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

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.

Pubmed ID: 8675700 RIS Download

Mesh terms: Animals | Base Sequence | Female | Hyperplasia | Mammary Glands, Animal | Mammary Neoplasms, Experimental | Mice | Mice, Transgenic | Molecular Sequence Data | Proto-Oncogene Proteins c-met | Proto-Oncogenes | Receptor Protein-Tyrosine Kinases

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Mouse Genome Informatics (MGI) (Data, Gene Annotation)

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