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PMID: 8675700 Published · ppublish English Journal Article 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.

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

The Journal of clinical investigation ·Vol. 97 ·No. 12 ·1996-06-15 ·Pages 2872-7

Liang TJ, Reid AE, Xavier R, Cardiff RD, Wang TC

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.

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
Chemicals
Proto-Oncogene Proteins c-met Receptor Protein-Tyrosine Kinases
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Liang T J
Department of Medicine, Massachusetts General Hospital, Boston 02114, USA. [email protected]
Reid A E
Xavier R
Cardiff R D
Wang T C
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Article Info
Journal
The Journal of clinical investigation
Abbr.
J Clin Invest
ISSN
0021-9738
Published
1996-06-15
Pages
2872-7
Language
English
Region
United States
NLM ID
7802877
PMCID
PMC507382
Subset
IM
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