The average age at time of EIN diagnosis is approximately 52 years, compared to approximately 61 years for carcinoma. The timeframe and likelihood of EIN progression to cancer, however, is not constant amongst all women. Some cases of EIN are first detected as residual premalignant disease in women who already have carcinoma, whereas other EIN lesions disappear entirely and never lead to cancer. For this reason, treatment benefits and risks must be individualized for each patient under the guidance of an experienced physician.

Risk factors for development of EIN and the endometrioid type of endometrial carcinoma include exposure to estrogens without opposing progestins, obesity, diabetes, and rare hereditary conditions such as hereditary nonpolyposis colorectal cancer. Protective factors include use of combined oral contraceptive pills (low dose estrogen and progestin), and prior use of a contraceptive intrauterine device.

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.

Some therapies for other forms of cancer increase the lifetime risk of endometrial cancer, which is a baseline 2–3%. Tamoxifen, a drug used to treat estrogen-positive breast cancers, has been associated with endometrial cancer in approximately 0.1% of users, particularly older women, but the benefits for survival from tamoxifen generally outweigh the risk of endometrial cancer. A one to two-year course of tamoxifen approximately doubles the risk of endometrial cancer, and a five-year course of therapy quadruples that risk. Raloxifene, a similar drug, did not raise the risk of endometrial cancer. Previously having ovarian cancer is a risk factor for endometrial cancer, as is having had previous radiotherapy to the pelvis. Specifically, ovarian granulosa cell tumors and thecomas are tumors associated with endometrial cancer.

Low immune function has also been implicated in endometrial cancer. 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 endometrial cancer. The risk is not negated by regular exercise, though it is lowered.

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.

Smoking and the use of progestin are both protective against endometrial cancer. 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.

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.

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.

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.

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.

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).

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%.

Surface epithelial-stromal tumors are a class of ovarian neoplasms that may be benign or malignant. Neoplasms in this group are thought to be derived from the ovarian surface epithelium (modified peritoneum) or from endometrial or Fallopian tube (tubal) tissue. Tumors of this type are also called ovarian adenocarcinoma. This group of tumors accounts for 90% to 95% of all cases of ovarian cancer. Serum CA-125 is often elevated but is only 50% accurate so it is not a useful tumor marker to assess the progress of treatment.

In pathology, serous carcinoma is an epithelial malignancy (carcinoma) that arises from the lining of a cavity that produces a serum-like fluid (a serous cavity).

Serous lined cavities include the peritoneum, pericardium and pleural space and tunica vaginalis.

Mucinous cystadenoma is a benign cystic tumor lined by a mucinous epithelium. It is a type of cystic adenoma (cystadenoma).

Mucinous cystadenoma may arise in a number of locations; however, mucinous cystadenoma at different locations are not generally considered to be related to one another.

EIN lesions have been discovered by a combination of molecular, histologic, and clinical outcome studies beginning in the 1990s which provide a multifaceted characterization of this disease. They are a subset of a larger mixed group of lesions previously called "endometrial hyperplasia". The EIN diagnostic schema is intended to replace the previous "endometrial hyperplasia" classification as defined by the World Health Organization in 1994, which have been separated into benign (benign endometrial hyperplasia) and premalignant (EIN) classes in accordance with their behavior and clinical management.

EIN should not be confused with an unrelated entity, serous intraepithelial carcinoma ("serous EIC"), which is an early stage of a different tumor type known as papillary serous adenocarcinoma that also occurs in the same location within the uterus.

Papillary serous cystadenocarcinomas may exhibit psammoma bodies upon histopathology.

Mucinous cystadenocarcinoma is a type of tumor in the cystadenocarcinoma grouping.

It can occur in the breast as well as in the ovary. Tumors are normally multilocular with various smooth, thin walled cysts. Within the cysts is found a haemorrhagic or cellular debris.

Serous cystadenocarcinoma is a type of tumor in the cystadenocarcinoma grouping.

Most commonly the primary site of serous cystadenocarcinoma is the ovary. Rare occurrence in the pancreas has been reported, although this is not typical, with the majority of microcystic pancreatic masses representing alternate disease processes such as the more benign serous cystadenoma.

The differential diagnosis of serous carcinoma not otherwise specified includes:

- Ovarian serous carcinoma, a type of ovarian cancer.

- Uterine serous carcinoma, also known as "uterine papillary serous carcinoma", a type of uterine cancer.

- Fallopian tube serous carcinoma, a type of uterine tube cancer.

- Cervical serous carcinoma, a rare type of cervical cancer.

- Primary peritoneal serous carcinoma, a very rare cancer that arise from the peritoneum.

There has been the suggestion that the above diagnoses really represent one entity.

Ovarian serous cystadenoma, also (less precisely) known as serous cystadenoma, is the most common ovarian neoplasm, representing 20% of ovarian neoplasms, and is benign.Human Reproduction. University of Utah Medpath http://library.med.utah.edu/kw/human_reprod/seminars/seminar4B2.html.

It has a very superficial resemblance to the most common type of ovarian cancer (serous carcinoma of the ovary) under the microscope; however, (1) it is virtually impossible to mix-up with its malignant counterpart (serous carcinoma), and (2) does not share genetic traits of indeterminate serous tumours, also called "serous borderline tumours", that may transform into serous carcinoma.

Serous cystadenomas (of the ovary) are not related to serous cystadenomas of the pancreas, i.e. the presence of an ovarian "or" pancreatic one does "not" suggest an increased risk for the other one.

The overall incidence is 0.5 to 1 cases per 100,000 people per year. It is slightly more common in women than men (male:female ratio = 9:11). The median age at presentation is typically about 50 years with a range of 20–25 years.

Ovarian cystadenoma is a cystic benign tumor of the ovary. Two types are recognized: serous and mucinous.

Pseudomyxoma peritonei (PMP) is a clinical condition caused by cancerous cells (mucinous adenocarcinoma) that produce abundant mucin or gelatinous ascites. The tumors cause fibrosis of tissues and impede digestion or organ function, and if left untreated, the tumors and mucin they produce will fill the abdominal cavity. This will result in compression of organs and will destroy the function of colon, small intestine, stomach, or other organs. Prognosis with treatment in many cases is optimistic, but the disease is lethal if untreated, with death by cachexia, bowel obstruction, or other types of complications.

This disease is most commonly caused by an appendiceal primary cancer (cancer of the appendix); mucinous tumors of the ovary have also been implicated, although in most cases ovarian involvement is favored to be a metastasis from an appendiceal or other gastrointestinal source. Disease is typically classified as low- or high-grade (with signet ring cells). When disease presents with low-grade histologic features the cancer rarely spreads through the lymphatic system or through the bloodstream.

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).

Variants with edema can be associated with Meigs' syndrome. They may be a part of nevoid basal cell carcinoma syndrome (Gorlin syndrome).