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The epithelial environment is complex, with many variables and influencing agents acting via the lumen. The cell is not a passive target, and contains inherent protective processes, which need to be disordered or overwhelmed before the progressively altered biology of tumorigenesis is set in motion. e. e. its anchorage to basement membrane. Cell birth and death (collectively often referred to simply as growth), relationship to environment, and cell locale become disturbed in a cancer cell. Proliferation: cell-cycle checkpoints The cycle of cell replication consists of five phases.

14 The possibility that a dysplastic lesion does not precede the invasive-cancer phenotype, however, seems unlikely. Small colorectal carcinomas normally arise in adenomas, whereas small carcinomas not associated with adenomas are relatively rare in Western countries. Recent observations in Japan and Europe, however, indicate that a sizeable minority of cancers do develop without recognizable adenomatous co-pathology. Overview of genetic events associated with tumorigenesis With progression of adenomas to carcinomas, there is a progressive accumulation of genetic abnormalities consistent with the multistep model.

Am J Epidemiol 1998; 147: 816–25. Ekbom A, Yuen J, Adami H-O et al, Cholecystectomy and colorectal cancer. Gastroenterology 1993; 105: 142–7. Howell MA, The association between colorectal cancer and breast cancer. J Chron Dis 1976; 29: 243–61. Rozen P, Hallak A, Rozen S et al, The value of screening women for large bowel tumors after breast or reproductive organ cancer. Front Gastrointest Res 1986; 10: 206–15. Travis LB, Curtis RE, Boice, JD Jr et al, Second malignant neoplasms among long-term survivors of ovarian cancer.

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