression and aberration patterns.
- GPCR mutations and changes in expression can serve as biomarkers of lymphoma.
- Better understanding of GPCRs in lymphoma will improve clinical outcomes.
B cell lymphoma consists of multiple individual diseases arising throughout the lifespan of B cell development. From pro-B cells in the bone marrow, through circulating mature memory B cells, each stage of B cell development is prone to oncogenic mutation and transformation, which can lead to a corresponding lymphoma. Therapies designed against individual types of lymphoma often target features that differ between malignant cells and the corresponding normal cells from which they arise. These genetic changes between tumor and normal cells can include oncogene activation, tumor suppressor gene repression and modified cell surface receptor expression. G protein-coupled receptors (GPCRs) are an important class of cell surface receptors that represent an ideal target for lymphoma therapeutics. GPCRs bind a wide range of ligands to relay extracellular signals through G protein-mediated signaling cascades. Each lymphoma subgroup expresses a unique pattern of GPCRs and efforts are underway to fully characterize these patterns at the genetic level. Aberrations such as overexpression, deletion and mutation of GPCRs have been characterized as having causative roles in lymphoma and such studies describing GPCRs in B cell lymphomas are summarized here.
Journal: Cellular Signalling - Volume 39, November 2017, Pages 95-107