Pancreatic carcinoma is nearly always fatal, with a 5-year survival rate of 3%–5%. Although cigarette smoking is considered to be a risk factor, the etiology of this cancer is essentially unknown. The hypothesis that accumulative genetic alterations underlie the multistage process of tumorigenesis is becoming increasingly accepted. Mutations activate the malignant potential of oncogenes and inactivate the repressor function of tumor suppressor genes (reviewed in Bishop 1991). The paradigmatic examples of these genes are the ras oncogenes and the P53 tumor suppressor gene.
KeywordsPancreatic Cancer Pancreatic Carcinoma Lynch Syndrome Hereditary Nonpolyposis Colorectal Cancer Mutator Mutation
Unable to display preview. Download preview PDF.
- Hruban RH, van Mansfeld ADM, Offerhaus GJ, van Weering DHJ, Allison D, Goodman SN, Kensler TW, Bose KK, CameronJL, Bos JL (1993). K-ras oncogene activation in adeno-carcinoma of the human pancreas. A study of 82 carcinomas using a combination of mutant-enriched polymerase chain reaction analysis and allelespecific oligonucleotide hybridization. Am J Pathol 143:545–554PubMedGoogle Scholar
- Love RR (1985) Small bowel cancers, B-cell lymphatic leukemia, and six primary cancers with metastases and prolonged survival in the cancer family syndrome of Lynch. Cancer Res 55:499–502Google Scholar
- Lynch HT, Lanspa S, Smyrk T, Boman B, Watson P, Lynch J (1991) Hereditary nonpolyposis colorectal cancer (Lynch syndrome I and II). Cancer Genet Cytogenet 143:160–170Google Scholar
- Perucho M, Forrester K, Almoguera C, Kahn S, Lama C, Shibata D, Arnheim N, Grizzle WE (1989) Expression and mutational activation of the c-Ki-ras gene in human carcinomas. Cancer Cells 7 (Mol Diagn Hum Cancer) 137–141Google Scholar