Untangling the genetics from the epigenetics in pancreatic cancer metastasis

Nat Genet. 2017 Feb 24;49(3):323-324. doi: 10.1038/ng.3798.

Abstract

Comparative genomic analyses of primary tumors and metastases within individuals with pancreatic cancer have exposed the complex clonal dynamics that underlie the dissemination of cancer cells to distant sites. Recent studies implicate non-genetic mechanisms in this process, particularly fluctuations in chromatin states and metabolism, which can endow rare cells within a primary tumor with metastatic potential.

MeSH terms

  • Adenocarcinoma / genetics*
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / secondary
  • Clonal Evolution
  • Clone Cells
  • Disease Progression
  • Epigenesis, Genetic*
  • Heterochromatin / metabolism*
  • Heterochromatin / pathology
  • Humans
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / secondary
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / secondary
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology
  • Phosphogluconate Dehydrogenase / genetics*
  • Phosphogluconate Dehydrogenase / metabolism
  • Proto-Oncogene Proteins p21(ras) / genetics
  • Proto-Oncogene Proteins p21(ras) / metabolism
  • Signal Transduction
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Heterochromatin
  • KRAS protein, human
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Phosphogluconate Dehydrogenase
  • Proto-Oncogene Proteins p21(ras)