ArticleThe American journal of pathology2002
Strain background alters mammary gland lesion phenotype in transforming growth factor-alpha transgenic mice.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
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- Transgene expression in the Nop-tTA driver line is not inherently restricted to the entorhinal cortex.Brain structure & function · 2016Article
- Bisphenol A increases mammary cancer risk in two distinct mouse models of breast cancer.Biology of reproduction · 2011Article
- RARα1 control of mammary gland ductal morphogenesis and wnt1-tumorigenesis.Breast cancer research : BCR · 2010Article
- Extranuclear coactivator signaling confers insensitivity to tamoxifen.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Short-term prophylactic tamoxifen reduces the incidence of antiestrogen-resistant/estrogen receptor-positive/progesterone receptor-negative mammary tumors.Cancer prevention research (Philadelphia, Pa.) · 2009Article
- Transgenic models to study actions of prolactin in mammary neoplasia.Journal of mammary gland biology and neoplasia · 2008Review
- Estrogen receptor-positive mammary tumorigenesis in TGFalpha transgenic mice progresses with progesterone receptor loss.Oncogene · 2007Article
- Dietary phytochemicals regulate whole-body CYP1A1 expression through an arylhydrocarbon receptor nuclear translocator-dependent system in gut.The Journal of clinical investigation · 2007Article
- Genetic mapping in mice identifies DMBT1 as a candidate modifier of mammary tumors and breast cancer risk.The American journal of pathology · 2007Article
- Prolactin potentiates transforming growth factor alpha induction of mammary neoplasia in transgenic mice.The American journal of pathology · 2006Article
- Bax regulates c-Myc-induced mammary tumour apoptosis but not proliferation in MMTV-c-myc transgenic mice.British journal of cancer · 2004Article
- A visual-quantitative analysis of fibroblastic stromagenesis in breast cancer progression.Journal of mammary gland biology and neoplasia · 2004Review
- Epidermal growth factor receptor stimulation activates the RNA binding protein CUG-BP1 and increases expression of C/EBPbeta-LIP in mammary epithelial cells.Molecular and cellular biology · 2004Article
- Proteotypic classification of spontaneous and transgenic mammary neoplasms.Breast cancer research : BCR · 2004Article
- Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice.Oncogene · 2003Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Whey acidic protein (WAP)-transforming growth factor (TGF)-alpha transgenic mice acquire both cancerous and noncancerous mammary lesions. For this study, we evaluated the effect of mouse strain background on the incidence, latency, and histotype of two noncancerous lesions, hyperplastic alveolar nodules (analogous to typical hyperplasias in women), and macrocysts. These lesions display characteristics of fibrocystic changes observed in breasts of women, and in both mice and humans are associated with an uncertain risk of progression to neoplasia. Virgin transgenic mice of the (C57BL/6J;SJL)F2 background developed very few hyperplastic alveolar nodules and no macrocysts. In contrast, when the WAP-TGF-alpha transgene was carried on the FVB/N strain, congenic virgin transgenic mice acquired both lesion types with approximately 100% penetrance. In the (FVB;C57BL/6J)F1 background, hyperplastic alveolar nodule incidence was reduced to approximately the nontransgenic mouse level, and macrocyst latency was increased dramatically. Crossing into C57BL/6 resulted in elimination of the macrocyst phenotype. Finally, FVB strain transgenic mammary epithelium transplanted into nontransgenic recipients of the FVB/N or (FVB;C57BL/6J)F1 backgrounds displayed macrocyst latency characteristic of the recipient, and not donor, mouse strain. Quantitative real-time polymerase chain reaction analysis demonstrated that, despite the difference in macrocyst incidence between (FVB;C57BL/6J)F1 and C57BL/6 virgin transgenic mice (81% versus 0%), the level of TGF-alpha expression was not different. FVB strain transgenic mice expressed only twofold more TGF-alpha than the other backgrounds. These findings indicate that C57BL/6J modifier alleles inhibit mammary lesion incidence and macrocyst latency in a semidominant manner, and that suppression of lesion development can involve host factors that are independent of mammary epithelial genotype.
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