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High-resolution genomic profiling of adenomas and carcinomas of the salivary glands reveals amplification, rearrangement, and fusion of HMGA2

Artikel i vetenskaplig tidskrift
Författare Fredrik Persson
Ywonne Andrén
Marta Winnes
Barbro Wedell
Anders Nordkvist
Gunnhildur Gudnadottir
R. Dahlenfors
Helene Sjögren
J. Mark
Göran Stenman
Publicerad i Genes Chromosomes Cancer
Volym 48
Nummer/häfte 1
Sidor 69-82
ISSN 1098-2264
Publiceringsår 2009
Publicerad vid Institutionen för biomedicin, avdelningen för patologi
Institutionen för kliniska vetenskaper
Sidor 69-82
Språk en
Länkar dx.doi.org/10.1002/gcc.20619
Ämnesord Adenoma/*genetics, Adult, Aged, Aged, 80 and over, Carcinoma/*genetics, Comparative Genomic Hybridization, Cytogenetic Analysis, Female, *Gene Amplification, Gene Fusion, *Gene Rearrangement, Gene Targeting, HMGA2 Protein/*genetics, Humans, Male, Middle Aged, Oligonucleotide Array Sequence Analysis, Proto-Oncogene Proteins c-mdm2/genetics, Receptor, erbB-2/genetics, Salivary Gland Neoplasms/*genetics
Ämneskategorier Cell- och molekylärbiologi

Sammanfattning

Carcinoma ex pleomorphic adenoma (Ca-ex-PA) is an epithelial malignancy developing within a benign salivary gland pleomorphic adenoma (PA). Here we have used genome-wide, high-resolution array-CGH, and fluorescence in situ hybridization to identify genes amplified in double min chromosomes and homogeneously staining regions in PA and Ca-ex-PA and to identify additional genomic imbalances characteristic of these tumor types. Ten of the 16 tumors analyzed showed amplification/gain of a 30-kb minimal common region, consisting of the 5'-part of HMGA2 (encoding the three DNA-binding domains). Coamplification of MDM2 was found in nine tumors. Five tumors had cryptic HMGA2-WIF1 gene fusions with amplification of the fusion oncogene in four tumors. Expression analysis of eight amplified candidate genes in 12q revealed that tumors with amplification/rearrangement of HMGA2 and MDM2 had significantly higher expression levels when compared with tumors without amplification. Analysis of individual HMGA2 exons showed that the expression of exons 3-5 were substantially reduced when compared with exons 1-2 in 9 of 10 tumors with HMGA2 activation, indicating that gene fusions and rearrangements of HMGA2 are common in tumors with amplification. In addition, recurrent amplifications/gains of 1q11-q32.1, 2p16.1-p12, 8q12.1, 8q22-24.1, and 20, and losses of 1p21.3-p21.1, 5q23.2-q31.2, 8p, 10q21.3, and 15q11.2 were identified. Collectively, our results identify HMGA2 and MDM2 as amplification targets in PA and Ca-ex-PA and suggest that amplification of 12q genes (in particular MDM2), deletions of 5q23.2-q31.2, gains of 8q12.1 (PLAG1) and 8q22.1-q24.1 (MYC), and amplification of ERBB2 may be of importance for malignant transformation of benign PA.

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