Mechanism of oncogenesis and activation of oncogene in human ovarian carcinoma

To investigate the specific chromosomal abnormalities and role of oncogene in human ovarian cancer, three cases of primary ovarian cancer tissues and cells line (HTB 161) were cultured and karyotyped after G-banding. DNA in situ hybridization and southern blot were also performed on the same materials for erb B2, N-ras and c-myc oncogenes. The case 1, had diploid 46, XX, showing HSR like regions in almost all cells. These HSR might have appeared due to amplification of erb-B2 oncogenes after translocation 17q21 to 9q12. In case 2 specific translocation t(1;7) (pter;q21) and amplification of N-ras were observed. However in case 3, the most common abnormality corresponded to del (1) (p13 or p22) with amplification of erb B2. In none of the cases the activation of c-myc was revealed in this study. This indicates that different karyotypic abnormalities may not interfere with activation of erb B2 or N-ras in cell lines. The paper also suggests that oncogenesis as a phenomenon might be progressed by the activation of an oncogene or may be combined with specific chromosomal translocation or even deletion (inactivation of antioncogene). Obviously, oncogenesis as a process may not be understood to adhere to fixed mechanisms but may show individual differences.