The frequent coexistence of adenoma with primary carcinoma of the colon and their association with higher incidences of both synchronous and metachronous carcinomas offers only circumstantial evidence that adenomas are premalignant lesions. Detailed histopathologic investigations, however, have documented the transition from adenoma to carcinoma. Although the common, minute adenomatous polyp has a low potential of malignancy, the risk increases with size, villous architecture and degree of epithelial dysplasia. Furthermore, the association of dysplasia, which shares many adenomatous features with carcinoma in patients with chronic ulcerative colitis, and the inevitable development of adenomatous polyps followed by carcinoma of the colon and rectum in patients with familial polyposis further support this concept. Most colorectal malignant lesions, therefore, are believed to progress through the adenoma to carcinoma sequence. Moreover, histochemical investigations have demonstrated that abnormalities of DNA content, enzyme activities, CEA expression and mucin composition are shared by both adenoma and carcinoma. Thus, the malignancy potential of adenoma of the colon and rectum is reflected not only in the overt histologic transition to carcinoma, but in the disruption of the genetic and biochemical control mechanisms of cellular function as well.