Signal transduction in cancer

Cold Spring Harb Perspect Med. 2015 Apr 1;5(4):a006098. doi: 10.1101/cshperspect.a006098.


Cancer is driven by genetic and epigenetic alterations that allow cells to overproliferate and escape mechanisms that normally control their survival and migration. Many of these alterations map to signaling pathways that control cell growth and division, cell death, cell fate, and cell motility, and can be placed in the context of distortions of wider signaling networks that fuel cancer progression, such as changes in the tumor microenvironment, angiogenesis, and inflammation. Mutations that convert cellular proto-oncogenes to oncogenes can cause hyperactivation of these signaling pathways, whereas inactivation of tumor suppressors eliminates critical negative regulators of signaling. An examination of the PI3K-Akt and Ras-ERK pathways illustrates how such alterations dysregulate signaling in cancer and produce many of the characteristic features of tumor cells.

Publication types

  • Review

MeSH terms

  • Cell Movement
  • Cell Polarity
  • Cell Proliferation
  • Genomic Instability
  • Humans
  • MAP Kinase Signaling System*
  • Mutation
  • Neoplasms / genetics*
  • Oncogenes*
  • Phosphatidylinositol 3-Kinases / genetics*
  • Proto-Oncogene Proteins c-akt / genetics*
  • Tumor Microenvironment


  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt