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Research Article Free access | 10.1172/JCI118744

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

T J Liang, A E Reid, R Xavier, R D Cardiff, and T C Wang

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

Published in Volume 97, Issue 12 on June 15, 1996
J Clin Invest. 1996;97(12):2872–2877. https://doi.org/10.1172/JCI118744.
© 1996 The American Society for Clinical Investigation
Published June 15, 1996 - Version history
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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.

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  • Version 1 (June 15, 1996): No description

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