Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia

Gastroenterology. 2012 Apr;142(4):730-733.e9. doi: 10.1053/j.gastro.2011.12.042. Epub 2012 Jan 5.

Abstract

More information is needed about genetic factors that initiate development of pancreatic intraepithelial neoplasms-the most common precursors of pancreatic ductal adenocarcinoma. We show that more than 99% of the earliest-stage, lowest-grade, pancreatic intraepithelial neoplasm-1 lesions contain mutations in KRAS, p16/CDKN2A, GNAS, or BRAF. These findings could improve our understanding of the development and progression of these premalignant lesions.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Baltimore
  • Carcinoma in Situ / genetics*
  • Carcinoma in Situ / pathology
  • Carcinoma, Pancreatic Ductal / genetics*
  • Carcinoma, Pancreatic Ductal / pathology
  • Chromogranins
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • DNA Mutational Analysis
  • GTP-Binding Protein alpha Subunits, Gs / genetics
  • Genetic Predisposition to Disease
  • Humans
  • Mutation*
  • Neoplasm Staging
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / pathology
  • Phenotype
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins / genetics

Substances

  • Chromogranins
  • Cyclin-Dependent Kinase Inhibitor p16
  • KRAS protein, human
  • Proto-Oncogene Proteins
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • GNAS protein, human
  • GTP-Binding Protein alpha Subunits, Gs
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins