[A case of huge papillary adenocarcinoma of the gallbladder with marked necrosis].

A 71-year-old woman was admitted to our hospital for evaluation of a right upper abdominal tumor. A contrast-CT scan demonstrated a huge tumor extending from the hepatic hilum to the pelvic space. The rim of tumor was enhanced. The center of the tumor was not enhanced and thus considered to consist of mucus or necrotic tissues. Preoperative diagnosis as gallbladder carcinoma without infiltrating to peripheral organ was made and subsequent cholecystectomy with full-thickness dissection has been performed. The tumor itself was in a swollen gallbladder, 18 cm in diameter, consisting of necrotic tissues in the lumen. Pathologic diagnosis was papillary adenocarcinoma, classified as pHinf1a, revealing fStage II. In many cases with undifferentiated carcinoma of the gallbladder, the neoplasms grow expansively to become large tumors with marked necrosis. We report a rare case of papillary adenocarcinoma of the gallbladder presenting both a clinical course and radiologic findings indistinguishable from undifferentiated carcinoma of the gallbladder.

Overexpression of protein kinase Cdelta enhances cisplatin-induced cytotoxicity correlated with p53 in gastric cancer cell line.

OBJECTIVE: An important issue in cancer therapy is to investigate the mechanism for cellular sensitivity to anticancer agents such as cisplatin. Cisplatin is one of the DNA-damaging agents and several factors including p53 are related to the sensitivity to cisplatin in cancer. Protein kinase C (PKC) delta is known as a positive regulator for cisplatin-induced cell death. In our present study, we examined whether overexpression of PKCdelta and p53 increases the sensitivity of the human gastric cancer cell line, MKN28, which has a mutation of p53 gene, to cisplatin. METHODS: Cell viability and DNA content were measured in MKN28 with adenovirus-mediated expression of PKCdelta and p53 after exposure to cisplatin. In addition, the active form of caspase-3 was detected by Western blotting. RESULTS: Overexpression of exogenous PKCdelta did not induce cell death in MKN28 but inhibited cell growth at 1 microg/ml cisplatin as compared to that by cisplatin alone. Moreover, overexpression of both wild-type p53 and exogenous PKCdelta in MKN28 increased cisplatin-induced cell death in MKN28. CONCLUSION: These results suggest that PKCdelta, in cooperation with p53, possibly regulates cisplatin-induced caspase-3-mediated cell death in gastric cancer.