ArticleThe American journal of pathology2002
A short mutational hot spot in the first intron of BCL-6 is associated with increased BCL-6 expression and with longer overall survival in large B-cell lymphomas.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 49 citations in OpenAlex.
- Genetic Polymorphisms and the Efficacy of Platinum-Based Chemotherapy: Review.Pharmacogenomics and personalized medicine · 2020Review
- Prognostic Significance of in situ Phenotypic Marker Expression in Diffuse Large B-cell Lymphomas.Biomarker insights · 2007Article
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- Point mutation of 5' noncoding region of BCL-6 gene in primary gastric lymphomas.World journal of gastroenterology · 2005Article
- Science review: Genetic variability in the systemic inflammatory response.Critical care (London, England) · 2003Review
- BCL6 controls the expression of the B7-1/CD80 costimulatory receptor in germinal center B cells.The Journal of experimental medicine · 2003Article
- Ambivalent role of BCL6 in cell survival and transformation.Oncogene · 2003Article
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BCL-6 somatic mutations have been described in normal and tumoral B lymphocytes, associated with germinal center transit. We analyzed mutations in the major mutation cluster of BCL-6 in a series of 45 large B-cell lymphomas (LBCLs) and 15 Burkitt's lymphomas, and their relation to the level of BCL-6 expression and clinical outcome. Mutations in LBCL cases revealed the existence of two distinct, short mutational hot spots, spanning positions 106 to 127 and 423 to 443, in which the mutation frequency was higher than expected (P < 0.001). Mutations in the 423 to 443 subcluster were associated with an increased level of expression, although this was not the case with the 106 to 127 cluster. Additionally, LBCL cases characterized by the presence of mutations in the 423 to 443 cluster showed an increased overall survival (P < 0.05) when compared with the nonmutated LBCL cases in these positions. Burkitt's lymphoma cases showed a slightly lower frequency of mutations with a nonclustered distribution and lacked any relationship with the level of expression or any clinical characteristic. Findings from LBCLs suggest that the 423 to 443 cluster includes a regulatory region that is of importance for BCL-6 expression. Deregulation of BCL-6 expression caused by these mutations could play an important role in lymphoma genesis or progression.
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