Risk factors include age, early menarche, nulliparity or late first pregnancy, high body-mass index, radiation exposure before age 30 years, hormone-replacement therapy (HRT), alcohol consumption, family history, presence of mutations in BRCA1 or BRCA2, and prior history of breast neoplasia. Models are able to predict a woman’s risk level (see www.cancer.gov/cancertopics/pdq/treatment/breast/healthprofessional#Section_627).
MRI scanning is a more effective screening tool than mammography in women with a familial breast cancer risk.
Women whose risk exceeds 1.66% in the next 5 years have been shown to have a 50% reduction in breast cancer from taking tamoxifen or raloxifene. Aromatase inhibitors have generally been superior to tamoxifen in the adjuvant treatment of hormone-sensitive breast cancer, and one of them (exemestane) reduces the risk of breast cancer by 65% in postmenopausal women at increased risk. Women with strong family histories should undergo testing for mutations in BRCA1 and BRCA2. Mutations in these genes carry a lifetime probability of >80% for developing breast cancer. Bilateral prophylactic mastectomy prevents at least 90% of these cancers but is a more radical prevention than the usual treatment for the disease. In addition, bilateral salpingo-oophorectomy reduces ovarian and fallopian tube cancer risk by about 96% in women with BRCA1 or BRCA2 mutations.
Risk factors include diets high in saturated fats and low in fruits and vegetables, smoking, and alcohol consumption. Stronger but less prevalent risk factors are the presence of inflammatory bowel disease or genetic disorders such as familial polyposis (autosomal dominant germline mutation in APC) and hereditary nonpolyposis colorectal cancer (mutations in DNA mismatch repair genes hMSH2 and hMLH1).
Pts with ulcerative colitis and familial polyposis generally undergo total colectomy. In familial polyposis, nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the number and size of polyps. Celecoxib, sulindac, and even aspirin appear to be effective, and celecoxib is approved by the U.S. Food and Drug Administration for this indication. Calcium supplementation can lead to a decrease in the recurrence of adenomas, but it is not yet clear that the risk of colorectal cancer is decreased and survival increased. The Women’s Health Study noted a significant reduction in the risk of colorectal cancer in women taking HRT, but the increase in thrombotic events and breast cancers counterbalanced this benefit. Studies are underway to assess NSAIDs with and without inhibitors of the epidermal growth factor (EGF) receptor in other risk groups.
Risk factors include smoking, exposure to radiation, asbestos, radon.
Smoking cessation is the only effective prevention (Chap. 204). NSAIDs and EGF receptor inhibitors are being evaluated. Carotenoids, selenium, retinoids, and α-tocopherol do not work.
Risk factors include age, family history, and possibly dietary fat intake. African Americans are at increased risk. The disease is highly prevalent, with autopsy studies finding prostate cancer in 70–80% of men over age 70.
In a group of men age ≥55 years with normal rectal examinations and PSA levels <3 ng/mL, daily finasteride reduced the incidence of prostate cancer by 25%. Finasteride also prevents the progression of benign prostate hyperplasia. However, some men experience decreased libido as a side effect. The Gleason grade of tumors seen in men taking finasteride prevention was somewhat higher than the controls; however, androgen deprivation alters the morphology of the cells and it is not yet clear that the Gleason grade is a reliable indicator of tumor aggressiveness in the setting of androgen deprivation. Dutasteride, another 5α-reductase inhibitor, had similar effects. The FDA has reviewed the data and concluded that the reduction in risk is primarily in the group of pts with low-grade tumors whose risk from prostate cancer is unclear. One additional high-grade tumor emerges for every 3–4 low-grade tumors averted. More follow-up is necessary to see if higher-grade tumors emerging on preventive therapy have the same aggressive behavior as those occurring in the absence of preventive hormone blockade.
Risk factors include early age at first intercourse, multiple sexual partners, smoking, and infection with human papillomavirus (HPV) types 16, 18, 45, and 56.
Regular Pap testing can detect nearly all cases of the premalignant lesion called cervical intraepithelial neoplasia. Untreated, the lesion can progress to carcinoma in situ and invasive cervical cancer. Surgical removal, cryotherapy, or laser therapy is used to treat the disease and is effective in 80%. Risk of recurrence is highest in women over age 30, those with prior HPV infection, and those who have had prior treatment for the same condition. A vaccine (Gardasil) containing antigens of strains 6, 11, 16, and 18 has been shown to be 100% effective in preventing HPV infections from those strains. The vaccine is recommended for all females and males age 9–26 years and could prevent up to 70% of all cervical cancer. The vaccine is not effective after infection has been established.
Risk factors include smoking, alcohol consumption, and possibly HPV infection.
Oral leukoplakia, white lesions of the oral mucosa, occur in 1–2 persons in 1000, and 2–3% of these pts go on to develop head and neck cancer. Spontaneous regression of oral leukoplakia is seen in 30–40% of pts. Retinoid treatment (13-cis retinoid acid) can increase the regression rate. Vitamin A induces complete remission in ~50% of pts. The use of retinoids in pts who have been diagnosed with head and neck cancer and received definitive local therapy has not produced consistent results. Initial studies claimed that retinoids prevented the development of second primary tumors, a common feature of head and neck cancer. However, large randomized studies did not confirm this benefit. Other studies are underway combining retinoids and NSAIDs with and without EGF receptor inhibitors.