Myc, Max, and Mnt: molecular mechanisms of enhancement of cholangiocarcinogenesis by cholestasis

Gastroenterology. 2011 Jul;141(1):32-4. doi: 10.1053/j.gastro.2011.05.022. Epub 2011 May 26.
No abstract available

Publication types

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

MeSH terms

  • Animals
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / metabolism*
  • Bile Duct Neoplasms / etiology*
  • Bile Duct Neoplasms / genetics
  • Bile Duct Neoplasms / metabolism
  • Bile Duct Neoplasms / pathology
  • Bile Ducts, Intrahepatic / metabolism*
  • Bile Ducts, Intrahepatic / pathology
  • Bile Ducts, Intrahepatic / surgery
  • Cell Cycle Proteins / metabolism
  • Cholangiocarcinoma / etiology*
  • Cholangiocarcinoma / genetics
  • Cholangiocarcinoma / metabolism
  • Cholangiocarcinoma / pathology
  • Cholestasis / complications*
  • Cholestasis / genetics
  • Cholestasis / metabolism
  • Cholestasis / pathology
  • Disease Models, Animal
  • Disease Progression
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Hyperplasia
  • Liver / metabolism*
  • Liver / pathology
  • Mice
  • MicroRNAs / metabolism
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism*
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism*
  • Signal Transduction
  • Time Factors

Substances

  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
  • Cell Cycle Proteins
  • MicroRNAs
  • Mnt protein, mouse
  • Myc protein, mouse
  • Proto-Oncogene Proteins c-myc
  • Repressor Proteins
  • Max protein, mouse