BACKGROUND: Gastrointestinal carcinogenesis generally follows the adenoma-adenocarcinoma sequence and tumor metastasis determines the survival time of the patients. The expressions of p53 and ki-67 in gastrointestinal adenoma and adenocarcinoma (GIA) were explored and their clinicopathological significance determined. MATERIALS AND METHODS: The expressions of mutant p53 and ki-67 were examined on tissue microarray containing GIA, adjacent mucosa or adenoma and metastases by immunostaining. Their expressions were compared with the clinicopathological parameters of tumors. RESULTS: The expressions of mutant p53 and ki-67 were gradually increased from gastrointestinal mucosa to adenocarcinoma through adenoma (p<0.05). Mutant p53 expression showed a positive association with depth of invasion, local invasion via vessels and lymph node metastasis of GIA (p<0.05). Ki-67 expression was positively correlated with local invasion via vessels and negatively with dedifferentiation and liver metastasis of GIA (p<0.05). The expressions of both markers in metastases of GIA were consistent with their corresponding primary foci (p < 0.05). A positive association between both markers was found in the primary foci of GIA (p<0.05). CONCLUSION: The up-regulated expressions of mutant p53 and ki-67 are involved in the carcinogenesis and progression of GIA. They appear to be objective and effective markers to reflect the development of GIA.
BACKGROUND:Gastrointestinal carcinogenesis generally follows the adenoma-adenocarcinoma sequence and tumor metastasis determines the survival time of the patients. The expressions of p53 and ki-67 in gastrointestinal adenoma and adenocarcinoma (GIA) were explored and their clinicopathological significance determined. MATERIALS AND METHODS: The expressions of mutant p53 and ki-67 were examined on tissue microarray containing GIA, adjacent mucosa or adenoma and metastases by immunostaining. Their expressions were compared with the clinicopathological parameters of tumors. RESULTS: The expressions of mutant p53 and ki-67 were gradually increased from gastrointestinal mucosa to adenocarcinoma through adenoma (p<0.05). Mutant p53 expression showed a positive association with depth of invasion, local invasion via vessels and lymph node metastasis of GIA (p<0.05). Ki-67 expression was positively correlated with local invasion via vessels and negatively with dedifferentiation and liver metastasis of GIA (p<0.05). The expressions of both markers in metastases of GIA were consistent with their corresponding primary foci (p < 0.05). A positive association between both markers was found in the primary foci of GIA (p<0.05). CONCLUSION: The up-regulated expressions of mutant p53 and ki-67 are involved in the carcinogenesis and progression of GIA. They appear to be objective and effective markers to reflect the development of GIA.