ArticleThe American journal of pathology2006
Mammary carcinogenesis is preceded by altered epithelial cell turnover in transforming growth factor-alpha and c-myc transgenic mice.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Manganese-induced Precocious Puberty Alters Mammary Epithelial Cell Proliferation in Female Rats.Endocrinology · 2025Article
- In-silico insights on the prognostic potential of immune cell infiltration patterns in the breast lobular epithelium.Scientific reports · 2016Article
- Mouse model for probing tumor suppressor activity of protein phosphatase 2A in diverse signaling pathways.Cell cycle (Georgetown, Tex.) · 2012Article
- Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.Cell cycle (Georgetown, Tex.) · 2011Review
- Short-term prophylactic tamoxifen reduces the incidence of antiestrogen-resistant/estrogen receptor-positive/progesterone receptor-negative mammary tumors.Cancer prevention research (Philadelphia, Pa.) · 2009Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Identification of biomarkers that indicate an increased risk of breast cancer or that can be used as surrogates for evaluating treatment efficacy is paramount to successful disease prevention and intervention. An ideal biomarker would be identifiable before lesion development. To test the hypothesis that changes in cell turnover precede mammary carcinogenesis, we evaluated epithelial cell proliferation and apoptosis in mammary glands from transgenic mice engineered to develop mammary cancer due to expression in mammary epithelia of transforming growth factor alpha (TGF-alpha) or c-myc. In transgenic glands, before lesion development, epithelial cell turnover was enhanced overall compared with nontransgenic glands, indicating that aberrant cell turnover in normal epithelia may contribute to tumorigenesis. In addition, in tumor-containing glands, proliferation in normal epithelia was higher than in tumor-free transgenic glands, suggesting these cell populations influence one another. Finally, although c-myc glands displayed a uniformly high epithelial cell turnover regardless of age, cell turnover was reduced with aging in nontransgenic and TGF-alpha mice, indicating that some growth and death regulatory mechanisms remain intact in TGF-alpha epithelia. These observations support the evaluation of cell turnover as a biomarker of cancer risk and indicator of prevention/treatment efficacy in preclinical models and warrant validation in human breast cancer.
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