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Colorectal Cancer Screening (PDQ®): Screening - Health Professional Information [NCI] - Significance

Colorectal cancer (CRC) is the third most common malignant neoplasm worldwide [1] and the second leading cause of cancer deaths in the United States.[2] 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.[2] 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.[3] 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.[3] About 5% of Americans are expected to develop the disease within their lifetime and about half of those will die from it.[3] 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.[5,6,7] 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.[8]

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Genetic,[9] experimental, and epidemiologic[10] 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.[11] In effect, measures that reduce the incidence and prevalence of adenomas may result in a subsequent decrease in the risk of CRCs [12]; 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.[13]

References:

  1. Shike M, Winawer SJ, Greenwald PH, et al.: Primary prevention of colorectal cancer. The WHO Collaborating Centre for the Prevention of Colorectal Cancer. Bull World Health Organ 68 (3): 377-85, 1990.
  2. American Cancer Society.: Cancer Facts and Figures 2013. Atlanta, Ga: American Cancer Society, 2013. Available online. Last accessed March 13, 2013.
  3. Howlader N, Noone AM, Krapcho M, et al., eds.: SEER Cancer Statistics Review, 1975-2009 (Vintage 2009 Populations). Bethesda, Md: National Cancer Institute, 2012. Also available online. Last accessed February 21, 2013.
  4. Imperiale TF, Wagner DR, Lin CY, et al.: Results of screening colonoscopy among persons 40 to 49 years of age. N Engl J Med 346 (23): 1781-5, 2002.
  5. Fuchs CS, Giovannucci EL, Colditz GA, et al.: A prospective study of family history and the risk of colorectal cancer. N Engl J Med 331 (25): 1669-74, 1994.
  6. Smith RA, von Eschenbach AC, Wender R, et al.: American Cancer Society guidelines for the early detection of cancer: update of early detection guidelines for prostate, colorectal, and endometrial cancers. Also: update 2001--testing for early lung cancer detection. CA Cancer J Clin 51 (1): 38-75; quiz 77-80, 2001 Jan-Feb.
  7. Levin B, Rozen P, Young GP: How should we follow up colorectal premalignant conditions? In: Rozen P, Young G, Levin B, et al.: Colorectal Cancer in Clinical Practice: Prevention, Early Detection, and Management. London, UK: Martin Dunitz, 2002, pp 67-76.
  8. Winawer SJ, Fletcher RH, Miller L, et al.: Colorectal cancer screening: clinical guidelines and rationale. Gastroenterology 112 (2): 594-642, 1997.
  9. Fearon ER, Vogelstein B: A genetic model for colorectal tumorigenesis. Cell 61 (5): 759-67, 1990.
  10. Young GP, Rozen P, Levin B: How does colorectal cancer develop? In: Rozen P, Young G, Levin B, et al.: Colorectal Cancer in Clinical Practice: Prevention, Early Detection, and Management. London, UK: Martin Dunitz, 2002, pp 23-37.
  11. Muto T, Bussey HJ, Morson BC: The evolution of cancer of the colon and rectum. Cancer 36 (6): 2251-70, 1975.
  12. Winawer SJ, Zauber AG, Ho MN, et al.: Prevention of colorectal cancer by colonoscopic polypectomy. The National Polyp Study Workgroup. N Engl J Med 329 (27): 1977-81, 1993.
  13. Loeve F, Boer R, Zauber AG, et al.: National Polyp Study data: evidence for regression of adenomas. Int J Cancer 111 (4): 633-9, 2004.
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WebMD Public Information from the National Cancer Institute

Last Updated: February 25, 2014
This information is not intended to replace the advice of a doctor. Healthwise disclaims any liability for the decisions you make based on this information.
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