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Chk2*1100delC Acts in synergy with the Ron receptor tyrosine kinase to accelerate mammary tumorigenesis in mice |
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| Authors: | Sara E. Meyer Belinda E. Peace El Mustapha Bahassi Gina M. Kavanaugh Purnima K. Wagh Susan B. Robbins Moying Yin Susanne I. Wells Glendon M. Zinser Peter J. Stambrook Susan E. Waltz |
| Affiliation: | 1. Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA;2. Department Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA;3. Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA |
| Abstract: | The CHEK2 (Chk2 in mice) polymorphic variant, CHEK2*1100delC, leads to genomic instability and is associated with an increased risk for breast cancer. The Ron receptor tyrosine kinase is overexpressed in a large fraction of human breast cancers. Here, we asked whether the low penetrance Chk2*1100delC allele alters the tumorigenic efficacy of Ron in the development of mammary tumors in a mouse model. Our data demonstrate that Ron overexpression on a Chk2*1100delC background accelerates the development of mammary tumors, and shows that pathways mediated by a tyrosine kinase receptor and a regulator of the cell cycle can act to hasten tumorigenesis in vivo. |
| Keywords: | MST1R Met receptor Breast cancer Receptor tyrosine kinase Hepatocyte growth factor-like protein (HGFL) CHEK2 |
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