Survivin is unique for its expression in human malignancies but not in normal adult cells. It has been implicated in sensitisation to chemotherapy and as a prognostic marker in several common cancers. Immunohistochemistry for Survivin, P53 and BCL-2 expression as well as cell proliferative index (Ki-67) and apoptosis index (TUNEL) was conducted on 52 pancreatic and 12 ampullary adenocarcinomas. Survivin was detected in the cytoplasm of carcinoma cells in 46 (88%) of pancreatic tumours. P53 and BCL-2 were detected in 54% and 12% of pancreatic tumours, respectively. Proliferative index was 26.2+10.5% and apoptosis index was 1.38+0.69%. Prevalence of Survivin expression was significantly higher in P53-positive than in P53-negative cases (P=0.05) but was not associated with BCL-2 expression. Incrementally higher weighted scores of Survivin expression were associated with increased proliferative index (P=0.001). Furthermore, there was linear correlation between increased proliferative index and higher apoptosis index (P50.001). Surprisingly, higher scores of Survivin expression were associated with increased apoptosis index (P=0.007). Survival characteristics were not influenced by Survivin, P53 or BCL-2 expression, apoptosis index or proliferative index. Ampullary carcinoma showed Survivin expression in 83% of cases. However, unlike pancreatic carcinoma, there was no correlation between Survivin and P53 expression or proliferative index. In conclusion, Survivin is expressed in the majority of pancreatic adenocarcinomas and correlates with both cellular proliferation and apoptosis. Molecular manipulation of Survivin expression may enhance chemotherapy and radiation therapy for pancreatic cancer.

Survivin expression within the tumor can identify patients with stage II colorectal carcinoma who are at increased risk of death from recurrent disease and might particularly benefit from adjuvant therapy.

p53 protein expression has been studied in epithelial inclusion cysts adjacent to and contralateral to serous carcinoma of the ovary and compared to epithelial inclusion cysts associated with borderline tumours and in normal ovaries. Atypia was found in epithelial inclusion cysts in eight of the thirteen advanced (stage III) serous ovarian carcinomas. Of these eight with atypical epithelial inclusion cysts, five showed immunoreactivity for p53. In the borderline tumours and normal ovaries no atypia in such cysts was found. p53 expression was also seen more frequently in surface epithelium associated with ovarian serous adenocarcinoma (ten of 13) than in normal ovaries (one of 13). We postulate that focal areas of atypia (ovarian intra-epithelial neoplasia) in epithelial inclusion cysts are the precursors of ovarian malignancy. In some cases, at least, p53 protein expression may precede overt cytological abnormalities.

No abstract