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

T. Jake Liang, Andrea E. Reid, Ramnik Xavier, Robert D. Cardiff, Timothy C. Wang

Research output: Contribution to journalArticle

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 roles 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.

Original languageEnglish (US)
Pages (from-to)2872-2877
Number of pages6
JournalJournal of Clinical Investigation
Volume97
Issue number12
Publication statusPublished - Jun 15 1996
Externally publishedYes

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Keywords

  • c-met
  • carcinogenesis
  • hepatocyte growth factor
  • receptor tyrosine kinase
  • sarcoma

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Liang, T. J., Reid, A. E., Xavier, R., Cardiff, R. D., & Wang, T. C. (1996). Transgenic expression of tpr-met oncogene leads to development of mammary hyperplasia and tumors. Journal of Clinical Investigation, 97(12), 2872-2877.