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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Role of SRC kinases in Neu-induced tumorigenesis: challenging the paradigm using Csk homologous kinase transgenic mice.

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.[1]

References

  1. Role of SRC kinases in Neu-induced tumorigenesis: challenging the paradigm using Csk homologous kinase transgenic mice. Kaminski, R., Zagozdzon, R., Fu, Y., Mroz, P., Fu, W., Seng, S., Avraham, S., Avraham, H.K. Cancer Res. (2006) [Pubmed]
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