Aims And Background: The literature data show that the most frequently affected chromosomes in ovarian carcinogenesis are 1, 8 and 17. In the present study we aimed to define more precisely at a high resolution the genomic imbalances of these chromosomes in ovarian cancer and to determine genomic markers separating tumors of different histological types and stages.
Methods: Array comparative genomic hybridization (CGH) with a resolution of approximately 0.
Background: We selected 5 oncogenes with well-established roles in carcinogenesis -- CCND1, ErbB1, ErbB2, c-myc and ZNF217 -- to investigate the coexistence of their copy imbalances in relation to the clinico-pathological characteristics of ovarian tumors.
Materials And Methods: Fluorescence in situ hybridization for the 5 genes was applied to a preexisting tissue microarray. 38 ovarian tumors were successfully analyzed for copy number changes of the 5 genes.
This study aimed to clarify the molecular mechanisms involved in ovarian carcinogenesis, and to identify candidate molecular targets for its diagnosis and treatment. The genome-wide gene expression profiles of 22 epithelial ovarian carcinomas were analyzed with a microarray representing 38,500 genes, in combination with laser microbeam microdissection. A total of 273 commonly up-regulated transcripts and 387 down-regulated transcripts were identified in the ovarian carcinoma samples.
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