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Amplification of the neu/erbB-2 oncogene in a mouse model of mammary tumorigenesis
Open accessAbstract
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 of Neu in the induction of mammary tumors, Neu expression in these models is driven by a strong viral promoter of questionable relevance to the human disease. To ascertain whether expression of activated Neu under the control of the endogenous promoter in the mammary gland could induce mammary tumors we have generated mice that conditionally express activated Neu under the transcriptional control of the intact endogenous Neu promoter. Expression of oncogenic neu in the mammary gland resulted in accelerated lobulo-alveolar development and formation of focal mammary tumors after a long latency period. However, expression of activated Neu under the normal transcriptional control of the endogenous promoter was not sufficient for the initiation of mammary carcinogenesis. Strikingly, all mammary tumors bear amplified copies (2-22 copies) of the activated neu allele relative to the wild-type allele and express highly elevated levels of neu transcript and protein. Thus, like human erbB-2-positive breast tumors, mammary tumorigenesis in this mouse model requires the amplification and commensurate elevated expression of the neu gene.
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“Consistent with its oncogenic activity, overexpression of wild-type Neu or HER2 under the control of a mammary-specific promoter leads to metastatic mammary tumors in transgenic mice (Andrechek et al., 2000; Finkle et al., 2004).”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Andrechek et al., 2000
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Metadata
- Authors
- Andrechek, E. R., Hardy, W. R., Siegel, P. M., Rudnicki, M. A., Cardiff, R. D., & Muller, W. J.
- Affiliations
- University of California, Davis (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2000-03-14
- Volume
- 97
- Issue
- 7
- Pages
- 3444-3449
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC16259
- OpenAlex
- W2041576667
- Cited by
- 230
- References
- 38
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 5 · 2023: 7 · 2022: 2 · 2021: 6 · 2020: 10 · 2019: 7 · 2018: 6 · 2017: 7 · 2016: 8 · 2015: 9 · 2014: 12 · 2013: 9 · 2012: 8
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (U01CA105490)
- Topics
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Breast Lesions and Carcinomas
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- neu oncogene, c-erbB-2, HER2, gene amplification, mammary carcinogenesis, transgenic mouse model, conditional gene expression, endogenous promoter, breast cancer, oncogene overexpression
- MeSH terms
- Animals, Disease Models, Animal, Gene Amplification, Humans, Immunohistochemistry, Mammary Neoplasms, Experimental, Mice, Transgenic, DNA, Complementary, Genes, erbB-2, Mice
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