作者: E. R. Andrechek , W. R. Hardy , P. M. Siegel , M. A. Rudnicki , R. D. Cardiff
关键词: Mammary gland 、 ErbB 、 Transgene 、 Immunohistochemistry 、 Transcriptional regulation 、 Endogeny 、 Oncogene 、 Genetically modified mouse 、 Biology 、 Molecular biology
摘要: The neu (c-erbB-2, Her-2) protooncogene is amplified and overexpressed in 20–30% of human breast cancers. Although transgenic mouse models have illustrated the role Neu induction mammary tumors, expression these driven by a strong viral promoter questionable relevance to disease. To ascertain whether activated under control endogenous gland could induce tumors we generated mice that conditionally express transcriptional intact promoter. Expression oncogenic resulted accelerated lobulo-alveolar development formation focal after long latency period. However, normal was not sufficient for initiation carcinogenesis. Strikingly, all bear copies (2–22 copies) allele relative wild-type highly elevated levels transcript protein. Thus, like erbB-2-positive tumorigenesis this model requires amplification commensurate gene.