Advertisement
Research Article Free access | 10.1172/JCI118744
Department of Medicine, Massachusetts General Hospital, Boston 02114, USA. liangt@bdg.niddk.nih.gov
Find articles by Liang, T. in: JCI | PubMed | Google Scholar
Department of Medicine, Massachusetts General Hospital, Boston 02114, USA. liangt@bdg.niddk.nih.gov
Find articles by Reid, A. in: JCI | PubMed | Google Scholar
Department of Medicine, Massachusetts General Hospital, Boston 02114, USA. liangt@bdg.niddk.nih.gov
Find articles by Xavier, R. in: JCI | PubMed | Google Scholar
Department of Medicine, Massachusetts General Hospital, Boston 02114, USA. liangt@bdg.niddk.nih.gov
Find articles by Cardiff, R. in: JCI | PubMed | Google Scholar
Department of Medicine, Massachusetts General Hospital, Boston 02114, USA. liangt@bdg.niddk.nih.gov
Find articles by Wang, T. in: JCI | PubMed | Google Scholar
Published June 15, 1996 - More info
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.