OP03. GENOMIC PROFILING OF OVARIAN CANCER FOR CHROMOSOME 17 BY ARRAY CGH ANALYSIS
DIMOVA I1, Orsetti B2, Rouge C2, Ursule L2, Lasorsa L2, Dimitrov R3, Doganov N3, Toncheva D1, Theillet Ch2 1 Department of Medical Genetics, Medical University - Sofia, Bulgaria 2 Genotype et Phenotype Tumoraux, EMI229 INSERM/Universite Montpellier I, CRLC Val D'Aurelle - Paul Lamarque, Montpellier, France 3 Clinics of Operative Gynecology, University Hospital of Obstetrics and Gynecology - Sofia, Bulgaria email: dragatoncheva@yahoo.com
*Corresponding Author:
page: 36

Abstract

We analyzed genomic imbalances affecting chromosome 17 by array-CGH in 28 primary ovarian cancers and 9 ovarian cancer cell lines, using a home made BAC-array covering this chromosome at a mean density of 1 BAC clone/0.8 Mb. We identified regions of highly frequent gains or losses, since they affected more than 40% of ovarian cancers and determined sites showing alterations of elevated amplitude (amplifications or homozygous deletions). Doing this we also identified at least two adjacent changed clones. Finally, we characterized the smallest regions of overlap for gains. This allowed us to determine anomalies strongly associated to the disease such as: deletions at 17p12-13 or amplifications at 17q12, 17q23.2, 17q24.3. The resolution of array-CGH gives an almost direct link to the human genome sequence and, hence, to a list of candidate genes. Our results defined more precisely the gains in 17q12-q24, finding as strong candidates for ovarian carcinogenesis the ge nes LASP1 (17q12), TGF11 (17q21.32), MUL (17q23.2), TBX2 (17q23.2), AXIN2 (17q24.3) and GRB2 (17q25.1). We were interested in verifying whether some of the anomalies we had identified were diagnostic in terms of separating tumors of different histological types or stage. We performed two comparisons: (1) serous and non-serous; (2) early and late stage ovarian tumors. To identify alterations, specific of a particular histological and stage group, we determined regions whose alterations was at least 40% more frequent in one group compared to another. We found that gains of 17q11.2-12 and 17q25 are associated with non-serous histology. Gains of 17q23.2 and 17q24.3 and losses of 17p and 17q were specific for late stage ovarian cancers.




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