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 148,810 new cases diagnosed in the United States in 2008 and 50,640 deaths due to this disease.[2] Between 1973 and 1995, mortality from CRC declined by 20.5%, and incidence declined by 7.4% in the United States. The incidence is higher in men than in women. It ranges from 48.3 per 100,000 per year in Hispanic men to 72.5 per 100,000 per year in African American men. In women it ranges from 32.3 per 100,000 per year in Hispanics to 56.0 per 100,000 per year in African Americans. The age-adjusted mortality rates for men and women are 24.8 per 100,000 per year in men and 17.4 per 100,000 per year in women.[3,4] About 6% of Americans are expected to develop the disease within their lifetime.[3] Age-specific incidence and mortality rates show that most cases are diagnosed after age 50 years.[3]

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; first-degree relative with adenomas diagnosed before age 60 years;[5] a personal history of ovarian, endometrial, or breast cancer; and a personal history of long-standing chronic ulcerative colitis or Crohn colitis.[6-8] 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.[9]

Genetic,[10] experimental, and epidemiologic [11] studies suggest that CRC results from complex interactions between inherited susceptibility and environmental or lifestyle factors. Efforts to identify causes and to develop effective preventive measures led to the hypothesis that adenomatous polyps (adenomas) are precursors for the vast majority of CRCs.[12] In effect, measures that reduce the incidence and prevalence of adenomas may result in a subsequent decrease in the risk of CRC.[13] In addition, the formation and spontaneous regression of adenomas may also be a dynamic process.[14]

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.  [PUBMED Abstract]
   
   
2. American Cancer Society.: Cancer Facts and Figures 2008. Atlanta, Ga: American Cancer Society, 2008. Also available online. Last accessed October 1, 2008. 
   
   
3. Ries LAG, Eisner MP, Kosary CL, et al., eds.: SEER Cancer Statistics Review, 1975-2002. Bethesda, Md: National Cancer Institute, 2005. Also available online. Last accessed May 30, 2008. 
   
   
4. Edwards BK, Howe HL, Ries LA, et al.: Annual report to the nation on the status of cancer, 1973-1999, featuring implications of age and aging on U.S. cancer burden. Cancer 94 (10): 2766-92, 2002.  [PUBMED Abstract]
   
   
5. Ahsan H, Neugut AI, Garbowski GC, et al.: Family history of colorectal adenomatous polyps and increased risk for colorectal cancer. Ann Intern Med 128 (11): 900-5, 1998.  [PUBMED Abstract]
   
   
6. 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.  [PUBMED Abstract]
   
   
7. 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.  [PUBMED Abstract]
   
   
8. 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. 
   
   
9. Winawer SJ, Fletcher RH, Miller L, et al.: Colorectal cancer screening: clinical guidelines and rationale. Gastroenterology 112 (2): 594-642, 1997.  [PUBMED Abstract]
   
   
10. Fearon ER, Vogelstein B: A genetic model for colorectal tumorigenesis. Cell 61 (5): 759-67, 1990.  [PUBMED Abstract]
    
    
11. 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. 
    
    
12. Muto T, Bussey HJ, Morson BC: The evolution of cancer of the colon and rectum. Cancer 36 (6): 2251-70, 1975.  [PUBMED Abstract]
    
    
13. 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.  [PUBMED Abstract]
    
    
14. 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.  [PUBMED Abstract]
    
    

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