These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: BCL-6 mutations are associated with immunoglobulin variable heavy chain mutations in B-cell chronic lymphocytic leukemia. Author: Pasqualucci L, Neri A, Baldini L, Dalla-Favera R, Migliazza A. Journal: Cancer Res; 2000 Oct 15; 60(20):5644-8. PubMed ID: 11059755. Abstract: The cell of origin of B-cell chronic lymphocytic leukemia (B-CLL) is still uncertain. Recent studies have indicated that a fraction of B-CLL displays somatically mutated immunoglobulin variable heavy chain (IgV(H)) genes, which suggests an origin from a post-germinal center (GC) B cell. It has been shown that the 5' noncoding region of the BCL-6 proto-oncogene is affected by mutations in normal GC B-lymphocytes and in lymphoid malignancies displaying GC/post-GC phenotype. To further explore the cellular origin of B-CLL, we have analyzed 34 cases for mutations in the BCL-6 5' noncoding region and in the IgV(H) genes. We found somatically mutated IgV(H) genes in 24 (73%) of 33 samples (average frequency, 6.5 x 10(-2)/bp) and BCL-6 mutations in 8 (24%) of 34 cases (average frequency, 0.14 x 10(-2)/bp in the mutated cases). The occurrence of BCL-6 mutations was restricted to those cases displaying IgV(H) mutations. Analysis of BCL-6 protein expression as a marker of GC phenotype showed that, regardless of the presence of IgV(H) or BCL-6 mutations, B-CLLs express BCL-6 at levels clearly below those found in normal or transformed GC B cells. These results indicate that a subset of B-CLL derives from a cell that has been exposed to the somatic hypermutation mechanism and support the hypothesis that BCL-6 mutations result from the same process that targets immunoglobulin genes.[Abstract] [Full Text] [Related] [New Search]