c-Src and cooperating partners in human cancer

Cancer Cell. 2004 Sep;6(3):209-14. doi: 10.1016/j.ccr.2004.09.001.


The proto-oncogene c-src is rarely mutated in human cancers, and when overexpressed in normal cells is non- or weakly oncogenic. These observations have raised doubts about the involvement of c-src in the etiology of human tumors. However, recent studies have shown that c-Src, a non-receptor tyrosine kinase, exhibits elevated protein levels and activity in numerous types of human cancers. Furthermore, it has been found to be a critical component of multiple signaling pathways that regulate proliferation, survival, metastasis, and angiogenesis. Because of its important role in these oncogenic processes, it represents a therapeutic target ripe for exploitation.

Publication types

  • Review

MeSH terms

  • Drug Delivery Systems
  • ErbB Receptors / metabolism
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases
  • Genes, src / physiology*
  • Humans
  • Neoplasms / genetics*
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Androgen
  • Receptors, Estrogen / metabolism
  • Receptors, Progesterone / metabolism
  • Signal Transduction


  • Receptors, Androgen
  • Receptors, Estrogen
  • Receptors, Progesterone
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases
  • PTK2 protein, human