Sakorafas G H, Tsiotou A G
251st Hellenic Airforce and V. A. General Hospital, Athens, Greece.
Eur J Surg. 1994 Oct;160(10):529-34.
Relatively little is known about the molecular basis of pancreatic cancer despite it being one of the most common cancers in the developed world. Recent studies have shown that in human pancreatic cancer there are abnormalities in the structure or function, or both, of several oncogenes, notably the c-erb B-2 proto-oncogene and the Ki-ras oncogene. These genetic alterations will have both diagnostic and therapeutic implications. The Ki-ras gene is mutated at codon 12 in about 90% of pancreatic cancers and there is abnormal expression of the c-erb B-2 oncogene in nearly 20%, although mutational activation of the latter is not seen in human pancreatic adenocarcinoma. There is considerable evidence to support the hypothesis that neoplastic transformation requires many genetic events, and it is likely therefore that there are other molecular abnormalities in pancreatic cancer. The sequence of their activation and the agents responsible for that activation have not yet been elucidated, and both laboratory and animal experiments are needed to define which molecular events activate the neoplastic genotype and phenotype and how.
