The risk factors for skin cancer (basal cell carcinoma and squamous cell carcinoma) and melanoma are similar yet different. Melanoma seems to be caused by intense, intermittent sun exposure, the blast of sun that you get when you are out sailing and have been in the office all week. Squamous cell carcinoma seems to have a direct relationship with the sun. After about 50-75,000 hours of sun exposure, the risk for SCC is quite linear. Basal cell carcinoma is somewhat inbetween and seems to be caused by both chronic sun exposure as well as intermittent sun exposure.

With any mastectomy, there is a small risk of cancer returning as it is physically impossible to remove every single breast cell. However if properly performed, the risks of recurrence are no higher with a skin-sparing or nipple-sparing procedure compared to a standard mastectomy.

Yes, your risk for melanoma, the deadliest form of skin cancer, may be increased if you have had other previous cancers, such as breast or thyroid cancer. In addition, having (or having had) any of the following puts a person at greater risk for getting skin cancer:

• Previous skin cancer.
• Organ transplant. The medicine that prevents the body from rejecting the organ also weakens the immune system, which increases the risk of skin cancer.
• Disease that weakens the immune system. Lymphoma and human immunodeficiency virus (HIV) are a few diseases that weaken the immune system.
• Gorlin’s syndrome (also called basal cell nevus syndrome). People who have this rare disease can get many basal cell carcinomas early in life. They also have a higher risk for getting melanoma and non-Hodgkin's lymphoma.

Many risk factors have been associated with an increased prevalence of ovarian cancer. Risks include a personal history of disease, family history, genetics, age, and reproductive factors.

Parity is another risk factor as nulliparous women have an increased risk of being diagnosed with ovarian cancer (2). Conversely, women who have given birth have a lower chance of developing ovarian cancer; in general, the lifetime risk of developing ovarian cancer decreases with each live birth (2). Lastly, nutrition plays a role, as a diet high in saturated fat and meat is associated with an increased risk of ovarian cancer. Factors associated with a decrease in risk include higher parity, use of oral contraception, and gynecologic procedures such as hysterectomy and tubal ligation (4). In fact, oral contraceptive use is one of the most significant methods for decreasing the risk of ovarian cancer.

The most important risk factor is a family history of breast or ovarian cancer. Women who have had breast cancer are at greater risk of developing ovarian cancer. The risk of ovarian cancer after breast cancer is highest in women who have a family history of breast cancer. In contrast to the 1.8% general population at risk for ovarian cancer, a family history of ovarian cancer in a first-degree relative (mother, daughter, sister) triples a woman’s lifetime risk of developing ovarian cancer (2). The risks further increase with two or more afflicted first-degree relatives (~7%). Up to 10% of ovarian cancers result from an inherited tendency to develop the disease. While 90% of diagnosed epithelial ovarian cancers occur sporadically, 10% are associated with the inheritance of an autosomal dominant genetic aberration (3). Women who have inherited high-penetrance cancer susceptibility genes, such as mutated BRCA1 or BRCA2 genes or those constituents of Lynch syndrome (hereditary nonpolyposis colorectal cancer, HNPCC), are at a greatly increased risk of developing ovarian cancer. Women who have had breast cancer are at greater risk of developing ovarian cancer. Women who have inherited high-penetrance cancer susceptibility genes, such as mutated BRCA1 or BRCA2 genes are at a greatly increased risk of developing ovarian cancer. A woman with BRCA1 mutation has a lifetime risk of 39% to 70 % of developing ovarian cancer and a risk of 11 to 25% for BRCA2 carriers (1). The NIH consensus statement concluded that women at increased risk should have at least an annual comprehensive gynecological examination (pelvic and rectovaginal), serum marker CA125, and transvaginal/abdominal ultrasound, despite the lack of data supporting the use of these measures for ovarian cancer screening (5). To reduce the morbidity and mortality from ovarian cancer one must identify early rather than advanced stage disease.

(1) Rock JA, Jones III HW. TeLinde’s operative gynecology. 10th ed. 2008. Philidephia, Pa. Lippincott Williams & Wilkins. Pp 1307-1312

(2) Schorge JO, Modesitt SC, Coleman RL, Cohn DE, Kauff ND, Duska LR, Herzog TJ. SGO White Paper on ovarian cancer: etiology, screening and surveillance. Gynecol Oncol. 2010; 119(1) 7-17

(3) Clarke-Pearson DL. Screening for ovarian cancer. N Engl J Med. 2009l 361(2): 170-177

(4) Rein BJD, Gupta S, Dada R, Safi J, Michener C, Argawal A. (Review Article) Potential markers for detection and monitoring of ovarian cancer. Journal of oncology. Vol 2011

(5) Ovarian Cancer: Screening, Treatment, and Followup. NIH Consensus Statement 1994 April 5-7;12(3):30

gender
age
race
high fat diet
early onset of mense and late menopause
late or no pregnancies
family history (BRCA-1, BRCA-2)
personal history (already had breast cancer)
dense breast tissue
alcohol consumption
hormone supplementation

Here are a couple of links that go into greater detail:
http://www.mayoclinic.com/health/breast-cancer/DS00328/DSECTION=risk-factors
http://www.cancer.org/cancer/breastcancer/detailedguide/breast-cancer-risk-factors

The risk assessment of prostate cancer is based on a combination of factors such as the PSA level at the time of diagnosis, the Gleason grade of the cancer which represents its aggressiveness (can vary from a low score of 2 to a high score of 10) and how the cancer feels on digital examination of the prostate (whether a cancerous nodule can be felt and if so does it extend beyond the confines of the prostate). High risk cancers are associated with a PSA > 20ng/ml, Gleason grade of 8-10 or a cancer that feels to be beyond the confines of prostate when felt with the finger in the rectum. Presence of any one of these characteristics renders a cancer to be high risk. The term high risk also connotes a high risk of recurrence of the cancer despite treatment.

Lung cancer risk is mostly determined by tobacco smoking history. The more one has smoked the higher the risk, but risk can be substantially reduced after stopping smoking. In addition, having chronic obstructive pulmonary disease (COPD, including chronic bronchitis and emphysema) also increase lung cancer risk, perhaps because of the damage caused by chronic inflammation in the lung. Some occupations increase lung cancer risk, especially those involving exposure to asbestos. A strong family history of lung cancer (parents, siblings) is also a risk factor. Considering all the risk factors, we can explain about 90% of lung cancer occurrence in men and 85% in women, so there are still factors we have not yet identified that can cause lung cancer.

The usual risk factors include a history of gastroesophageal reflux, smoking and alcohol use. Unfortunately we don’t have any biomarkers or xrays to help us determine who is high risk. There are certain diseases which can increase the risk, such as Barrett’s esophagus, achalasia, or a history of a caustic injection that damages the esophagus; these patients should be monitored long-term for developing esophageal cancer. Patient with high grade Barrett’s disease may already have invasive cancer present.

Bladder cancer presents in two forms, the non-muscle invasive form and the muscle invasive form. The former is a more serious form than the latter, requiring more aggressive therapy. Individual tumors in each form can have a high risk and a low risk profile in regard to its own category. The most important determinants of risk are the classical pathological features of the cancer such as grade, stage and lymphovascular invasion. These features are important in both non-muscle invasive and invasive bladder cancer. In addition with progress and molecular Identification of the genes driving bladder cancer we have further knowledge and classification of the cancer (1).

1. Flaig, T.W., and Theodorescu, D. 2012. Bladder cancer in 2011: the dawn of personalized medicine. Nature reviews. Urology 9:65-66.

The National Cancer Institute has a tool on their website, The Gail Model, that helps women over 35 determine their risk for invasive breast cancer. It can be accessed through this link http://www.cancer.gov/bcrisktool/