| First Author | Meyer SE | Year | 2010 |
| Journal | Cancer Lett | Volume | 296 |
| Issue | 2 | Pages | 186-93 |
| PubMed ID | 20434834 | Mgi Jnum | J:162668 |
| Mgi Id | MGI:4819473 | Doi | 10.1016/j.canlet.2010.04.011 |
| Citation | Meyer SE, et al. (2010) Chk2*1100delC Acts in synergy with the Ron receptor tyrosine kinase to accelerate mammary tumorigenesis in mice. Cancer Lett 296(2):186-93 |
| abstractText | 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. |
