Genomic Consequences of Ovarian Cancer with Respect to DNA Damage and Repair Mechanism

Ovarian cancer is not a single disorder having different histological types which are associated with germline or somatic mutations. Histological types include epithelial cancers that account for ~90% of ovarian cancers and include serous, endometrioid, clear-cell and mucinous carcinomas. There are several risk factors for developing ovarian cancer which includes a genetic factor, age, use of hormonal therapy after menopause, null parity, infertility and other factors including obesity, lifestyle, dietary habits. BRCA1 and BRCA2 are germ line mutations which are completely associated with epithelial ovarian cancer. Germ line mutations in DNA repair pathway which increase the risk of ovarian cancer such as RAD51C, RAD51D, BRIP1, BARD1, and PALB2. To understand the mechanism of progression of ovarian cancer it is very important to explore the mechanism behind the abruption of DNA repair genes that are associated with a high risk of ovarian cancer (such as BRCA1 and BRCA2). The study of these DNA repair genes holds a promise for identifying the women at high risk of developing the ovarian cancer in early stages. The main aim of this review is to investigate the development and progression of ovarian cancer and to explore the various genetic and non-genetic perspectives of cancer with special emphasis to personalized medicine.