Transgenic expression of tpr-met oncogene leads to development of mammary hyperplasia and tumors.
AUTOR(ES)
Liang, T J
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=507382Documentos Relacionados
- Characterization of the rearranged tpr-met oncogene breakpoint.
- tpr-met Oncogene Product Induces Maturation-Promoting Factor Activation in Xenopus Oocytes
- tpr-met oncogene product induces maturation-producing factor activation in Xenopus oocytes.
- Characterization of the TPR-MET oncogene p65 and the MET protooncogene p140 protein-tyrosine kinases.
- The TPR-MET oncogenic rearrangement is present and expressed in human gastric carcinoma and precursor lesions.