Colorectal cancer (CRC) is the third most common malignant neoplasm worldwide  and the second leading cause of cancer deaths in the United States. It is estimated that there will be 142,820 new cases diagnosed in the United States in 2013 and 50,830 deaths due to this disease. From 2005 to 2009, CRC incidence declined by 4.1% per year among adults aged 50 years and older. However, in adults younger than 50 years, CRC incidence rates have been increasing by 1.1% per year. From 2005 to 2009, mortality from CRC declined by 2.4% per year in men and 3.1% per year in women. The incidence is higher in men than in women. It ranges from 46.1 per 100,000 per year in Hispanic men to 66.9 per 100,000 per year in African American men. In women, it ranges from 31.9 per 100,000 per year in Hispanics to 50.3 per 100,000 per year in African Americans. The age-adjusted mortality rates for men and women are 20.2 per 100,000 per year in men and 14.1 per 100,000 per year in women. About 5% of Americans are expected to develop the disease within their lifetime and about half of those will die from it. Age-specific incidence and mortality rates show that the vast majority of cases are diagnosed after age 50 years; about 4% of CRCs occur younger than age 50 years.[3,4]
Among the groups that have a high incidence of CRC are those with hereditary conditions, such as familial adenomatous polyposis and hereditary nonpolyposis CRC (inherited in an autosomal dominant manner). Combined, the two groups account for no more than 6% of CRCs. More common conditions associated with an increased risk include a personal history of CRC or adenomas; first-degree relative with CRC; a personal history of ovarian, endometrial, or breast cancer; and a personal history of long-standing chronic ulcerative colitis or Crohn colitis.[5-7] These high-risk groups account for about a quarter of all CRCs. Limiting screening or early cancer detection to only these high-risk groups would miss the majority of CRCs.
Genetic, experimental, and epidemiologic  studies suggest that CRC results from complex interactions between inherited susceptibility and environmental or lifestyle factors. Efforts to identify causes led to the hypothesis that adenomatous polyps (adenomas) are precursors for the vast majority of CRCs. In effect, measures that reduce the incidence and prevalence of adenomas may result in a subsequent decrease in the risk of CRCs; however, some CRC mortality may be caused by fast-growing lesions and even lesions that do not pass through an adenomatous phase. Overall, the details of growth rates of adenomas and cancer are unknown; most likely there is a broad spectrum of growth patterns, including formation and spontaneous regression of adenomas.References
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