Ovarian cancer (OC) is the seventh most common cancer in women globally and the tenth in China. It is primarily epithelial in origin, with five major histotypes: high-grade serous (HGSOC), endometrioid (ENOC), clear cell (CCOC), mucinous (MOC), and low-grade serous (LGSOC). Genetic factors, including rare inherited mutations in BRCA1 and BRCA2, contribute to hereditary cases. Genome-wide association studies have identified 29 common susceptibility alleles, including 14 subtype-specific ones. Reproductive and hormonal factors such as parity, oral contraceptive use, and lactation may lower risk, while older age at menopause and hormone replacement therapy increase it. These associations vary by histotype, especially for mucinous OC. Endometrioid and clear cell OC are associated with increased risk in women with endometriosis and decreased risk with tubal ligation. Other risk factors include environmental and lifestyle factors like asbestos and talc exposure, and cigarette smoking. The epidemiology of OC provides insights into its etiology, prevention, early detection, and potential therapeutic strategies. OC incidence varies geographically, with higher rates in developed countries. In the US, racial disparities exist, with higher rates among white women. OC incidence and mortality have declined in most developed countries since the 1990s, while they have increased in less developed countries with recent economic growth. Genetic epidemiology shows that BRCA1 and BRCA2 mutations significantly increase OC risk, accounting for most hereditary cases. Genome-wide association studies have identified 22 susceptibility alleles for invasive OC, with some associated with specific histotypes. Risk factors include hormonal and reproductive factors such as parity, age at menarche and menopause, and oral contraceptive use. Parity is associated with lower OC risk, with each additional full-term pregnancy reducing risk by about 15%. Lactation is associated with a slight protective effect. Infertility is a risk factor in many studies, but not all. Endometriosis is linked with OC, particularly endometrioid and clear cell subtypes. PID is associated with increased OC risk, especially among younger women. HRT is associated with increased OC risk, particularly for unopposed estrogen therapy. Obesity is associated with increased OC risk, especially for non-serous and low-grade serous subtypes. Diet and nutrition are not clearly linked to OC risk, but higher vegetable intake is associated with lower risk. Exercise is associated with lower OC risk, but the effect is not consistent across histotypes. Cigarette smoking is associated with increased risk for mucinous OC. Alcohol consumption has inconsistent associations with OC risk. Asbestos and talc exposure are associated with increased OC risk, though evidence is not conclusive. Drug use, including aspirin and NSAIDs, is associated with lower OC risk. Overall, OC risk is influenced by a complex interplayOvarian cancer (OC) is the seventh most common cancer in women globally and the tenth in China. It is primarily epithelial in origin, with five major histotypes: high-grade serous (HGSOC), endometrioid (ENOC), clear cell (CCOC), mucinous (MOC), and low-grade serous (LGSOC). Genetic factors, including rare inherited mutations in BRCA1 and BRCA2, contribute to hereditary cases. Genome-wide association studies have identified 29 common susceptibility alleles, including 14 subtype-specific ones. Reproductive and hormonal factors such as parity, oral contraceptive use, and lactation may lower risk, while older age at menopause and hormone replacement therapy increase it. These associations vary by histotype, especially for mucinous OC. Endometrioid and clear cell OC are associated with increased risk in women with endometriosis and decreased risk with tubal ligation. Other risk factors include environmental and lifestyle factors like asbestos and talc exposure, and cigarette smoking. The epidemiology of OC provides insights into its etiology, prevention, early detection, and potential therapeutic strategies. OC incidence varies geographically, with higher rates in developed countries. In the US, racial disparities exist, with higher rates among white women. OC incidence and mortality have declined in most developed countries since the 1990s, while they have increased in less developed countries with recent economic growth. Genetic epidemiology shows that BRCA1 and BRCA2 mutations significantly increase OC risk, accounting for most hereditary cases. Genome-wide association studies have identified 22 susceptibility alleles for invasive OC, with some associated with specific histotypes. Risk factors include hormonal and reproductive factors such as parity, age at menarche and menopause, and oral contraceptive use. Parity is associated with lower OC risk, with each additional full-term pregnancy reducing risk by about 15%. Lactation is associated with a slight protective effect. Infertility is a risk factor in many studies, but not all. Endometriosis is linked with OC, particularly endometrioid and clear cell subtypes. PID is associated with increased OC risk, especially among younger women. HRT is associated with increased OC risk, particularly for unopposed estrogen therapy. Obesity is associated with increased OC risk, especially for non-serous and low-grade serous subtypes. Diet and nutrition are not clearly linked to OC risk, but higher vegetable intake is associated with lower risk. Exercise is associated with lower OC risk, but the effect is not consistent across histotypes. Cigarette smoking is associated with increased risk for mucinous OC. Alcohol consumption has inconsistent associations with OC risk. Asbestos and talc exposure are associated with increased OC risk, though evidence is not conclusive. Drug use, including aspirin and NSAIDs, is associated with lower OC risk. Overall, OC risk is influenced by a complex interplay