Treatment may include the following:

- Surgery with or without radiation

- Radiotherapy

Fast neutron therapy has been used successfully to treat salivary gland tumors, and has shown to be significantly more effective than photons in studies treating unresectable salivary gland tumors.

- Chemotherapy

The relative risk of breast cancer based on a median follow-up of 8 years, in a case control study of US registered nurses, is 3.7.

The specific causes of DCIS are still unknown. The risk factors for developing this condition are similar to those for invasive breast cancer.

Some women are however more prone than others to developing DCIS. Women considered at higher risks are those who have a family history of breast cancer, those who have had their periods at an early age or who have had a late menopause. Also, women who have never had children or had them late in life are also more likely to get this condition.

Long-term use of estrogen-progestin hormone replacement therapy (HRT) for more than five years after menopause, genetic mutations (BRCA1 or BRCA2 genes), atypical hyperplasia, as well as radiation exposure or exposure to certain chemicals may also contribute in the development of the condition. Nonetheless, the risk of developing noninvasive cancer increases with age and it is higher in women older than 45 years.

Ductal carcinoma is a type of tumor that primarily presents in the ducts of a gland.

Types include:

- Mammary

- Ductal carcinoma in situ

- Invasive ductal carcinoma

- Pancreatic ductal carcinoma

Due to the diverse nature of salivary gland tumours, many different terms and classification systems have been used. Perhaps the most widely used currently is that system proposed by the World Health Organization in 2004, which classifies salivary neoplasms as primary or secondary, benign or malignant, and also by tissue of origin. This system defines five broad categories of salivary gland neoplasms:

Benign epithelial tumors

- Pleomorphic adenoma

- Warthin's tumor

- Myoepithelioma

- Basal cell adenoma

- Oncocytoma

- Canalicular adenoma

- Lymphadenoma

- "Sebaceous lymphadenoma"

- "Nonsebaceous lymphadenoma"

- Ductal papilloma

- "Inverted ductal papilloma"

- "Intraductal papilloma"

- "Sialadenoma papilliferum"

- Cystadenoma

- Malignant epithelial tumors

- Acinic cell carcinoma

- Mucoepidermoid carcinoma

- Adenoid cystic carcinoma

- Polymorphous low-grade adenocarcinoma

- Epithelial-myoepithelial carcinoma

- Clear cell carcinoma, not otherwise specified

- Basal cell adenocarcinoma

- Sebaceous carcinoma

- Sebaceous lymphadenocarcinoma

- Cystadenocarcinoma

- Low-grade cribriform cystadenocarcinoma

- Mucinous adenocarcinoma

- Oncocytic carcinoma

- Salivary duct carcinoma

- Salivary duct carcinoma, not otherwise specified

- Adenocarcinoma, not otherwise specified

- Myoepithelial carcinoma

- Carcinoma ex pleomorphic adenoma

- Mammary analogue secretory carcinoma

- Carcinosarcoma

- Metastasizing pleomorphic adenoma

- Squamous cell carcinoma

- Large cell carcinoma

- Lymphoepithelial carcinoma

- Sialoblastoma

- Soft tissue tumors

- Hemangioma

- Hematolymphoid tumors

- Hodgkin lymphoma

- Diffuse large B-cell lymphoma

- Extranodal marginal zone B cell lymphoma

- Secondary tumors (i.e. a tumor which has metastasized to the salivary gland from a distant location)

Others, not included in the WHO classification above, include:

- Intraosseous (central) salivary gland tumors

- Hybrid tumors (i.e. a tumor displaying combined forms of histologic tumor types)

- Hybrid carcinoma

- Others

- Others

- Keratocystoma

- Sialolipoma

Mammary analogue secretory carcinoma (MASC) (also termed MASC; the "SG" subscript indicates salivary gland)) is a salivary gland neoplasm that shares a genetic mutation with certain types of breast cancer. MASC was first described by Skálová et al. in 2010. The authors of this report found a chromosome translocation in certain salivary gland tumors that was identical to the (12;15)(p13;q25) fusion gene mutation found previously in secretory carcinoma, a subtype of invasive ductal carcinoma of the breast.

Uterine sarcoma are rare, out of all malignancies of the uterine body only about 4% will be uterine sarcomas. Generally, the cause of the lesion is not known, however patients with a history of pelvic radiation are at higher risk. Most tumors occur after menopause.

Women who take long-term tamoxifen are at higher risk.

80% of cases in the United States are diagnosed by mammography screening.

Most mammary tumors in rats are benign fibroadenomas, which are also the most common tumor in the rat. Less than 10 percent are adenocarcinomas. They occur in male and female rats. The tumors can be large and occur anywhere on the trunk. There is a good prognosis with surgery. Spayed rats have a decreased risk of developing mammary tumors.

Bartholin gland carcinoma is an uncommon type of malignancy in the Bartholin gland that accounts for 1% of all vulvar malignant neoplasms. It is most common in women in their mid-60s. The tumor can become large before a woman is aware of symptoms. One of the first symptoms can be dyspareunia. In other instances a woman may find a mass or ulcer in the vulva area. Many clincians assume that an enlarged Bartholin gland is malignant in postmenopausal woman until proven otherwise. The growth of the tumor can spread to nearby areas such as the ischiorectal fossa and inguinal lymph nodes. Approximately 50% of bartholin gland carcinomas originate from squamous cell carcinomas. Another uncommon characteristic of Bartholin gland malignancies is that the growth of a lesion originates from the three types of epithelial tissue present in the gland: mucinous, transitional, and squamous.

Atypical ductal hyperplasia, abbreviated ADH, is the term used for a benign lesion of the breast that indicates an increased risk of breast cancer.

The name of the entity is descriptive of the lesion; ADH is characterized by cellular proliferation (hyperplasia) within one or two breast ducts and (histomorphologic) architectural abnormalities, i.e. the cells are arranged in an abnormal or atypical way.

In the context of a core (needle) biopsy, ADH is considered an indication for a breast lumpectomy, also known as a surgical (excisional) biopsy, to exclude the presence of breast cancer.

Mammary tumors are the third most common neoplasia in cats, following lymphoid and skin cancers. The incidence of mammary tumors in cats is reduced by 91 percent in cats spayed prior to six months of age and by 86 percent in cats spayed prior to one year, according to one study. Siamese cats and Japanese breeds seem to have increased risk, and obesity also appears to be a factor in tumor development. Malignant tumors make up 80 to 96 percent of mammary tumors in cats, almost all adenocarcinomas. Male cats may also develop mammary adenocarcinoma, albeit rarely, and the clinical course is similar to female cats. As in dogs, tumor size is an important prognostic factor, although for tumors less than three centimeters the individual size is less predictive. According to one study, cats with tumors less than three cm had an average survival time of 21 months, and cats with tumors greater than three cm had an average survival of 12 months. About 10 percent of cat mammary tumors have estrogen receptors, so spaying at the time of surgery has little effect on recurrence or survival time. Metastasis tends to be to the lungs and lymph nodes, and rarely to bone. Diagnosis and treatment is similar to the dog. There is a better prognosis with bilateral radical surgery (removing the both mammary chains) than with more conservative surgery. Doxorubicin has shown some promise in treatment.

Bartholin gland can be differentiated by histology to determine whether the malignancy is due to squamous cell carcinoma, adenoid cystic carcinoma, or adenocarcinomas.

A perianal gland tumor is a type of tumor found near the anus in dogs that arises from specialized glandular tissue found in the perineum. Perianal glands do not exist in cats. It is also known as a hepatoid tumor because of the similarity in cell shape to hepatocytes (liver cells). It is most commonly seen in intact (not neutered) dogs and is the third most common tumor type in intact male dogs. There are two types of perianal gland tumors, perianal gland adenomas, which are benign, and perianal gland adenocarcinomas, which are malignant. Both have receptors for testosterone. Perianal gland adenomas are three times more likely to be found in intact male dogs than females, and perianal gland adenocarcinomas are ten times more common in male dogs than females. The most commonly affected breeds for adenomas are the Siberian Husky, Cocker Spaniel, Pekingese, and Samoyed; for adenocarcinomas the most commonly affected breeds are the Siberian Husky, Bulldog, and Alaskan Malamute.

Perianal gland tumors are located most commonly in the skin around the anus, but can also be found on the tail or groin. Adenomas are more common, making up 91 percent of perianal gland tumors in one study. Adenomas and adenocarcinomas look alike, both being round, pink and usually less than three centimeters in width. Adenocarcinomas are more likely to be multiple and invasive into the underlying tissue, and they can metastasize to the lymph nodes, liver, and lungs.

Both types should be removed and sent to a pathologist for identification. However, 95 percent of perianal gland adenomas will disappear after neutering the dog. Removing the tumor and neutering the dog at the same time will help prevent recurrence. Dogs with perianal gland adenocarcinomas should be treated with aggressive surgery and the radiation therapy and chemotherapy if necessary.

MASC is currently treated as a low-grade (i.e. Grade 1) carcinoma with an overall favorable prognosis. These cases are treated by complete surgical excision. However, the tumor does have the potential to recur locally and/or spread beyond surgically dissectible margins as well as metastasize to regional lymph nodes and distant tissues, particularly in tumors with histological features indicating a high cell growth rate potential. One study found lymph node metastasis in 5 of 34 MASC patients at initial surgery for the disease; these cases, when evidencing no further spread of disease, may be treated with radiation therapy. The treatment of cases with disease spreading beyond regional lymph nodes has been variable, ranging from simple excision to radical resections accompanied by adjuvant radiotherapy and/or chemotherapy, depending on the location of disease. Mean disease-free survival for MASC patients has been reported to be 92 months in one study.

The tyrosine kinase activity of NTRK3 as well as the ETV6-NTRK3 protein is inhibited by certain tyrosine kinase inhibitory drugs such as Entrectinib and LOXO-101; this offers a potential medical intervention method using these drugs to treat aggressive MASC disease. Indeed, one patient with extensive head and neck MASC disease obtained an 89% fall in tumor size when treated with entrectinib. This suppression lasted only 7 months due to the tumor's acquirement of a mutation in the "ETV6-NTRK3" gene. The newly mutated gene encoded an entrectinib-reisistant "ETV6-NTRK3" protein. Treatment of aggressive forms of MASC with NTRK3-inhibiting tyrosine kinase inhibiting drugs, perhaps with switching to another type of tyrosine kinase inhibitor drug if the tumor acquires resistance to the initial drug, is under study.STARTRK-2

Mammary myofibroblastoma, abbreviated MMFB, (aka "Wargotz tumor") is a rare, benign tumor of the breast.

These tumors are painless masses that manifest as breast lumps and may be found on a mammogram.

Carcinosarcomas are malignant tumors that consist of a mixture of carcinoma (or epithelial cancer) and sarcoma (or mesenchymal/connective tissue cancer). Carcinosarcomas are rare tumors, and can arise in diverse organs, such as the skin, salivary glands, lungs, the esophagus, pancreas, colon, uterus and ovaries.

Four main hypotheses have been proposed for the cellular origins of carcinosarcoma, based largely on the pathology of the disease. First, the collision tumor hypothesis, which proposes the collision of two independent tumors resulting in a single neoplasm, based on the observation that skin cancers and superficial malignant fibrous histiocytomas are commonly seen in patients with sun-damaged skin; second, the composition hypothesis, which suggests that the mesenchymal component represents a pseudosarcomatous reaction to the epithelial malignancy; third, the combination hypothesis, which suggests that both the epithelial and mesenchymal components of the tumor arise from a common pluripotential stem cell that undergoes divergent differentiation; and fourth, the conversion/divergence hypothesis, which argues that the sarcomatous component of the tumor represents a metaplastic sarcomatous transformation of the epithelial component. Despite the remaining uncertainty on the mechanisms that generate these tumors, recent immunohistochemical, ultrastructural, and molecular genetic studies suggest and favor the notion of monoclonality in carcinosarcoma. In addition, identical p53 and KRAS mutations have been identified in both epithelial and mesenchymal components of carcinosarcoma, findings that suggest an early alteration in the histogenesis of the tumor with late transformation or degeneration of the epithelial component into the sarcomatous component.

Pheochromocytoma is seen in between two and eight in 1,000,000, with approximately 1000 cases diagnosed in United States yearly. It mostly occurs in young or middle age adults, though it presents earlier in hereditary cases.

- About 10% of adrenal cases are bilateral (suggesting hereditary disease)

- About 10% of adrenal cases occur in children (also suggesting hereditary disease)

- About 15% are extra-adrenal (located in any orthosympathetic tissue): Of these 9% are in the abdomen, and 1% are located elsewhere. Some extra-adrenal pheochromocytomas are probably actually paragangliomas, but the distinction can only be drawn after surgical resection.

- About 11.1% of adrenal cases are malignant, but this rises to 30% for extra-adrenal cases

- About 15–20% are hereditary

- About 5% are caused by VHL disease

- About 3% recur after being resected

- About 14% of affected individuals do not have arterial hypertension (Campbell's Urology)

Atypical hyperplasia is a high-risk premalignant lesion of the breast. It is believed that atypical ductal hyperplasia (ADH) is a direct precursor for low-grade mammary ductal carcinoma, whereas atypical lobular hyperplasia (ALH) serves as a risk indicator.

In some population studies moderate alcohol consumption is associated with increase the breast cancer risk.

In contrast, research by the Danish National Institute for Public Health, comprising 13,074 women aged 20 to 91 years, found that moderate drinking had virtually no effect on breast cancer risk.

Studies that control for screening incidence show no association with moderate drinking and breast cancer, e.g.. Moderate drinkers tend to screen more which results in more diagnoses of breast cancer, including mis-diagnoses. A recent study of 23 years of breast cancer screening in the Netherlands concluded that 50% of diagnoses were over-diagnoses.

The main etiologic factor of adrenocortical cancer is unknown. Families with Li–Fraumeni syndrome have increased risk. The p53, retinoblastoma protein (RB) tumor suppressor genes located on chromosomes 17p, 13q respectively, may be changed. The genes h19, insulin-like growth factor II (IGF-II), p57 are important for fetal growth and development. They are located on chromosome 11p. Expression of the h19 gene is markedly reduced in both nonfunctioning and functioning adrenal cortical carcinomas, especially in tumors producing cortisol and aldosterone. There is also a loss of activity of the p57 gene product in virilizing adenomas and adrenal cortical carcinomas. In contrast, IGF-II gene expression has been shown to be high in adrenal cortical carcinomas. Finally, c-myc gene expression is relatively high in neoplasms, and it is often linked to poor prognosis.

Bilateral adrenocortical tumors are less common than unilateral. The majority of bilateral tumours can be distinguished according to size and aspect of the nodules: primary pigmented nodular adrenocortical disease which can be sporadic or part of Carney complex and primary bilateral macro nodular adrenal hyperplasia.

Adrenocortical carcinoma (ACC, adrenal cortical carcinoma, adrenal cortical cancer, adrenal cortex cancer, etc.) is an aggressive cancer originating in the cortex (steroid hormone-producing tissue) of the adrenal gland. Adrenocortical carcinoma is a rare tumor, with incidence of 1–2 per million population annually. Adrenocortical carcinoma has a bimodal distribution by age, with cases clustering in children under 5, and in adults 30–40 years old. Adrenocortical carcinoma is remarkable for the many hormonal syndromes which can occur in patients with steroid hormone-producing ("functional") tumors, including Cushing's syndrome, Conn syndrome, virilization, and feminization. Adrenocortical carcinoma has often invaded nearby tissues or metastasized to distant organs at the time of diagnosis, and the overall 5-year survival rate is only 20–35%. The widely used angiotensin-II-responsive steroid-producing cell line H295R was originally isolated from a tumor diagnosed as adrenocortical carcinoma.

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.

Atypical hyperplasia is a benign (noncancerous) cellular hyperplasia in which cells show some atypia. In this condition, cells look abnormal under a microscope and are increased in number.