Evidence for a Common Molecular Pathogenesis in Colorectal, Gastric, and Pancreatic Cancer

✍ Scribed by Wilma L. Neuman; Marina L. Wasylyshyn; Russell Jacoby; Francesca Erroi; Imerio Angriman; Anthony Montag; Thomas Brasitus; Fabrizio Michelassi; Carol A. Westbrook

• Book ID: 102844533
• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 733 KB
• Volume: 3
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/gcc.2870030609

✦ Synopsis

W e examined tissue extracted from 19 gastric, 7 pancreatic, and 23 colorectal carcinoma specimens to determine the comparative incidence of allele loss on chromosomes 5, 17, and I 8 and that of KRAS2 point mutations. Chromosome 5 allele loss occurred at the same frequency in all three gastrointestinal tumors (approximately 30%), whereas chromosome I7 and I 8 allele losses were seen at a significantly lower frequency in gastric (20%) and pancreatic (0%) malignancies than in colorectal cancer (57%). Point mutations in KRASZ were seen in 83% of pancreatic and 52% of colon cancers, but not in gastric cancer specimens. In pancreatic tumors, these mutations were always found in the second nucleotide of codon 12. In colorectal cancer, the distribution was more variable, involving the second nucleotide of codon I 3 and both the first and second nucleotides of codon 12. These results suggest that inactivation of the adenomatous polyposis coli gene on chromosome 5 may be an initiating step for carcinomas of the stomach and pancreas as well as of the colon, but that the genes involved in tumor progression events may be tissue-or tumor-specific.