Author/Authors :
Meyer، نويسنده , , Sara E. and Peace، نويسنده , , Belinda E. and Bahassi، نويسنده , , El Mustapha and Kavanaugh، نويسنده , , Gina M. and Wagh، نويسنده , , Purnima K. and Robbins، نويسنده , , Susan B. and Yin، نويسنده , , Moying and Wells، نويسنده , , Susanne I. and Zinser، نويسنده , , Glendon M. and Stambrook، نويسنده , , Peter J. and Waltz، نويسنده , , Susan E.، نويسنده ,
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 , breast cancer , Receptor tyrosine kinase , CHEK2 , Hepatocyte growth factor-like protein (HGFL) , Met receptor
