| First Author | Kaminski R | Year | 2006 |
| Journal | Cancer Res | Volume | 66 |
| Issue | 11 | Pages | 5757-62 |
| PubMed ID | 16740714 | Mgi Jnum | J:110109 |
| Mgi Id | MGI:3639376 | Doi | 10.1158/0008-5472.CAN-05-3536 |
| Citation | Kaminski R, et al. (2006) Role of SRC kinases in Neu-induced tumorigenesis: challenging the paradigm using Csk homologous kinase transgenic mice. Cancer Res 66(11):5757-62 |
| abstractText | Amplification of the HER-2/neu (ErbB2) gene is observed in approximately 30% of human breast cancers, correlating with a poor clinical prognosis. Src kinases are also involved in the etiology of breast cancer, and their activation was suggested to be necessary for Neu-induced oncogenesis. To address whether Src activity is essential for Neu-mediated tumorigenesis, we used a physiologic inhibitor of Src kinase activity, the Csk homologous kinase (CHK), expressed as a mammary tissue-specific transgene. Our data, using a physiologic inhibitor of Src activity (CHK), showed that blocking of Neu-induced Src activity without altering Src expression levels had no significant effects on Neu-mediated mammary tumorigenesis in vivo. This contradicts the current paradigm that activation of Src kinases is essential for Neu-induced oncogenesis. This study is the first to distinguish between the kinase-dependent and kinase-independent actions of Src and shows that its kinase-dependent properties are not requisite for Neu-induced tumorigenesis. |
