Cancer genes and the pathways they control

Nat Med. 2004 Aug;10(8):789-99. doi: 10.1038/nm1087.

Abstract

The revolution in cancer research can be summed up in a single sentence: cancer is, in essence, a genetic disease. In the last decade, many important genes responsible for the genesis of various cancers have been discovered, their mutations precisely identified, and the pathways through which they act characterized. The purposes of this review are to highlight examples of progress in these areas, indicate where knowledge is scarce and point out fertile grounds for future investigation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Adenomatous Polyposis Coli Protein / metabolism
  • Apoptosis / genetics
  • Apoptosis / physiology
  • DNA Repair / genetics
  • DNA Repair / physiology*
  • DNA-Binding Proteins / metabolism
  • Genes, Tumor Suppressor / physiology*
  • Humans
  • Hypoxia-Inducible Factor 1
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Mutation / genetics*
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Nuclear Proteins / metabolism
  • Oncogenes / genetics
  • Oncogenes / physiology*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Retinoblastoma Protein / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / physiology*
  • Smad Proteins
  • Trans-Activators / metabolism
  • Transcription Factors / metabolism
  • Tumor Suppressor Protein p53 / metabolism
  • Zinc Finger Protein GLI1

Substances

  • Adenomatous Polyposis Coli Protein
  • DNA-Binding Proteins
  • GLI1 protein, human
  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Nuclear Proteins
  • Retinoblastoma Protein
  • Smad Proteins
  • Trans-Activators
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Zinc Finger Protein GLI1
  • Phosphatidylinositol 3-Kinases
  • Receptor Protein-Tyrosine Kinases