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.

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.

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.

Tubal cancer is thought to be a relatively rare primary cancer among women accounting for 1 to 2 percent of all gynecologic cancers, In the USA tubal cancer had an incidence of 0.41 per 100,000 women from 1998 to 2003. Demographic distribution is similar to ovarian cancer, and the highest incidence was found in white, non-Hispanic women and women aged 60–79. However, recent evidence suggests tubal cancer to be much more frequent .

Evidence is accumulating that individuals with mutations of BRCA1 and BRCA2 are at higher risks for the development of PFTC.

Prognosis depends to a large degree on the stage of the condition. In 1991 it was reported that about half of the patients with advanced stage disease survived 5 years with a surgical approach followed by cisplatinum-based chemotherapy.

There are two primary types of vaginal cancer: squamous-cell carcinoma and adenocarcinoma.

- Vaginal squamous-cell carcinoma arises from the squamous cells (epithelium) that line the vagina. This is the most common type of vaginal cancer. It is found most often in women aged 60 or older.

- Vaginal adenocarcinoma arises from the glandular (secretory) cells in the lining of the vagina that produce some vaginal fluids. Adenocarcinoma is more likely to spread to the lungs and lymph nodes.

- Clear cell adenocarcinoma occurs in a small percentage of women (termed "DES-Daughters") born between 1938 and 1973 (later outside the United States) that were exposed to the drug diethylstilbestrol (DES) in utero. DES was prescribed to 5 to 10 million mothers period to prevent possible miscarriages and premature births. Typically, women develop DES-related adenocarcinoma before age 30, but increasing evidence suggests possible effects or cancers (including other forms of vaginal glandular tumors) at a later age. DES-exposure in women is also linked to various infertility and pregnancy complications. Daughters exposed to DES in utero may also have an increased risk of moderate/severe cervical squamous cell dysplasia and an increased risk of breast cancer. Approximately one in 1,000 (0.1%) DES Daughters will be diagnosed with clear cell adenocarcinoma. The risk is virtually non-existent among premenopausal women not exposed to DES.

- Vaginal germ cell tumors (primarily teratoma and endodermal sinus tumor) are rare. They are found most often in infants and children.

- Sarcoma botryoides, a rhabdomyosarcoma also is found most often in infants and children.

- Vaginal melanoma, a melanoma that appears in the vagina.

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.

Cancer of the vagina is rare and is only 2% of all gynecological cancers less than 0.5% of all cancers in women Estimated new cases in the United States in 2017 are 4,810. Deaths from vaginal during the same time were 1,240. It is more common in older women.

In the UK, 254 cases of Vaginal cancer were identified in 2014. Deaths from vaginal cancer in this period were 110. Out of those with vaginal cancer, 53% are related to HPV infection.

In a recent study, about 60% of USCs were found to overexpress the protein HER2/neu—the same one that is overexpressed in some breast cancers. The monoclonal antibody trastuzumab (Herceptin) is currently being tested as a therapy for this subset of USCs.

The antibody trastuzumab (Herceptin), which is used to treat breast cancers that overexpress the HER2/neu protein, has been tried with some success in a phase II trial in women with UPSCs that overexpress HER2/neu.

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.

Uterine serous carcinoma (USC), also known as uterine papillary serous carcinoma (UPSC) and uterine serous adenocarcinoma, is an uncommon form of endometrial cancer that typically arises in postmenopausal women.

It is typically diagnosed on endometrial biopsy, prompted by post-menopausal bleeding.

Unlike the more common low-grade "endometrioid endometrial adenocarcinoma", USC does not develop from endometrial hyperplasia and is not hormone-sensitive. It arises in the setting of endometrial atrophy and is classified as a type II endometrial cancer.

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.

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.

Endometrial polyps usually occur in women in their 40s and 50s. Endometrial polyps occur in up to 10% of women. It is estimated that they are present in 25% of women with abnormal vaginal bleeding.

Endometrial polyps are usually benign although some may be precancerous or cancerous. About 0.5% of endometrial polyps contain adenocarcinoma cells. Polyps can increase the risk of miscarriage in women undergoing IVF treatment. If they develop near the fallopian tubes, they may lead to difficulty in becoming pregnant. Although treatments such as hysteroscopy usually cure the polyp concerned, recurrence of endometrial polyps is frequent. Untreated, small polyps may regress on their own.

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.

A malignant mixed Müllerian tumor, also known as malignant mixed mesodermal tumor, MMMT and carcinosarcoma, is a malignant neoplasm found in the uterus, the ovaries, the fallopian tubes and other parts of the body that contains both carcinomatous (epithelial tissue) and sarcomatous (connective tissue) components. It is divided into two types, homologous (in which the sarcomatous component is made of tissues found in the uterus such as endometrial, fibrous and/or smooth muscle tissues) and a heterologous type (made up of tissues not found in the uterus, such as cartilage, skeletal muscle and/or bone). MMMT account for between two and five percent of all tumors derived from the body of the uterus, and are found predominantly in postmenopausal women with an average age of 66 years. Risk factors are similar to those of adenocarcinomas and include obesity, exogenous estrogen therapies, and nulliparity. Less well-understood but potential risk factors include tamoxifen therapy and pelvic irradiation.

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%.

Villoglandular adenocarcinoma of the cervix, also villoglandular papillary adenocarcinoma, papillary villoglandular adenocarcinoma and well-differentiated villoglandular adenocarcinoma, abbreviated VGA, is a rare type of cervical cancer that, in relation to other cervical cancers, is typically found in younger women and has a better prognosis.

A similar lesion, "villoglandular adenocarcinoma of the endometrium", may arise from the inner lining of the uterus, the endometrium.

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

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.

There is debate over the naming of MMMT; the term carcinosarcoma was formerly used to describe lesions with homologous tumors, and "malignant mixed Müllerian tumor" or "mixed mesodermal tumor" was used to describe heterologous tumors. While "carcinosarcoma" now considered standard, "malignant mixed Müllerian tumor" has a lengthy history within gynecological literature and is expected to continue to be used. The naming issue to a certain extent reflects histological characteristics and development of the tumors, in which the different types of tissues are believed to either develop separately and join into a single mass (the "collision" theory), that an adenocarcinoma stimulates the stroma to create a tumor (the "composition" theory), or that the tumor is the result of a stem cell that differentiates into different cell types (the "combination" theory). "Collision" tumors are normally easily recognized and not considered true MMMTs; the "combination" theory is most widely held, and is due to evidence that the tumors develop from a single line of cells, developing in a fashion similar to the fundus of the uterus from the Müllerian duct - first from a stem cell into a population of cells, that then differentiates into epithelial and stromal components.

There is evidence that some tumors are better explained by the composition theory, due to the aggressive nature of the epithelial cells involved which tend to metastasize much more readily than the sarcomal component. The behavior of MMMT overall is more related to the type and grade of the epithelium than the sarcoma, which suggests the sarcomal portion is an atypical "bystander" than primary driver of the tumor. Despite this, when purely endometrial tumors are compared to MMMTs, the MMMT tumor tends to have a worse prognosis.

The treatment is dependent on the stage. As the prognosis of this tumour is usually good, fertility sparing approaches (conization, cervicectomy) may be viable treatment options.