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

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.

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.

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.

Spermatocytic seminomas are not considered a subtype of seminoma and unlike other germ cell tumours do not arise from intratubular germ cell neoplasia.

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

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.

Malignant germ cell tumors of the mediastinum are uncommon, representing only 3 to 10% of tumors originating in the mediastinum. They are much less common than germ cell tumors arising in the testes, and account for only 1 to 5% of all germ cell neoplasms.

Syndromes associated with mediastinal germ cell tumors include Hematologic Neoplasia and Klinefelter's syndrome.

Some investigators suggest that this distribution arises as a consequence of abnormal migration of germ cells during embryogenesis. Others hypothesize a widespread distribution of germ cells to multiple sites during normal embryogenesis, with these cells conveying genetic information or providing regulatory functions at somatic sites.

Extragonadal germ cell tumors were thought initially to be isolated metastases from an undetected primary tumor in a gonad, but it is now known that many germ cell tumors are congenital and originate outside the gonads. The most notable of these is sacrococcygeal teratoma, the single most common tumor diagnosed in babies at birth.

Of all anterior mediastinal tumors, 15–20% are germ cell tumors of which approximately 50% are benign teratomas.

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.

Germ cell neoplasia in situ, abbreviated GCNIS, represents the precursor lesion for many types of testicular germ cell tumors. As the name suggests, it represents a neoplastic process of germ cells that is confined to the spermatogonial niche.

The term GCNIS was introduced with the 2016 edition of the WHO classification of urological tumours. It replaces the previous term intratubular germ cell neoplasia, abbreviated ITGCN or IGCN and also known as testicular intratubular germ cell neoplasia and intratubular germ cell neoplasia of the testis. GCNIS more accurate describes the lesion as it arises between the basement membrane and Sertoli cells (the cells that 'nurse' the developing germ cell). The common, unspecified variant of the entity was once considered to be a carcinoma in situ although the term "carcinoma "in situ"" is now largely historical as it is not an accurate description of the process.

While cancer is generally considered a disease of old age, children can also develop cancer. In contrast to adults, carcinomas are exceptionally rare in children..

The two biggest risk factors for ovarian carcinoma are age and family history.

The World Health Organisation classification of testicular tumours subdivides ITGCN into (1) a more common, unspecified type (ITGCNU), and (2) other specific subtypes. The most common specific subtypes are intratubular embryonal carcinoma and intratubular seminoma.

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%

Sertoli–Leydig cell tumour is a group of tumours composed of variable proportions of Sertoli cells, Leydig cells, and in the case of intermediate and poorly differentiated neoplasms, primitive gonadal stroma and sometimes heterologous elements.

Sertoli–Leydig cell tumour is a member of the sex cord-stromal tumour group of ovarian and testicular cancers. The tumour is rare, comprising less than 1% of testicular tumours. While the tumour can occur at any age, it occurs most often in young adults. Recent studies have shown that many cases of Sertoli–Leydig cell tumor of the ovary are caused by germline mutations in the "DICER1" gene. These hereditary cases tend to be younger, often have a multinodular thyroid goiter and there may be a personal or family history of other rare tumors such as pleuropulmonary blastoma, Wilms tumor and cervical rhabdomyosarcoma.

Closely related terms include arrhenoblastoma and androblastoma. Both terms are classified under Sertoli–Leydig cell tumour in MeSH.

Since gestational choriocarcinoma (which arises from a hydatidiform mole) contains paternal DNA (and thus paternal antigens), it is exquisitely sensitive to chemotherapy. The cure rate, even for metastatic gestational choriocarcinoma, is around 90–95%.

At present, treatment with single-agent methotrexate is recommended for low-risk disease, while intense combination regimens including EMACO (etoposide, methotrexate, actinomycin D, cyclosphosphamide and vincristine (Oncovin) are recommended for intermediate or high-risk disease.

Hysterectomy (surgical removal of the uterus) can also be offered to patients > 40 years of age or those for whom sterilisation is not an obstacle. It may be required for those with severe infection and uncontrolled bleeding.

Choriocarcinoma arising in the testicle is rare, malignant and highly resistant to chemotherapy. The same is true of choriocarcinoma arising in the ovary. Testicular choriocarcinoma has the worst prognosis of all germ-cell cancers.

Leydig cell tumour, also Leydig cell tumor (US spelling), (testicular) interstitial cell tumour and (testicular) interstitial cell tumor (US spelling), is a member of the sex cord-stromal tumour group of ovarian and testicular cancers. It arises from Leydig cells. While the tumour can occur at any age, it occurs most often in young adults.

A Sertoli-Leydig cell tumour is a combination of a Leydig cell tumour and a Sertoli cell tumour from Sertoli cells.

Dysgerminomas, like other seminomatous germ cell tumors, are very sensitive to both chemotherapy and radiotherapy. For this reason, with treatment patients' chances of long-term survival, even cure, is excellent.

A dysgerminoma is a type of germ cell tumor; it usually is malignant and usually occurs in the ovary.

A tumor of the identical histology but not occurring in the ovary may be described by an alternate name: seminoma in the testis or germinoma in the central nervous system or other parts of the body.

Dysgerminoma accounts for less than 1% of ovarian tumors overall. Dysgerminoma usually occurs in adolescence and early adult life; about 5% occur in pre-pubertal children. Dysgerminoma is extremely rare after age 50. Dysgerminoma occurs in both ovaries in 10% of patients and, in a further 10%, there is microscopic tumor in the other ovary.

Abnormal gonads (due to gonadal dysgenesis and androgen insensitivity syndrome) have a high risk of developing a dysgerminoma. Most dysgerminomas are associated with elevated serum lactic dehydrogenase (LDH), which is sometimes used as a tumor marker.

Embryonal carcinoma is a relatively uncommon type of germ cell tumour that occurs in the ovaries and testes.

Seminoma (also known as "pure seminoma" or "classical seminoma") is a germ cell tumor of the testicle or, more rarely, the mediastinum or other extra-gonadal locations. It is a malignant neoplasm and is one of the most treatable and curable cancers, with a survival rate above 95% if discovered in early stages.

Testicular seminoma originates in the germinal epithelium of the seminiferous tubules. About half of germ cell tumors of the testicles are seminomas. Treatment usually requires removal of one testicle. However, fertility usually isn't affected. All other sexual functions will remain intact.

Spermatocytic seminoma is not considered a subtype of seminoma and, unlike seminoma and most other germ cell tumours, it does not arise from "intratubular germ cell neoplasia". It has not been described as arising in locations outside the testis, and does not occur in association with other germ cell tumours.

The new WHO classification, due to be published in 2016, will rename the condition spermatocytic tumour to avoid confusion with classical seminoma as the biology and treatment are different.

Spermatocytic seminoma is a neoplasm of the testis ("i.e." a tumour of the testis), and classified as a germ cell tumour.

The name of the tumour comes from the similarity (under the microscope) between the small cells of the tumour and secondary spermatocytes.

Choriocarcinoma of the placenta during pregnancy is preceded by:

- hydatidiform mole (50% of cases)

- spontaneous abortion (20% of cases)

- ectopic pregnancy (2% of cases)

- normal term pregnancy (20–30% of cases)

- hyperemesis gravidarum

Rarely, choriocarcinoma occurs in primary locations other than the placenta; very rarely, it occurs in testicles. Although trophoblastic components are common components of mixed germ cell tumors, pure choriocarcinoma of the adult testis is rare. Pure choriocarcinoma of the testis represents the most aggressive pathologic variant of germ cell tumors in adults, characteristically with early hematogenous and lymphatic metastatic spread. Because of early spread and inherent resistance to anticancer drugs, patients have poor prognosis. Elements of choriocarcinoma in a mixed testicular tumor have no prognostic importance.

Choriocarcinomas can also occur in the ovaries.