Alcohol consumption does not appear to be related to ovarian cancer. 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 ovarian cancer. 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 ovarian cancer, but using talc more often does not create a greater risk. Use of talc elsewhere on the body is unrelated to ovarian cancer. Sitting regularly for prolonged periods is associated with higher mortality from epithelial ovarian cancer. The risk is not negated by regular exercise, though it is lowered.

Increased age (up to the 70s) is a risk factor for epithelial ovarian cancer 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 ovarian cancer; after smoking cessation, the risk eventually returns to normal.A diet high in animal fats may be associated with ovarian cancer, but the connection is unclear. Diet seems to play a very small role, if any, in ovarian cancer risk.

Higher levels of C-reactive protein are associated with a higher risk of developing ovarian cancer.

Industrialized nations, with the exception of Japan, have high rates of epithelial ovarian cancer, which may be due to diet in those countries. Caucasian are at a 30–40% higher risk for ovarian cancer when compared to Black and Hispanic people, likely due to socioeconomic factors; white women tend to have fewer children and different rates of gynecologic surgeries that affect risk for ovarian cancer.

Cohort studies have found a correlation between dairy consumption and ovarian cancer, but case-control studies do not show this correlation. There is mixed evidence regarding the effect of red meat and processed meat in ovarian cancer.

Tentative evidence suggests that talc, pesticides, and herbicides increase the risk of ovarian cancer. 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 ovarian cancer.

A prospective study of ovarian sex cord–stromal tumours in children and adolescents began enrolling participants in 2005.

Prognosis and treatment is the same as for the most common type of ovarian cancer, which is epithelial ovarian cancer.

The median survival of primary peritoneal carcinomas is usually shorter by 2–6 months time when compared with serous ovarian cancer. Studies show median survival varies between 11.3–17.8 months. One study reported 19-40 month median survival (95% CI) with a 5-year survival of 26.5%.

Elevated albumin levels have been associated with a more favorable prognosis.

10-year survival rates for mucinous tumors is excellent in the absence of invasion.

In the case of borderline tumors confined to the ovary and malignant tumors without invasion, the survival rates are 90% or greater. In invasive mucinous cystadenocarcinomas, the survival is approximately 30%

Krukenberg tumors can be seen in all age groups, with an average age of 45 years. In most countries, cancer that has metastasized to the ovary accounts for only about 1 to 2% of ovarian cancer; in the remainder, the ovary itself is the primary cancer site. However, in Japan they represent a much higher percentage of malignancies in the ovary (almost 20%) due to the increased prevalence of gastric cancer.

Krukenberg tumors account for about 15% of metastatic cancers that initially appear to have arisen in the ovary, and as such is less common than metastasis arising from ovarian epithelial and germ-cell tumors.

In people who have had nongynecologic malignancy, approximately 20% of adnexal masses are malignant, and 60% of these are Krukenberg tumors.

Fertility subsequent to treatment of surface epithelial-stromal tumors depends mainly on histology and initial

staging to separate it into early borderline (or more benign) versus advanced stages of borderline (or more malignant). Conservative management (without bilateral oophorectomy) of early stage borderline tumors have been estimated to result in chance of over 50% of spontaneous pregnancy with a low risk of lethal recurrence of the tumor (0.5%). On the other hand, in cases of conservative treatment in advanced stage borderline tumors, spontaneous pregnancy rates have been estimated to be 35% and the risk of lethal recurrence 2%.

It is associated with hormone replacement therapy (estrogen). The risk is higher in white women than other ethnicities, incidence, prevalence, age distribution, and sex ratio

Although the precise causes are not known, a link with certain variants of BRCA1/2 has been described. Furthermore, women with BRCA1/2 mutation have a 5% risk of developing primary peritoneal cancer even after prophylactic oophorectomy.

Primary peritoneal carcinoma shows similar rates of tumor suppressor gene dysfunction (p53, BRCA, WT1) as ovarian cancer and can also show an increased expression of HER-2/neu.

An association with vascular endothelial growth factor has been observed.

For surface epithelial-stromal tumors, the most common sites of metastasis are the pleural cavity (33%), the liver (26%), and the lungs (3%).

A retrospective study of 83 women with sex cord–stromal tumours (73 with granulosa cell tumour and 10 with Sertoli-Leydig cell tumour), all diagnosed between 1975 and 2003, reported that survival was higher with age under 50, smaller tumour size, and absence of residual disease. The study found no effect of chemotherapy. A retrospective study of 67 children and adolescents reported some benefit of cisplatin-based chemotherapy.

A number of genes are associated with HBOC. The most common of the known causes of HBOC are:

- BRCA mutations: Harmful mutations in the "BRCA1" and "BRCA2" genes can produce very high rates of breast and ovarian cancer, as well as increased rates of other cancers.

Other identified genes include:

- "TP53": Mutations cause Li-Fraumeni syndrome. It produces particularly high rates of breast cancer among younger women with mutated genes, and despite being rare, 4% of women with breast cancer under age 30 have a mutation in this gene.

- "PTEN": Mutations cause Cowden syndrome, which produces hamartomas (benign polyps) in the colon, skin growths, and other clinical signs, as well as an increased risk for many cancers.

- "CDH1": Mutations are associated with lobular breast cancer and gastric cancer.

- "STK11": Mutations produce Peutz–Jeghers syndrome. It is extremely rare, and creates a predisposition to breast cancer, intestinal cancer, and pancreatic cancer.

- "CHEK2": Approximately one out of 40 northern Europeans have a mutation in this gene, making it a common mutation. Considered a moderate-risk mutation, it may double or triple the carrier's lifetime risk of breast cancer, and also increase the risk of colon cancer and prostate cancer.

- "ATM": Mutations cause ataxia telangectasia; female carriers have approximately double the normal risk of developing breast cancer.

- "PALB2": Studies vary in their estimate of the risk from mutations in this gene. It may be moderate risk, or as high as "BRCA2".

Approximately 45% of HBOC cases involve unidentified genes, or multiple genes.

Benign tumors of the ovary include ovarian cysts, such as borderline tumor cysts.

Ovarian tumors, or ovarian neoplasms, are tumors arising from the ovary. They can be benign or malignant (ovarian cancer).

A Krukenberg tumor refers to a malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source. Krukenberg tumors are often (over 80%) found in both ovaries, consistent with its metastatic nature.

Papillary serous cystadenocarcinomas are the most common form of malignant ovarian cancer making up 26 percent of ovarian tumours in women aged over 20 in the United States.

As with most ovarian tumours, due to the lack of early signs of disease these tumours can be large when discovered and have often metastasized, often by spreading along the peritoneum.

These tumours do better than other types of epithelial tumours of the ovary.

Transitional cell carcinoma of the ovary, abbreviated TCC of the ovary, is a rare type of ovarian cancer that has an appearance similar to urothelial carcinoma (also known as transitional cell carcinoma).

Serous tumours are part of the surface epithelial-stromal tumour group of ovarian neoplasms, which derive from Mullerian epithelium.

They are common neoplasms with a strong tendency to bilaterality, and they account for 50% of all ovarian tumours.

Sixty percent are benign (cystadenoma), 10% are borderline and 30% are malignant (cystadenocarcinoma).

The 1997 International Germ Cell Consensus Classification is a tool for estimating the risk of relapse after treatment of malignant germ cell tumor.

A small study of ovarian tumors in girls reports a correlation between cystic and benign tumors and, conversely, solid and malignant tumors. Because the cystic extent of a tumor can be estimated by ultrasound, MRI, or CT scan before surgery, this permits selection of the most appropriate surgical plan to minimize risk of spillage of a malignant tumor.

Access to appropriate treatment has a large effect on outcome. A 1993 study of outcomes in Scotland found that for 454 men with non-seminomatous (non-germinomatous) germ cell tumors diagnosed between 1975 and 1989, 5-year survival increased over time and with earlier diagnosis. Adjusting for these and other factors, survival was 60% higher for men treated in a cancer unit that treated the majority of these men, even though the unit treated more men with the worst prognosis.

Choriocarcinoma of the testicles has the worst prognosis of all germ cell cancers

Papillary serous cystadenocarcinomas may exhibit psammoma bodies upon histopathology.

The exact cause of Sertoli-Leydig Cell Tumor is not known.

Research studies seem to indicate that certain genetic mutations (in the DICER1 gene) may play a role in many cases.

Clear-cell adenocarcinoma is a type of adenocarcinoma that shows clear cells.

Types include:

- Clear-cell adenocarcinoma of the vagina

- Clear-cell ovarian carcinoma

- Uterine clear-cell carcinoma

- Clear-cell adenocarcinoma of the lung (which is a type of Clear-cell carcinoma of the lung)

See also:

- Clear-cell squamous cell carcinoma of the lung

Women with benign germ cell tumors such as mature teratomas (dermoid cysts) are cured by ovarian cystectomy or oophorectomy. In general, all patients with malignant germ cell tumors will have the same staging surgery that is done for epithelial ovarian cancer. If the patient is in her reproductive years, an alternative is unilateral salpingoophorectomy, while the uterus, the ovary, and the fallopian tube on the opposite side can be left behind. This isn't an option when the cancer is in both ovaries. If the patient has finished having children, the surgery involves complete staging including salpingoophorectomy on both sides as well as hysterectomy.

Most patients with germ cell cancer will need to be treated with combination chemotherapy for at least 3 cycles. The chemotherapy regimen most commonly used in germ cell tumors is called PEB (or BEP), and consists of bleomycin, etoposide, a platinum-based antineoplastic (cisplatin).

Mucinous tumors are part of the surface epithelial-stromal tumor group of ovarian neoplasms, and account for approximately 36% of all ovarian tumors.

Approximately 75% are benign, 10% are borderline and 15% are malignant.

Rarely, the tumor is seen bilaterally; approximately 5% of primary mucinous tumors are bilateral.

"Benign" mucinous tumors are typically multilocular (have several lobes), and the cysts have a smooth lining of epithelium that resembles endocervical epithelial cells with small numbers of gastrointestinal-type epithelial cells.

"Borderline" and "malignant" mucinous tumors often have papillae and solid areas.

There may also be hemorrhage and necrosis.

It is well documented that malignancy may be only focally present in mucinous neoplasms of the ovary, so thorough sampling is imperative.

The major distinguishing features of mucinous tumors are that the tumors are filled with a mucus-like material, which gives them their name; this mucus is produced by mucus-secreting goblet cells very similar to the cells lining normal intestine.

These tumors may become very large, some have been weighed as large as 25 kilograms.

Cystadenocarcinomas (malignant tumors) contain a more solid growth pattern with the hallmarks of malignancy: cellular atypia and stratification, loss of the normal architecture of the tissue, and necrosis. The appearance can look similar to colonic cancer.

Clear stromal invasion is used to differentiate borderline tumors from malignant tumors.

Pseudomyxoma peritonei may present as a result of an ovarian mucinous tumor, however this is a rare cause of this condition, which is a rare condition. A more common cause of pseudomyxoma peritonei is a mucin-producing tumor of the appendix.

Since mucinous tumors arising from the ovary usually only involve one ovary, the presence of involvement in both ovaries with a mucinous tumor suggests that the tumor may have arisen in another location, and further study is warranted.

The risk of mucinous tumors is significantly associated with smoking: relative risk for current smokers 2.22 (2.22 times the risk for non-smokers) and 2.02 for past smokers. Risk is also associated with smoking duration: relative risk per 20 years was 1.44. See article by Tworoger SS in Cancer March 1, 2008 using data from the Nurses Health Study.