Ovarian cancer is the leading cause of death from gynecological malignancies, and the fourth leading cause of death. among women. Development of a comprehensive model of ovarian carcinogenesis is a major objective of Current ovarian cancer research efforts. The molecular pathogenesis of ovarian cancer is heterogeneous and this is reflected in the variability of clinical characteristics. The precise Molecular mechanisms in ovarian tumorigenesis, both inherited and sporadic, are largely unknown, and several chromosomal regions and genes have been implicated in the tumorigenic process. Both familial and sporadic cases of ovarian cancer require the accumulation of genetic changes. Notably, loss of the wild-type allele at the BRCA1 (17q21) or BRCA2 (13q12) loci has been reported in ovarian tumors, though somatic point Mutations have rarely been detected. Inactivation of p53 at 17p and allelic loss targeting a distinct region oil proximal 17p also have been reported to be early events in ovarian cancer and overexpression of Putative oncogenes such as HER2/Neu have been described in ovarian cancer, and although controversial, has been associated with poor prognosis. The development of new diagnostic, preventive and treatment approaches requires an in-depth understanding of the mechanisms of the complex multistep process of tumorigenesis in ovarian cancer. However, relatively little is known regarding the molecular pathogenesis and progression of ovarian cancer compared to other solid tumors. Elucidation of the genes that are involved in ovarian tumorigenesis and analysis of the genome for regions may be Sources of insight to potential future therapeutic and intervention strategies.