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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]


  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.
  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.
  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.
  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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Last Updated: September 04, 2014
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