Cellular DNA, Ras p21 and p53 expression in the carcinogenesis of adenomatous colorectal polyps

OBJECTIVE: To explore the possible roles of cellular DNA, oncogene ras and tumor suppressor gene p53 in the carcinogenesis of colorectal adenomatous p olyps (CAP). STUDY DESIGN: Cellular DNA content, oncogene ras and tumor suppressor gene p53 expression at the protein level were quantitatively studied with flow c ytometry (FCM) in 16 cases of CAP with mild epithelial dysplasia (CAP-MD), 16 cases of CAP with moderate/severe epithelial dysplasia (CAP-M/SD) and 11 cases of cancer in adenomatous polyps (CIAP). RESULTS: Nuclear DNA contents of CAP-M/SD (DNA [DI] = 1.11 +/- 0.06) and CI AP (DI = 1.29 +/- 0.03) Tr,ere significantly higher than those of CAP-MD (D I = 1.06 +/- 0.06) and normal controls (DI = 1.00, P <.005) and were in the FCM DNA aneuploidy range. The rates and amount las determined by the fluor esence index) of mutant p53 protein expression in CAP-M/SD and CIAP were si gnificantly higher than those in the control and CAP-MD groups. Positive ra tes of ras p21 expression were all high in CAP-MD, CAP-M/SD and CIAP (80%, 75% and 100%, respectively), yet the in-tensity of expression in the last w as significantly stronger than those in the former two groups. DNA aneuploi d, ras p21 and p53 coexpression were found in 10 of II cases of CIAP. CONCLUSION: The results suggest that cellular DNA, ras p21 and p53 are al i nvolved in the carcinogenesis of CAP. Clinically, the appearance of DNA ane uploidy, ras p21 or p53 overexpression should be considered markers of mali gnant conversion in CAP.