51. Correlations between c-myc gene copy-number and clinicopathological parameters of ovarian tumours
- Author
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D. Toncheva, I. Dimova, N. Doganov, S. Raitcheva, and R. Dimitrov
- Subjects
Cancer Research ,endocrine system diseases ,Gene Dosage ,Genes, myc ,Biology ,Protein Serine-Threonine Kinases ,Malignancy ,Gene dosage ,Ovarian tumor ,Aurora Kinases ,Gene duplication ,medicine ,Humans ,Telomerase ,In Situ Hybridization, Fluorescence ,Aurora Kinase A ,Ovarian Neoplasms ,Tissue microarray ,Gene Amplification ,Histology ,medicine.disease ,female genital diseases and pregnancy complications ,DNA-Binding Proteins ,Phenotype ,Oncology ,Cancer research ,Female ,Ovarian cancer ,Clear cell - Abstract
The objective of this study was to investigate increases in c-myc gene copy-number in ovarian tumours, and to analyze their correlations with clinicopathological parameters. Here we applied FISH on TMA (tissue microarrays) containing 507 ovarian tumour samples from different malignancy, histology, stage and grade. Overall, we found high frequency for c-myc copy-number increases (38.5%) in ovarian cancers: 22.1% amplifications and 16.4% gains. We established c-myc amplification in more than 30% in endometrioid and mixed epithelial ovarian carcinomas. c-myc gains were found in a high proportion (42.9%) of clear cell carcinomas. We found associations between c-myc copy-number changes and clinicopathological parameters of ovarian tumours such as degree of malignancy and histological type. We suggested that c-myc amplifications are characteristics for endometrioid, and c-myc gains for clear cell ovarian cancers. We suggest that copy-number increases of c-myc and 20q13.2 represent a possible mechanism for the regulation of the pathway STK15--c-myc--hTERT.
- Published
- 2005