rdf:type |
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lifeskim:mentions |
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pubmed:issue |
20
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pubmed:dateCreated |
1998-10-22
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pubmed:abstractText |
The molecular mechanism involved in the process of antigen-driven somatic hypermutation of Ig genes is unknown, but it is commonly believed that this mechanism is restricted to the Ig loci. B cell lymphomas commonly display multiple somatic mutations clustering in the 5'-regulatory region of BCL-6, a proto-oncogene encoding for a POZ/Zinc finger transcriptional repressor expressed in germinal center (GC) B cells and required for GC formation. To determine whether BCL-6 mutations represent a tumor-associated phenomenon or reflect a physiologic mechanism, we screened single human tonsillar GC B cells for mutations occurring in the BCL-6 5'-noncoding region and in the Ig variable heavy chain sequences. Thirty percent of GC B cells, but not naive B cells, displayed mutations in the 742 bp region analyzed within the first intron of BCL-6 (overall frequency: 5 x 10(-4)/bp). Accordingly, an expanded survey in lymphoid malignancies showed that BCL-6 mutations are restricted to B cell tumors displaying GC or post-GC phenotype and carrying mutated Ig variable heavy chain sequences. These results indicate that the somatic hypermutation mechanism active in GC B cells physiologically targets non-Ig sequences.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9751748-1420357,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9751748-1760840,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9751748-9624052
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0027-8424
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pubmed:author |
pubmed-author:BaldiniLL,
pubmed-author:ChagantiR SRS,
pubmed-author:Dalla-FaveraRR,
pubmed-author:FracchiollaNN,
pubmed-author:KüppersRR,
pubmed-author:KleinUU,
pubmed-author:MigliazzaAA,
pubmed-author:OwenW GWG,
pubmed-author:PasqualucciLL,
pubmed-author:RajewskyKK,
pubmed-author:WilliamCC
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pubmed:issnType |
Print
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pubmed:day |
29
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pubmed:volume |
95
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11816-21
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9751748-B-Lymphocytes,
pubmed-meshheading:9751748-Cell Transformation, Neoplastic,
pubmed-meshheading:9751748-DNA-Binding Proteins,
pubmed-meshheading:9751748-Genes, Immunoglobulin,
pubmed-meshheading:9751748-Germinal Center,
pubmed-meshheading:9751748-Humans,
pubmed-meshheading:9751748-Immunoglobulin Heavy Chains,
pubmed-meshheading:9751748-Immunoglobulin Variable Region,
pubmed-meshheading:9751748-Leukemia, B-Cell,
pubmed-meshheading:9751748-Lymphoma, B-Cell,
pubmed-meshheading:9751748-Mutation,
pubmed-meshheading:9751748-Neoplasms,
pubmed-meshheading:9751748-Polymerase Chain Reaction,
pubmed-meshheading:9751748-Polymorphism, Single-Stranded Conformational,
pubmed-meshheading:9751748-Proto-Oncogene Proteins,
pubmed-meshheading:9751748-Proto-Oncogene Proteins c-bcl-6,
pubmed-meshheading:9751748-Transcription Factors
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pubmed:year |
1998
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pubmed:articleTitle |
BCL-6 mutations in normal germinal center B cells: evidence of somatic hypermutation acting outside Ig loci.
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pubmed:affiliation |
Departments of Pathology and Genetics and Development, Columbia University, New York, NY 10032, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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