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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2005-6-8
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pubmed:abstractText |
Activation of an oncogene via its juxtaposition to the IGH locus by a chromosomal translocation or, less frequently, by genomic amplification is considered a major mechanism of B-cell lymphomagenesis. However, amplification of an IGH/oncogene fusion, coined a complicon, is a rare event in human cancers and has been associated with poor outcome and resistance to treatment. In this article are descriptions of two cases of germinal-center-derived B-cell lymphomas with IGH/BCL2 fusion that additionally displayed amplification of an IGH/MYC fusion. As shown by fluorescence in situ hybridization, the first case contained a IGH/MYC complicon in double minutes, whereas the second case showed a BCL2/IGH/MYC complicon on a der(8)t(8;14)t(14;18). Additional molecular cytogenetic and mutation analyses revealed that the first case also contained a chromosomal translocation affecting the BCL6 oncogene and a biallelic inactivation of TP53. The second case harbored a duplication of REL and acquired a translocation affecting IGL and a biallelic inactivation of TP53 during progression. Complicons affecting Igh/Myc have been reported previously in lymphomas of mouse models simultaneously deficient in Tp53 and in genes of the nonhomologous end-joining DNA repair pathway. To the best of our knowledge, this is the first time that IGH/MYC complicons have been reported in human lymphomas. Our findings imply that the two mechanisms resulting in MYC deregulation, that is, translocation and amplification, can occur simultaneously.
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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 |
Aug
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pubmed:issn |
1045-2257
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pubmed:author |
pubmed-author:AgirreXabierX,
pubmed-author:ArdanazMaría TMT,
pubmed-author:CalasanzMaría JoséMJ,
pubmed-author:CigudosaJuan CruzJC,
pubmed-author:GascoyneRandy DRD,
pubmed-author:HernandezRobertoR,
pubmed-author:Martín-SuberoJosé IgnacioJI,
pubmed-author:NovoFrancisco JavierFJ,
pubmed-author:OderoMaría DoloresMD,
pubmed-author:SaezBorjaB,
pubmed-author:Sanz-GarcíaEduardoE,
pubmed-author:SiebertReinerR
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pubmed:copyrightInfo |
Copyright 2005 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
414-23
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15852472-Adult,
pubmed-meshheading:15852472-DNA-Binding Proteins,
pubmed-meshheading:15852472-Gene Amplification,
pubmed-meshheading:15852472-Genes, bcl-2,
pubmed-meshheading:15852472-Genes, myc,
pubmed-meshheading:15852472-Genes, rel,
pubmed-meshheading:15852472-Germinal Center,
pubmed-meshheading:15852472-Humans,
pubmed-meshheading:15852472-Immunoglobulin Heavy Chains,
pubmed-meshheading:15852472-In Situ Hybridization, Fluorescence,
pubmed-meshheading:15852472-Lymphoma, B-Cell,
pubmed-meshheading:15852472-Male,
pubmed-meshheading:15852472-Oncogene Proteins, Fusion,
pubmed-meshheading:15852472-Proto-Oncogene Proteins,
pubmed-meshheading:15852472-Proto-Oncogene Proteins c-bcl-6,
pubmed-meshheading:15852472-Transcription Factors,
pubmed-meshheading:15852472-Translocation, Genetic,
pubmed-meshheading:15852472-Tumor Suppressor Protein p53
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pubmed:year |
2005
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pubmed:articleTitle |
Amplification of IGH/MYC fusion in clinically aggressive IGH/BCL2-positive germinal center B-cell lymphomas.
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pubmed:affiliation |
Institute of Human Genetics, University Hospital Schleswig-Holstein Campus Kiel, Germany.
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pubmed:publicationType |
Journal Article,
Case Reports,
Research Support, Non-U.S. Gov't
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