<unk>  is related to the amount of time spent ovulating. Thus, not having children is a risk factor for<unk> , likely because ovulation is suppressed via pregnancy. During ovulation, cells are constantly stimulated to divide while ovulatory cycles continue. Therefore, women who have not borne children are at twice the risk of<unk>  than those who have. A longer period of ovulation caused by early first menstruation and late menopause is also a risk factor. Both obesity and hormone replacement therapy also raise the risk. The risk of developing<unk>  is less for women who have fewer menstrual cycles, no menstrual cycles, breast feeding, take oral contraceptives, have multiple pregnancies, and have a pregnancy at an early age. The risk of developing<unk>  is reduced in women who have had tubal ligation (colloquially known as having one's "tubes tied"), both ovaries removed, or hysterectomy (an operation in which the uterus, and sometimes the cervix, is removed). Age is also a risk factor. Hormones The use of fertility medication may contribute to ovarian borderline tumor formation, but the link between the two is disputed and difficult to study. Fertility drugs may be associated with a higher risk of borderline tumors. Those who have been treated for infertility but remain nulliparous are at higher risk for epithelial<unk> ; however, those who are successfully treated for infertility and subsequently give birth are at no higher risk. This may be due to shedding of precancerous cells during pregnancy, but the cause remains unclear. The risk factor may instead be infertility itself, not the treatment. Hormonal conditions such as polycystic ovary syndrome and endometriosis are associated with<unk> , but the link is not completely confirmed. Postmenopausal hormone replacement therapy (HRT) with estrogen likely increases the risk of<unk> . The association has not been confirmed in a large-scale study, but notable studies including the Million Women Study have supported this link. Postmenopausal HRT with combined estrogen and progesterone may increase contemporaneous risk if used for over 5 years, but this risk returns to normal after cessation of therapy. Estrogen HRT with or without progestins increases the risk of endometrioid and serous tumors but lowers the risk of mucinous tumors. Higher doses of estrogen increase this risk. Endometriosis is another risk factor for<unk> , as is pain with menstruation. Endometriosis is associated with clear-cell and endometrioid subtypes, low-grade serous tumors, stage I and II tumors, grade 1 tumors, and lower mortality. Before menopause, obesity can increase a person's risk of<unk> , but this risk is not present after menopause. This risk is also relevant in those who are both obese and have never used HRT. A similar association with<unk>  appears in taller women. Genetics Women with ovarian or breast cancer in a pedigree chart of a family A family history of<unk>  is a risk factor for<unk> . Women with hereditary nonpolyposis colon cancer (Lynch syndrome), and those with BRCA-1 and BRCA-2 genetic abnormalities are at increased risk. The major genetic risk factor for<unk>  is a mutation in BRCA1 or BRCA2 genes, or in DNA mismatch repair genes, which is present in 10% of<unk>  cases. Only one allele need be mutated to place a person at high risk. The gene can be inherited through either the maternal or paternal line, but has variable penetrance. Though mutations in these genes are usually associated with increased risk of breast cancer, they also carry a substantial lifetime risk of<unk> , a risk that peaks in a person's 40s and 50s. The lowest risk cited is 30% and the highest 60%. Mutations in BRCA1 have a lifetime risk of developing<unk>  of 15–45%. Mutations in BRCA2 are less risky than those with BRCA1, with a lifetime risk of 10% (lowest risk cited) to 40% (highest risk cited). On average, BRCA-associated cancers develop 15 years before their sporadic counterparts because people who inherit the mutations on one copy of their gene only need one mutation to start the process of carcinogenesis, whereas people with two normal genes would need to acquire two mutations. In the United States, five of 100 women with a first-degree relative with<unk>  will eventually get<unk>  themselves, placing those with affected family members at triple the risk of women with unaffected family members. Seven of 100 women with two or more relatives with<unk>  will eventually get<unk> . In general, 5–10% of<unk>  cases have a genetic cause. BRCA mutations are associated with high-grade serous nonmucinous epithelial<unk> . A strong family history of endometrial cancer, colon cancer, or other gastrointestinal cancers may indicate the presence of a syndrome known as hereditary nonpolyposis colorectal cancer (also known as Lynch syndrome), which confers a higher risk for developing a number of cancers, including<unk> . Lynch syndrome is caused by mutations in mismatch repair genes, including MSH2, MLH1, MLH6, PMS1, and PMS2. The risk of<unk>  for an individual with Lynch syndrome is between 10 and 12 percent. Women of Icelandic descent, European Jewish descent/Ashkenazi Jewish descent, and Hungarian descent are at higher risk for epithelial<unk> . Estrogen receptor beta gene (ESR2) seems to be a key to pathogenesis and response to therapy. Other genes that have been associated with<unk>  are BRIP1, MSH6, RAD51C and RAD51D. CDH1, CHEK2, PALB2 and RAD50 have also been associated with<unk> . Several rare genetic disorders are associated with specific subtypes of<unk> . Peutz–Jeghers syndrome, a rare genetic disorder, also predisposes women to sex cord tumour with annular tubules. Ollier disease and Maffucci syndrome are associated with granulosa cell tumors in children and may also be associated with Sertoli-Leydig tumors. Benign fibromas are associated with nevoid basal cell carcinoma syndrome. Diet Alcohol consumption does not appear to be related to<unk> . The American Cancer Society recommends a healthy eating pattern that includes plenty of fruits, vegetables, whole grains, and a diet that avoids or limits red and processed meats and processed sugar. High consumption of total, saturated and trans-fats increases<unk>  risk. A 2021 umbrella review found that coffee, egg, and fat intake significantly increases the risk of<unk> . There is mixed evidence from studies on<unk>  risk and consumption of dairy products. Environmental factors Industrialized nations, with the exception of Japan, have high rates of epithelial<unk> , which may be due to diet in those countries. White women are at a 30–40% higher risk for<unk>  when compared to Black women and Hispanic women, likely due to socioeconomic factors; white women tend to have fewer children and different rates of gynecologic surgeries that affect risk for<unk> . Tentative evidence suggests that talc, pesticides, and herbicides increase the risk of<unk> . The American Cancer Society notes that as of now, no study has been able to accurately link any single chemical in the environment, or in the human diet, directly to mutations that cause<unk> . Other Other factors that have been investigated, such as smoking, low levels of vitamin D in the blood, presence of inclusion ovarian cysts, and infection with human papilloma virus (the cause of some cases of cervical cancer), have been disproven as risk factors for<unk> . The carcinogenicity of perineal talc is controversial, because it can act as an irritant if it travels through the reproductive tract to the ovaries. Case-control studies have shown that use of perineal talc does increase the risk of<unk> , but using talc more often does not create a greater risk. Use of talc elsewhere on the body is unrelated to<unk> . Sitting regularly for prolonged periods is associated with higher mortality from epithelial<unk> . The risk is not negated by regular exercise, though it is lowered. Increased age (up to the 70s) is a risk factor for epithelial<unk>  because more mutations in cells can accumulate and eventually cause cancer. Those over 80 are at slightly lower risk. Smoking tobacco is associated with a higher risk of mucinous<unk> ; after smoking cessation, the risk eventually returns to normal. Higher levels of C-reactive protein are associated with a higher risk of developing<unk> . Protective factors Suppression of ovulation, which would otherwise cause damage to the ovarian epithelium and, consequently, inflammation, is generally protective. This effect can be achieved by having children, taking combined oral contraceptives, and breast feeding, all of which are protective factors. A longer period of breastfeeding correlates with a larger decrease in the risk of<unk> . Each birth decreases risk of<unk>  more, and this effect is seen with up to five births. Combined oral contraceptives reduce the risk of<unk>  by up to 50%, and the protective effect of combined oral contraceptives can last 25–30 years after they are discontinued. Regular use of aspirin or acetaminophen (paracetamol) may be associated with a lower risk of<unk> ; other NSAIDs do
Ovarian cancer
Uterine fibroid  s  1
Breast cancer
Uterine cancer
Cervical cancer
Endometrial cancer
Ovarian cyst
Fallopian tube cancer