Risk factors for<unk>  include obesity, diabetes mellitus, breast cancer, use of tamoxifen, never having had a child, late menopause, high levels of estrogen, and increasing age. Immigration studies (migration studies), which examine the change in cancer risk in populations moving between countries with different rates of cancer, show that there is some environmental component to<unk> . These environmental risk factors are not well characterized. Hormones Most of the risk factors for<unk>  involve high levels of estrogens. An estimated 40% of cases are thought to be related to obesity. In obesity, the excess of adipose tissue increases conversion of androstenedione into estrone, an estrogen. Higher levels of estrone in the blood causes less or no ovulation and exposes the endometrium to continuously high levels of estrogens. Obesity also causes less estrogen to be removed from the blood. Polycystic ovary syndrome (PCOS), which also causes irregular or no ovulation, is associated with higher rates of<unk>  for the same reasons as obesity. Specifically, obesity, type II diabetes, and insulin resistance are risk factors for Type I<unk> . Obesity increases the risk for<unk>  by 300–400%. Estrogen replacement therapy during menopause when not balanced (or "opposed") with progestin is another risk factor. Higher doses or longer periods of estrogen therapy have higher risks of<unk> . Women of lower weight are at greater risk from unopposed estrogen. A longer period of fertility—either from an early first menstrual period or late menopause—is also a risk factor. Unopposed estrogen raises an individual's risk of<unk>  by 2–10 fold, depending on weight and length of therapy. In trans men who take testosterone and have not had a hysterectomy, the conversion of testosterone into estrogen via androstenedione may lead to a higher risk of<unk> . Genetics alt=A diagram of the autosomal dominant inheritance pattern, showing how a gene can be passed from an affected parent to an affected child. Genetic disorders can also cause<unk> . Overall, hereditary causes contribute to 2–10% of<unk>  cases. Lynch syndrome, an autosomal dominant genetic disorder that mainly causes colorectal cancer, also causes<unk> , especially before menopause. Women with Lynch syndrome have a 40–60% risk of developing<unk> , higher than their risk of developing colorectal (bowel) or ovarian cancer. Ovarian and<unk>  develop simultaneously in 20% of people.<unk>  nearly always develops before colon cancer, on average, 11 years before. Carcinogenesis in Lynch syndrome comes from a mutation in MLH1 or MLH2: genes that participate in the process of mismatch repair, which allows a cell to correct mistakes in the DNA. Other genes mutated in Lynch syndrome include MSH2, MSH6, and PMS2, which are also mismatch repair genes. Women with Lynch syndrome represent 2–3% of<unk>  cases; some sources place this as high as 5%. Depending on the gene mutation, women with Lynch syndrome have different risks of<unk> . With MLH1 mutations, the risk is 54%; with MSH2, 21%; and with MSH6, 16%. Women with a family history of<unk>  are at higher risk. Two genes most commonly associated with some other women's cancers, BRCA1 and BRCA2, do not cause<unk> . There is an apparent link with these genes but it is attributable to the use of tamoxifen, a drug that itself can cause<unk> , in breast and ovarian cancers. The inherited genetic condition Cowden syndrome can also cause<unk> . Women with this disorder have a 5–10% lifetime risk of developing<unk> , compared to the 2–3% risk for unaffected women. Common genetic variation has also been found to affect<unk>  risk in large-scale genome-wide association studies. Sixteen genomic regions have been associated with<unk>  and the common variants explain up to 7% of the familial relative risk. Other health problems Some therapies for other forms of cancer increase the lifetime risk of<unk> , which is a baseline 2–3%. Tamoxifen, a drug used to treat estrogen-positive breast cancers, has been associated with<unk>  in approximately 0.1% of users, particularly older women, but the benefits for survival from tamoxifen generally outweigh the risk of<unk> . A one to two-year course of tamoxifen approximately doubles the risk of<unk> , and a five-year course of therapy quadruples that risk. Raloxifene, a similar drug, did not raise the risk of<unk> . Previously having ovarian cancer is a risk factor for<unk> , as is having had previous radiotherapy to the pelvis. Specifically, ovarian granulosa cell tumors and thecomas are tumors associated with<unk> . Low immune function has also been implicated in<unk> . High blood pressure is also a risk factor, but this may be because of its association with obesity. Sitting regularly for prolonged periods is associated with higher mortality from<unk> . The risk is not negated by regular exercise, though it is lowered. Protective factors Smoking and the use of progestin are both protective against<unk> . Smoking provides protection by altering the metabolism of estrogen and promoting weight loss and early menopause. This protective effect lasts long after smoking is stopped. Progestin is present in the combined oral contraceptive pill and the hormonal intrauterine device (IUD). Combined oral contraceptives reduce risk more the longer they are taken: by 56% after four years, 67% after eight years, and 72% after twelve years. This risk reduction continues for at least fifteen years after contraceptive use has been stopped. Obese women may need higher doses of progestin to be protected. Having had more than five infants (grand multiparity) is also a protective factor, and having at least one child reduces the risk by 35%. Breastfeeding for more than 18 months reduces risk by 23%. Increased physical activity reduces an individual's risk by 38–46%. There is preliminary evidence that consumption of soy is protective.
Endometrial cancer
Cervical cancer
Uterine cancer
Ovarian cancer
Vaginal cancer
Breast cancer
Intravenous leiomyomatosis
Ovarian disease