담낭암 발생에서 담췌관합류이상의 역할 규명과 암화과정에 관한 연구

Abstract

Background/Aims : To clarify the carcinogenesis of gallbladder cancer (GBC) in patients/ with anomalous pancreaticobiliary ductal union (APBDU), we investigated the expression of mutated p53 protein and c-erbB2, the cell proliferation indices of Ki-67 and the histopathologic changes in gallbladder carcinoma and noncancerous mucosa which are associated with APBDU. Methods : In the clinical review, we analysed 62 patients (27 patients of GBC with APBDU and 35 patients of GBC without APBDU) who were diagnosed in Sevrance Hospital from January, 1992 to December, 1994. Immunohistochemical staining and histologic examination were performed on the specimens obtained from surgically resected gallbladders from the patients. For comparative study, the specimens were grouped as follows: 5 cases of carcinoma with APBDU, 4 cases of noncancerous mucosa with APBDU associated with GHC, 11 cases of noncancerous mucosa with APBDU not associated with GBC, 19 cases of carcinoma without APBDU and 7 cases of chronic inflammatory mucosa of gallbladder stones as controls. Results: GBC developed in 33.3% of patients with APBDU (especially, 66.1% of PC type) and showed no gallbladder stones. The frequency of papillary carcinoma was higher and depth of invasion was less in GBC with APBDU than in GBC without APBDU. Among 15 cases of noncancerous mucosa with APBDU, isolated dysplasia and adenomyomatous hyperplasia were noted in 10 cases and 4 cases, respectively. In one case of APBDU with GBC, the expression of p53 protein was noted in the focal area of low grade dysplasia. Cell proliferation indices of Ki-67 were stepwise increased with the progression of histologic findings from inflammation, papillary hyperplasia, metaplasia and adenomyomatous hyperplasia to dysplasia. Particularly, remarkable increase was observed in adenomyomatous hyperplasia and dysplasia. Conclusions : The high incidence of isolated dysplasia and adenomyoma accompanying with increased cell proliferative indices seems to be closely related to the carcinogenesis of GBC in patients with APBDU. Additionally, the mutation of p53 may contribute to early event of carcinogenesis in some patients with APBDU.