Aryl hydrocarbon receptor activation during pregnancy, and in adult nulliparous mice, delays the subsequent development of DMBA-induced mammary tumors.

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 veh

SUBMITTER: Wang T 

PROVIDER: S-EPMC2974771 | biostudies-literature | 2011 Apr

REPOSITORIES: biostudies-literature