Ovarian cancer has no single cause, but rather a combination of genetic, hormonal, and reproductive factors that increase or decrease risk. The average woman has about a 1.4% lifetime risk of developing ovarian cancer, but that number shifts dramatically based on inherited gene mutations, ovulation history, and certain medical conditions. Understanding these factors can help you assess your own risk profile.
Where Ovarian Cancer Actually Starts
For decades, scientists assumed ovarian cancer originated on the surface of the ovary itself. That view has shifted significantly. Research now shows that the most common and aggressive form, called high-grade serous carcinoma, frequently begins not in the ovary but in the fallopian tubes. Specifically, tiny clusters of abnormal cells form in the fimbriae, the finger-like projections at the far end of the fallopian tube that sit close to the ovary. These precursor lesions can be as small as a nest of roughly 13 cells.
These abnormal cells shed from the fallopian tube and land on the ovarian surface or nearby tissue, where they take root and grow. By the time the cancer is detected, it appears to be an ovarian tumor, but its origin was the tube. This discovery is one reason why removing the fallopian tubes (while leaving the ovaries) has become a risk-reduction strategy for some women.
Genetic Mutations and Inherited Risk
The strongest known risk factor for ovarian cancer is inheriting a mutation in the BRCA1 or BRCA2 genes. These genes normally help repair damaged DNA in your cells. When they don’t work properly, cells are more likely to accumulate errors that lead to cancer. Women with a BRCA1 mutation face a 39% to 44% lifetime risk of ovarian cancer. For BRCA2 carriers, the lifetime risk is 11% to 17%. Compare that to the 1.4% risk in the general population, and the magnitude of these mutations becomes clear.
Lynch syndrome, a lesser-known inherited condition that also raises the risk of colon and uterine cancers, carries an 8% lifetime risk of ovarian cancer. While that’s lower than BRCA-related risk, it’s still roughly six times higher than average. Lynch syndrome results from mutations in genes responsible for fixing small errors that occur when DNA copies itself during cell division.
Not everyone with these mutations develops cancer, and most ovarian cancers occur in women without any known hereditary syndrome. But if you have a close relative (mother, sister, daughter) who had ovarian cancer, or a family history of breast, colon, or uterine cancer, genetic counseling can help determine whether testing makes sense for you.
How Ovulation Damages Cells Over Time
Each time you ovulate, your body essentially creates a small wound. The surface of the ovary ruptures to release an egg, triggering an inflammatory response. Inflammatory cells rush to the site and generate reactive oxygen species, molecules that can directly damage DNA. Your body has built-in repair mechanisms to fix this damage, but over hundreds of ovulation cycles across a lifetime, errors can slip through.
This is known as the “incessant ovulation” theory, and it explains why factors that reduce the total number of ovulations in your lifetime also reduce ovarian cancer risk. Pregnancy, breastfeeding, and oral contraceptive use all suppress ovulation for extended periods. Women who started menstruating early, went through menopause late, or never had children accumulate more ovulatory cycles, and with them, more opportunities for DNA damage to go unrepaired.
Pregnancy, Breastfeeding, and Oral Contraceptives
Reproductive history has a surprisingly powerful influence on ovarian cancer risk. Breastfeeding, in particular, shows a strong protective effect. Women who breastfed at all had a 22% lower risk of ovarian cancer compared to those who never breastfed. Those who breastfed for 18 months or more saw a 43% reduction in risk. Among women with only one child, breastfeeding for 18 months or longer was associated with nearly a 70% reduction in risk.
Oral contraceptives offer similar protection through a different mechanism: they suppress ovulation entirely. Women who have ever used the pill have a 30% to 50% lower risk of ovarian cancer than those who never used it. The longer you use oral contraceptives, the greater the protection, and the benefit persists for up to 30 years after stopping.
Endometriosis and Ovarian Cancer
Endometriosis, a condition where tissue similar to the uterine lining grows outside the uterus, is a meaningful risk factor. A large study published in JAMA found that endometriosis was associated with a 4.2-fold increased risk of ovarian cancer overall. For a specific category called type I ovarian cancers (which includes endometrioid, clear cell, and mucinous subtypes), the risk jumped to 7.5 times higher than in women without endometriosis.
The risk isn’t uniform across all types of endometriosis. Women with deep infiltrating endometriosis or ovarian endometriomas (cysts on the ovary caused by endometriosis) had nearly 19 times the risk of type I ovarian cancer compared to women without the condition. These are the more severe forms of endometriosis, and they create a chronic inflammatory environment on or near the ovaries that may promote cancer development over years or decades.
It’s worth noting that type I ovarian cancers tend to be slower-growing and diagnosed at earlier stages than the more aggressive high-grade serous type. Having endometriosis does not mean ovarian cancer is inevitable, but it’s a factor worth discussing with your doctor, especially if you have the more advanced forms.
Hormone Replacement Therapy
Menopausal hormone therapy has a modest but real association with ovarian cancer risk. The risk increases with prolonged use, particularly beyond 10 years. Estrogen-only therapy appears to carry a slightly higher risk than combined estrogen-progesterone therapy, especially with extended use. For women who need hormone therapy to manage menopause symptoms, the absolute increase in ovarian cancer risk remains small, but it’s one factor to weigh alongside the benefits.
Talcum Powder
The relationship between genital talc use and ovarian cancer has been debated for years. A study from the National Institute of Environmental Health Sciences found a persistent positive association between genital talc use and ovarian cancer, with the strongest links seen in women who used talc frequently, over long periods, and during their reproductive years. The study used advanced statistical methods to account for reporting bias, which had been a criticism of earlier research. While the association is real, the absolute increase in risk from talc use is smaller than the increases seen with genetic mutations or endometriosis.
Age, Obesity, and Other Factors
Most ovarian cancers are diagnosed after age 50, with risk increasing steadily through the 60s and 70s. Obesity raises risk modestly, likely through hormonal changes: excess fat tissue produces estrogen, which can stimulate cell growth in reproductive organs. A diet high in processed foods and low in vegetables has been loosely linked to higher risk in some population studies, though the effect is much weaker than genetic or reproductive factors.
Fertility treatments have been studied extensively, and current evidence suggests they do not significantly increase ovarian cancer risk on their own. The underlying infertility itself, which often means more years of uninterrupted ovulation, may be the actual contributor.
Why It’s Hard to Detect Early
One reason ovarian cancer is so dangerous is that it rarely produces obvious symptoms in its early stages. When symptoms do appear, they tend to be vague: bloating, pelvic discomfort, feeling full quickly, or urinary urgency. These overlap with dozens of common, benign conditions, which is why most cases aren’t caught until the cancer has spread beyond the ovary. There is currently no reliable screening test for ovarian cancer in the general population. Pap smears do not detect it, and routine ultrasounds and blood tests have not been shown to reduce deaths from the disease in average-risk women.
For women at high genetic risk, more intensive monitoring and preventive surgery (removing the fallopian tubes and ovaries) are options that substantially reduce risk. The timing of these decisions depends on the specific mutation, family history, and whether you’ve completed childbearing.