The most successful treatment for angiosarcoma is amputation of the affected limb if possible. Chemotherapy may be administered if there is metastatic disease. If there is no evidence of metastasis beyond the lymphedematous limb, adjuvant chemotherapy may be given anyway due to the possibility of micrometastatic disease. Evidence supporting the effectiveness of chemotherapy is, in many cases, unclear due to a wide variety of prognostic factors and small sample size. However, there is some evidence to suggest that drugs such as paclitaxel, doxorubicin, ifosfamide, and gemcitabine exhibit antitumor activity.

Women may reduce their risk of breast cancer by maintaining a healthy weight, drinking less alcohol, being physically active and breastfeeding their children. These modifications might prevent 38% of breast cancers in the US, 42% in the UK, 28% in Brazil and 20% in China. The benefits with moderate exercise such as brisk walking are seen at all age groups including postmenopausal women. High levels of physical activity reduce the risk of breast cancer by about 14%. Strategies that encourage regular physical activity and reduce obesity could also have other benefits, such as reduced risks of cardiovascular disease and diabetes.

High intake of citrus fruit has been associated with a 10% reduction in the risk of breast cancer.

Marine omega-3 polyunsaturated fatty acids appear to reduce the risk. High consumption of soy-based foods may reduce risk.

Removal of both breasts before any cancer has been diagnosed or any suspicious lump or other lesion has appeared (a procedure known as prophylactic bilateral mastectomy) may be considered in people with BRCA1 and BRCA2 mutations, which are associated with a substantially heightened risk for an eventual diagnosis of breast cancer. Evidence is not strong enough to support this procedure in anyone but those at the highest risk. BRCA testing is recommended in those with a high family risk after genetic counseling. It is not recommended routinely. This is because there are many forms of changes in "BRCA" genes, ranging from harmless polymorphisms to obviously dangerous frameshift mutations. The effect of most of the identifiable changes in the genes is uncertain. Testing in an average-risk person is particularly likely to return one of these indeterminate, useless results. It is unclear if removing the second breast in those who have breast cancer in one is beneficial.

Cancer affects approximately 1 in 1,000 pregnant women. The most common cancers found during pregnancy are the same as the most common cancers found in non-pregnant women during childbearing ages: breast cancer, cervical cancer, leukemia, lymphoma, melanoma, ovarian cancer and colorectal cancer.

Diagnosing a new cancer in a pregnant woman is difficult, in part because any symptoms are commonly assumed to be a normal discomfort associated with pregnancy. As a result, cancer is typically discovered at a somewhat later stage than average. Some imaging procedures, such as MRIs (magnetic resonance imaging), CT scans, ultrasounds and mammograms with fetal shielding are considered safe during pregnancy; some others, such as PET scans, are not.

Treatment is generally the same as for non-pregnant women. However, radiation and radioactive drugs are normally avoided during pregnancy, especially if the fetal dose might exceed 100 cGy. In some cases, some or all treatments are postponed until after birth if the cancer is diagnosed late in the pregnancy. Early deliveries are often used to advance the start of treatment. Surgery is generally safe, but pelvic surgeries during the first trimester may cause miscarriage. Some treatments, especially certain chemotherapy drugs given during the first trimester, increase the risk of birth defects and pregnancy loss (spontaneous abortions and stillbirths).

Elective abortions are not required and, for the most common forms and stages of cancer, do not improve the mother's survival. In a few instances, such as advanced uterine cancer, the pregnancy cannot be continued and in others, the patient may end the pregnancy so that she can begin aggressive chemotherapy.

Some treatments can interfere with the mother's ability to give birth vaginally or to breastfeed. Cervical cancer may require birth by Caesarean section. Radiation to the breast reduces the ability of that breast to produce milk and increases the risk of mastitis. Also, when chemotherapy is given after birth, many of the drugs appear in breast milk, which could harm the baby.

Most people with cancer of unknown primary origin have widely disseminated and incurable disease, although a few can be cured through treatment. With treatment, typical survival with CUP ranges from 6 to 16 months. Survival rates are lower in cases with visceral metastatic disease, ranging from 6 to 9 months. Survival rates are higher when the cancer is more limited to lymph nodes, pleura, or peritoneal metastasis, which ranges from 14 to 16 months. Long-term prognosis is somewhat better if a particular source of cancer is strongly suggested by clinical evidence.

Some patients with metastatic breast cancer opt to try alternative therapies such as vitamin therapy, homeopathic treatments, a macrobiotic diet, chiropractic or acupuncture. There is no evidence that any of these therapies are effective; they may be harmful, either because patients pass up effective conventional therapies such as chemotherapy or anti-estrogen therapy in favor of alternative treatments, or because the treatments themselves are harmful (as in the case of apricot-pit therapy—which exposes the patient to cyanide—or in chiropractic, which can be dangerous to patients with cancer metastatic to the spinal bones or spinal cord. A macrobiotic diet is neither effective nor safe as it could hypothetically induce weight loss due to severe dietary restriction. There is limited evidence that acupuncture might relive pain in cancer patients, but data so far is insufficient to recommend its use outside of clinical trials.

There is free peer support and an online platform to interact with others going through various therapies, including Abraxane.

Medications can be used to prevent cancer in a few circumstances. In the general population, NSAIDs reduce the risk of colorectal cancer; however, due to cardiovascular and gastrointestinal side effects, they cause overall harm when used for prevention. Aspirin has been found to reduce the risk of death from cancer by about 7%. COX-2 inhibitors may decrease the rate of polyp formation in people with familial adenomatous polyposis; however, it is associated with the same adverse effects as NSAIDs. Daily use of tamoxifen or raloxifene reduce the risk of breast cancer in high-risk women. The benefit versus harm for 5-alpha-reductase inhibitor such as finasteride is not clear.

Vitamin supplementation does not appear to be effective at preventing cancer. While low blood levels of vitamin D are correlated with increased cancer risk, whether this relationship is causal and vitamin D supplementation is protective is not determined. One 2014 review found that supplements had no significant effect on cancer risk. Another 2014 review concluded that vitamin D may decrease the risk of death from cancer (one fewer death in 150 people treated over 5 years), but concerns with the quality of the data were noted.

Beta-carotene supplementation increases lung cancer rates in those who are high risk. Folic acid supplementation is not effective in preventing colon cancer and may increase colon polyps. It is unclear if selenium supplementation has an effect.

Scheduling of drug treatments and combination treatment can have substantial impact on treatment efficacy.

CUP sometimes runs in families. It has been associated with familial lung, kidney, and colorectal cancers, which suggests that these sites may often be the origin of unidentifiable CUP cancers.

Children with cancer are at risk for developing various cognitive or learning problems. These difficulties may be related to brain injury stemming from the cancer itself, such as a brain tumor or central nervous system metastasis or from side effects of cancer treatments such as chemotherapy and radiation therapy. Studies have shown that chemo and radiation therapies may damage brain white matter and disrupt brain activity.

Vitamin A is associated with a lower risk as are vitamin B12, vitamin C, vitamin E, and beta-Carotene.

Factors that contribute to the development of hypopharyngeal cancer include:

- Smoking

- Chewing tobacco

- Heavy alcohol use

- Poor diet

Smoking, like lung cancer, can cause hypopharyngeal cancer because it contains carcinogens that alter the DNA or RNA in a dividing cell. These alterations may change a normal DNA sequence to an oncogene, a gene that causes cancer after exposure to a carcinogen.

Squamous cells, a type of cell that lines hollow organs like the throat, mouth, lungs, and outer layer of skin, are particularly vulnerable when exposed to cigarette smoke.

Chewing tobacco can have the same effects as smoking and is also linked to hypopharyngeal cancer. The chewing tobacco is placed into the mouth, leaving it exposed to enzymes, like amylase, which partly digests the carcinogenic material. Saliva is swallowed, along with the cancer-promoting material, which passes through the hypopharynx on its way to the esophagus.

Heavy alcohol use is linked to Hypopharyngeal Cancer as well. Alcohol damages the lining of the hypopharynx, increasing the amount of chemicals that are allowed to seep into the underlying membranes. Heavy alcohol use is also associated with nutritional deficiencies.

A disease called Plummer-Vinson syndrome, a genetic disorder that causes a long-term iron deficiency, may also lead to Hypopharyngeal Cancer. Other factors like a deficiency in certain vitamins also appear to contribute to this type of cancer.

Familial and genetic factors are identified in 5-15% of childhood cancer cases. In <5-10% of cases, there are known environmental exposures and exogenous factors, such as prenatal exposure to tobacco, X-rays, or certain medications. For the remaining 75-90% of cases, however, the individual causes remain unknown. In most cases, as in carcinogenesis in general, the cancers are assumed to involve multiple risk factors and variables.

Aspects that make the risk factors of childhood cancer different from those seen in adult cancers include:

- Different, and sometimes unique, exposures to environmental hazards. Children must often rely on adults to protect them from toxic environmental agents.

- Immature physiological systems to clear or metabolize environmental substances

- The growth and development of children in phases known as "developmental windows" result in certain "critical windows of vulnerability".

Also, a longer life expectancy in children avails for a longer time to manifest cancer processes with long latency periods, increasing the risk of developing some cancer types later in life.

There are preventable causes of childhood malignancy, such as delivery overuse and misuse of ionizing radiation through computed tomography scans when the test is not indicated or when adult protocols are used.

Treatment of hypopharyngeal cancer depends on the prognosis (chance of recovery), age, stage, and general health of the patient. Because hypopharyngeal cancer is often advanced at the time of diagnosis, treatment also depends on the overall goal. The goal may simply be to keep the patient talking, eating, and breathing normally.

Treatment usually begins with surgery and then a course of radiation for cancer that has progressed past Stage I. For cancer that is advanced, which is typical of hypopharyngeal cancer, neoadjuvant chemotherapy may be used. This is performed by administering chemotherapy before surgery. Neoadjuvant chemotherapy in conjunction with radiation and surgery has yielded the best results in patients with Stage III and Stage IV cancers.

While an active area of research, no immunotherapy has been shown to be effective as of 2013. However, trials of the antibody and VEGF inhibitor bevacizumab, which can slow the growth of new blood vessels in the cancer, have shown promising results, especially in combination with pazopanib, which also slows the process of blood vessel growth. Bevacizumab has been particularly effective in preliminary studies on stage-III and -IV cancer and has been cited as having at least a 15% response rate. It is being investigated particularly in mucinous ovarian cancers.

There are several experimental therapies for endometrial cancer under research, including immunologic, hormonal, and chemotherapeutic treatments. Trastuzumab (Herceptin), an antibody against the Her2 protein, has been used in cancers known to be positive for the Her2/neu oncogene, but research is still underway. Immunologic therapies are also under investigation, particularly in uterine papillary serous carcinoma.

Cancers can be analyzed using genetic techniques (including DNA sequencing and immunohistochemistry) to determine if certain therapies specific to mutated genes can be used to treat it. PARP inhibitors are used to treat endometrial cancer with PTEN mutations, specifically, mutations that lower the expression of PTEN. The PARP inhibitor shown to be active against endometrial cancer is olaparib. Research is ongoing in this area as of the 2010s.

Research is ongoing on the use of metformin, a diabetes medication, in obese women with endometrial cancer before surgery. Early research has shown it to be effective in slowing the rate of cancer cell proliferation. Preliminary research has shown that preoperative metformin administration can reduce expression of tumor markers. Long-term use of metformin has not been shown to have a preventative effect against developing cancer, but may improve overall survival.

Temsirolimus, an mTOR inhibitor, is under investigation as a potential treatment. Research shows that mTOR inhibitors may be particularly effective for cancers with mutations in PTEN. Ridaforolimus (deforolimus) is also being researched as a treatment for people who have previously had chemotherapy. Preliminary research has been promising, and a stage II trial for ridaforolimus was completed by 2013. There has also been research on combined ridaforolimus/progestin treatments for recurrent endometrial cancer. Bevacizumab and tyrosine kinase inhibitors, which inhibit angiogenesis, are being researched as potential treatments for endometrial cancers with high levels of vascular endothelial growth factor. Ixabepilone is being researched as a possible chemotherapy for advanced or recurrent endometrial cancer. Treatments for rare high-grade undifferentiated endometrial sarcoma are being researched, as there is no established standard of care yet for this disease. Chemotherapies being researched include doxorubicin and ifosfamide.

There is also research in progress on more genes and biomarkers that may be linked to endometrial cancer. The protective effect of combined oral contraceptives and the IUD is being investigated. Preliminary research has shown that the levonorgestrel IUD placed for a year, combined with 6 monthly injections of gonadotropin-releasing hormone, can stop or reverse the progress of endometrial cancer in young women. An experimental drug that combines a hormone with doxorubicin is also under investigation for greater efficacy in cancers with hormone receptors. Hormone therapy that is effective in treating breast cancer, including use of aromatase inhibitors, is also being investigated for use in endometrial cancer. One such drug is anastrozole, which is currently being researched in hormone-positive recurrences after chemotherapy. Research into hormonal treatments for endometrial stromal sarcomas is ongoing as well. It includes trials of drugs like mifepristone, a progestin antagonist, and aminoglutethimide and letrozole, two aromatase inhibitors.

Research continues into the best imaging method for detecting and staging endometrial cancer. In surgery, research has shown that complete pelvic lymphadenectomy along with hysterectomy in stage 1 endometrial cancer does not improve survival and increases the risk of negative side effects, including lymphedema. Other research is exploring the potential of identifying the sentinel lymph nodes for biopsy by injecting the tumor with dye that shines under infrared light. Intensity modulated radiation therapy is currently under investigation, and already used in some centers, for application in endometrial cancer, to reduce side effects from traditional radiotherapy. Its risk of recurrence has not yet been quantified. Research on hyperbaric oxygen therapy to reduce side effects is also ongoing. The results of the PORTEC 3 trial assessing combining adjuvant radiotherapy with chemotherapy were awaited in late 2014.

MDV3100 was in phase III trials for CRPC (chemo-naive and post-chemo patient populations) and gained FDA approval in 2012 as enzalutamide for the treatment of castration-resistant prostate cancer.

Alpharadin completed a phase 3 trial for CRPC patients with bone metastasis. A pre-planned interim analysis showed improved survival and quality of life. The study was stopped for ethical reasons to give the placebo group the same treatment. Alpharadin uses bone targeted Radium-223 isotopes to kill cancer cells by alpha radiation. It was approved by the U.S. Food and Drug Administration (FDA) on May, 15th 2013 ahead of schedule under the priority review program. Alpharadin still waits for approval by the European Medicines Agency (EMA).

While some dietary factors have been associated with prostate cancer the evidence is still tentative. Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence. Red meat and processed meat also appear to have little effect in human studies. Higher meat consumption has been associated with a higher risk in some studies.

Lower blood levels of vitamin D may increase the risk of developing prostate cancer.

Folic acid supplements have no effect on the risk of developing prostate cancer.

It was previously a relatively common complication of the massive lymphedema of the arm which followed removal of axillary (arm pit) lymph nodes and lymphatic channels as part of the classical Halstedian radical mastectomy, as a treatment for breast cancer. The classical radical mastectomy was abandoned in most areas of the world in the late 1960s to early 1970s, being replaced by the much more conservative modified radical mastectomy and, more recently, by segmental breast tissue excision and radiation therapy. Because of this change in clinical practice lymphedema is now a rarity following breast cancer treatment—and post-mastectomy lymphangiosarcoma is now vanishingly rare. When it occurs following mastectomy it is known as Stewart-Treves syndrome (which can be both lymphangiosarcoma and hemangiosarcoma following mastectomy). The pathogenesis of lymphangiosarcoma has not been resolved, however several vague mechanisms have been proposed. Stewart and Treves, proposed that a cancer causing agent is present in lymphedematous limbs. Schreiber "et al." proposed that local immunodeficiency as a result of lymphedema results in a "immunologically privileged site" in which the sarcoma is able to develop.

Long-term use of oral contraceptives is associated with increased risk of cervical cancer. Women who have used oral contraceptives for 5 to 9 years have about three times the incidence of invasive cancer, and those who used them for 10 years or longer have about four times the risk.

mTOR inhibitors were a highly investigated potential treatment in the 2000s and 2010s, but the side effects of these drugs (particularly hyperglycemia and hyperlipidemia) were not well tolerated and the survival benefit not confirmed. PI3 kinase inhibitors have been of interest, but they tend to be highly toxic and cause diarrhea. Another investigated drug is selumetinib, a MAPK inhibitor. It improved survival, but did not correlate with any mutations found in tumors.

Bevacizumab can also be combined with platinum chemotherapy, a combination that has had positive preliminary results in PFS, but equivocal results regarding overall survival. One disadvantage to these treatments is the side effect profile, which includes high blood pressure and proteinuria. The drug can also exacerbate bowel disease, leading to fistulae or bowel perforation. Vintafolide, which consists of an antifolate conjugated with vinblastine, is also in clinical trials; it may prove beneficial because folate receptors are overexpressed in many ovarian cancers. Another potential immunotherapy is trastuzumab, which is active against tumors positive for Her2/neu mutations. Other angiogenesis inhibitors are also being investigated as potential ovarian cancer treatments. Combretastatin and pazopanib are being researched in combination for recurrent ovarian cancer. Trebananib and tasquinimod are other angiogenesis inhibitors being investigated. The monoclonal antibody farletuzumab is being researched as an adjuvant to traditional chemotherapy. Another type of immunotherapy involves vaccines, including TroVax.

An alternative to BEP chemotherapy, a regimen of 3 cycles of carboplatin and etoposide, is a current topic of research for germ cell malignancies.

Intraperitoneal chemotherapy has also been under investigation during the 2000s and 2010s for its potential to deliver higher doses of cytotoxic agent to tumors. Preliminary trials with cisplatin and paclitaxel have shown it is not well tolerated, but does improve survival, and more tolerable regimens are being researched. Cisplatin and paclitaxel are both being researched as intraperitoneal chemotherapy agents. A specific chemotherapy regimen for rare clear-cell cancers is also under investigation: irinotecan combined with cisplatin.

PARP inhibitors have also shown promise in early trials, particularly in people with "BRCA" gene mutations, since the BRCA protein interacts with the PARP pathway. It is also being studied in recurrent ovarian cancer in general, where preliminary studies have shown longer PFS. Specifically, olaparib has shown greater survival compared to doxorubicin, though this treatment is still being investigated. It is not clear yet which biomarkers are predictive of responsiveness to PARP inhibitors. Rucaparib is another PARP inhibitor being researched in BRCA-positive and BRCA-negative recurrent advanced ovarian cancer. Niraparib is a PARP inhibitor being tested in BRCA-positive recurrent ovarian cancer.

Tyrosine kinase inhibitors are another investigational drug class that may have applications in ovarian cancer. Angiogenesis inhibitors in the receptor tyrosine kinase inhibitor group, including pazopanib, cediranib, and nintedanib, have also been shown to increase progression free survival (PFS), but their benefit for overall survival has not been investigated as of 2015. Preliminary research showed that cediranib combined with platins in recurrent ovarian cancer increased the time to second recurrence by 3–4 months and increased survival by 3 months. MK-1775 is a tyrosine kinase inhibitor that is being used in combination with paclitaxel and carboplatin in platinum-sensitive cancers with p53 mutations. Nintedanib is being researched as a potential therapy in combination with cyclophosphamide for people with recurrences.

A urogenital neoplasm is a tumor of the urogenital system.

Types include:

- Cancer of the breast and female genital organs: (Breast cancer, Vulvar cancer, Vaginal cancer, Cervical cancer, Uterine cancer, Endometrial cancer, Ovarian cancer)

- Cancer of the male genital organs (Carcinoma of the penis, Prostate cancer, Testicular cancer)

- Cancer of the urinary organs (Renal cell carcinoma, Bladder cancer)

Since many, if not most, anal cancers derive from HPV infections, and since the HPV vaccine before exposure to HPV prevents infection by some strains of the virus and has been shown to reduce the incidence of potentially precancerous lesions, scientists surmise that HPV vaccination may reduce the incidence of anal cancer.

On 22 December 2010, the U.S. Food and Drug Administration approved Gardasil vaccine to prevent anal cancer and pre-cancerous lesions in males and females aged 9 to 26 years. The vaccine has been used before to help prevent cervical, vulvar, and vaginal cancer, and associated lesions caused by HPV types 6, 11, 16, and 18 in women.

Treatment largely follows patterns that have been set for the management of postmenopausal breast cancer. The initial treatment is surgical and consists of a modified radical mastectomy with axillary dissection or lumpectomy and radiation therapy with similar treatment results as in females. Also, mastectomy with sentinel lymph node biopsy is a treatment option. In males with node-negative tumors, adjuvant therapy is applied under the same considerations as in females with node-negative breast cancer. Similarly, with node-positive tumors, males increase survival using the same adjuvants as affected females, namely both chemotherapy plus tamoxifen and other hormonal therapy. There are no controlled studies in males comparing adjuvant options. In the vast majority of males with breast cancer hormone receptor studies are positive, and those situations are typically treated with hormonal therapy.

Locally recurrent disease is treated with surgical excision or radiation therapy combined with chemotherapy. Distant metastases are treated with hormonal therapy, chemotherapy, or a combination of both. Bones can be affected either by metastasis or weakened from hormonal therapy; bisphosphonates and calcitonin may be used to counterbalance this process and strengthen bones.

Chemotherapeutic options include:

- Cyclophosphamide plus methotrexate plus fluorouracil (CMF).

- Cyclophosphamide plus doxorubicin plus fluorouracil (CAF).

- Trastuzumab (monoclonal antibody therapy).

Hormonal options include:

- Orchiectomy.

- Gonadotropin hormone releasing hormone agonist (GNRH agonist) with or without total androgen blockage (anti-androgen).

- Tamoxifen for estrogen receptor–positive patients.

- Progesterone.

- Aromatase inhibitors.