Transgenic expression of tpr-met oncogene leads to development of mammary hyperplasia and tumors. |
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Authors: | T J Liang A E Reid R Xavier R D Cardiff T C Wang |
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Affiliation: | Department of Medicine, Massachusetts General Hospital, Boston 02114, USA. liangt@bdg.niddk.nih.gov |
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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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