Abstract:
Objective To identify copy number variations in the oncogene c-myc and antioncogene Rb1 in epithelial ovarian cancer.
Methods Tumor cells from ascites were collected from epithelial ovarian cancer patients. Karyotype analysis was performed to distinguish and exclude aneuploid samples. Probe DNA prepared from bacterial artificial chromosomes (BACs) selected according to c-myc and Rb1 was labeled with Spectrum Green and PromoFluor-590 by nick translation. Duo-color fluorescent in situ hybridization (D-FISH) analysis was then performed. The hybridization was performed strictly according to a previously published method.
Results Three aneuploid samples were excluded from the samples. In 41 of the 58 diploid samples, c-myc amplification was identified (70.69%), whereas Rb1 deletion appeared in 24 of the 58 samples (41.38%). C-myc amplification and Rb1 deletion were found simultaneously in 20 samples (34.48%). Only one sample showed c-myc amplification in a benign ovarian tumor. Neither amplification nor deletion was seen in normal ovarian tissues. The deletion of Rb1 is related to the International Federation of Gynecology and Obstetrics staging and pathological grading.
Conclusion Genome abnormalities were abundantly observed in epithelial ovarian cancer, among which, the amplification of c-myc and Rb1 deletion are the most common. Copy number variations in both oncogenes and antioncogenes may play an important role in the development and progress of advanced epithelial ovarian cancer.
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