ArticleInternational journal of cancer2011
Aryl hydrocarbon receptor activation during pregnancy, and in adult nulliparous mice, delays the subsequent development of DMBA-induced mammary tumors.
Article in International journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Carotenoids from StarfishMarine drugs · 2023Article
- Review
- Role of the aryl hydrocarbon receptor in carcinogenesis and potential as an anti-cancer drug target.Archives of toxicology · 2017Review
- Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds.Molecular nutrition & food research · 2016Review
- The impact of p53 on DNA damage and metabolic activation of the environmental carcinogen benzo[a]pyrene: effects in Trp53(+/+), Trp53(+/-) and Trp53(-/-) mice.Archives of toxicology · 2016Article
- Carcinogenic polycyclic aromatic hydrocarbons induce CYP1A1 in human cells via a p53-dependent mechanism.Archives of toxicology · 2016Article
- Mammalian models of chemically induced primary malignancies exploitable for imaging-based preclinical theragnostic research.Quantitative imaging in medicine and surgery · 2015Review
- Pulmonary Inflammation Impacts on CYP1A1-Mediated Respiratory Tract DNA Damage Induced by the Carcinogenic Air Pollutant Benzo[a]pyrene.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- The aryl hydrocarbon receptor ligand omeprazole inhibits breast cancer cell invasion and metastasis.BMC cancer · 2014Article
- The Aryl Hydrocarbon Receptor: A Target for Breast Cancer Therapy.Journal of cancer therapy · 2013Article
- Role of the aryl hydrocarbon receptor in carcinogenesis and potential as a drug target.Toxicological sciences : an official journal of the Society of Toxicology · 2013Review
- Mechanisms underlying the varied mammary carcinogenicity of the environmental pollutant 6-nitrochrysene and its metabolites (-)-[R,R]- and (+)-[S,S]-1,2-dihydroxy-1,2-dihydro-6-nitrochrysene in the rat.Chemical research in toxicology · 2013Article
- Alcohol consumption suppresses mammary tumor metastasis in a syngeneic tumor transplantation model.Breast cancer research and treatment · 2012Article
- Exposure to polychlorinated biphenyl (PCB) congeners measured shortly after giving birth and subsequent risk of maternal breast cancer before age 50.Breast cancer research and treatment · 2012Article
- Differential gene expression and a functional analysis of PCB-exposed children: understanding disease and disorder development.Environment international · 2012Article
- Activation of the aryl hydrocarbon receptor by TCDD inhibits mammary tumor metastasis in a syngeneic mouse model of breast cancer.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Breast cancer stem-like cells are inhibited by a non-toxic aryl hydrocarbon receptor agonist.PloS one · 2010Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the prototypic ligand for the aryl hydrocarbon receptor (AhR), promotes tumor formation in some model systems. However, with regard to breast cancer, epidemiological and animal studies are inconclusive as to whether exposure increases tumor incidence or may instead be protective. We have previously reported that mice exposed to TCDD during pregnancy have impaired differentiation of mammary tissue, including decreased branching and poor development of lobuloalveolar structures. Because normal pregnancy-induced mammary differentiation may protect against subsequent neoplastic transformation, we hypothesized that TCDD-treated mice would be more susceptible to chemical carcinogenesis after parturition. To test this, mice were treated with TCDD or vehicle during pregnancy. Four weeks later, 7,12-dimethylbenz[a]anthracene (DMBA) was administered to induce mammary tumor formation. Contrary to our hypothesis, TCDD-exposed parous mice showed a 4-week delay in tumor formation relative to controls, and they had a lower tumor incidence throughout the 27-week time course. The same results were obtained in nulliparous mice given TCDD and DMBA on the same schedule. We next addressed whether the delayed tumor incidence was a reflection of decreased tumor initiation, by testing the formation of DMBA-DNA adducts and preneoplastic lesions, induction of cytochrome P450s, and cell proliferation. None of these markers of tumor initiation differed between vehicle- and TCDD-treated animals. The expression of CXCL12 and CXCR4 was also measured to address their possible role in tumorigenesis. Taken together, our results suggest that AhR activation by TCDD slows the promotion of preneoplastic lesions to overt mammary tumors.
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