Transgenic expression of tpr-met oncogene leads to development of mammary hyperplasia and tumors

J Clin Invest. 1996 Jun 15;97(12):2872-7. doi: 10.1172/JCI118744.

Abstract

Receptor tyrosine kinases are important in cell signal transduction and proliferation. Abnormal expression of tyrosine kinases often leads to malignant transformation. C-met is a tyrosine kinase receptor and its ligand is hepatocyte growth factor (HGF). HGF/c-met plays diverse role in regulation of cell growth, shape and movement. Constitutively activated met, such as tpr-met, is a potent oncogene in vitro, but its carcinogenic role in vivo remains unclear. Our study demonstrates that expression of tpr-met leads to development of mammary tumors and other malignancies in transgenic mice, and suggests that deregulated met expression may be involved in mammary carcinogenesis.

Publication types

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

MeSH terms

  • Animals
  • Base Sequence
  • Female
  • Hyperplasia
  • Mammary Glands, Animal / pathology*
  • Mammary Neoplasms, Experimental / etiology*
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Proto-Oncogene Proteins c-met
  • Proto-Oncogenes*
  • Receptor Protein-Tyrosine Kinases / genetics*

Substances

  • Proto-Oncogene Proteins c-met
  • Receptor Protein-Tyrosine Kinases