Source:http://linkedlifedata.com/resource/pubmed/id/11929130
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2002-4-3
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pubmed:abstractText |
CD95 (Apo-1/Fas) is crucial for the negative selection of B cells within the germinal center (GC). Impairment of CD95-mediated apoptosis results in defective affinity maturation and the persistence of autoreactive B-cell clones. CD95 was defined recently as a tumor-suppressor gene and is silenced in many tumor entities. In contrast to other malignancies, in GC-derived B-cell lymphomas, inactivation of the CD95 gene is often a result of deleterious mutations. Such mutations occur also at a low frequency in normal GC, but not naive, B cells. We propose that CD95 mutations in B-cell lymphomas originate from the GC reaction and are introduced most probably as targeting errors of the somatic hypermutation machinery, which bears--besides its physiological role--an inherent risk of malignant transformation and the persistence of autoreactive B-cell specificities.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1471-4906
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
75-80
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
2002
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pubmed:articleTitle |
The origin of CD95-gene mutations in B-cell lymphoma.
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pubmed:affiliation |
Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Universität zu Köln, Germany. markus.mueschen@uni-koeln.de
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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