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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Oncología > Genética > DA - CIMA - Oncología - Genética - Artículos de revista >

Amplification of IGH/MYC fusion in clinically aggressive IGH/BCL2-positive germinal center B-cell lymphomas
Authors: Martin-Subero, J.I. (José Ignacio)
Odero, M.D. (María D.)
Hernandez, R. (Roberto)
Cigudosa, J.C. (Juan Cruz)
Aguirre, X. (Xavier)
Saez, B. (Borja)
Sanz-Garcia, E. (Eduardo)
Ardanaz, M.T. (M.T.)
Novo, F.J. (Francisco Javier)
Gascoyne, R.D (R. D.)
Calasanz, M.J. (María José)
Siebert, R. (Reiner)
Keywords: Gene Amplification
Genes, bcl-2
Genes, myc
Germinal Center
Oncogene Proteins, Fusion/genetics
Issue Date: 2005
Publisher: Wiley-Blackwell
Publisher version: http://onlinelibrary.wiley.com/doi/10.1002/gcc.20187/abstract
ISSN: 1098-2264
Citation: Martin-Subero JI, Odero MD, Hernandez R, Cigudosa JC, Agirre X, Saez B, et al. Amplification of IGH/MYC fusion in clinically aggressive IGH/BCL2-positive germinal center B-cell lymphomas. Genes Chromosomes Cancer 2005 Aug;43(4):414-423.
Abstract
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.
Permanent link: http://hdl.handle.net/10171/19527
Appears in Collections:DA - CIMA - Oncología - Genética - Artículos de revista
DA - Ciencias - Genética - Artículos de revista

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