To determine the nature of the interaction between the ligand-activated AHR and ER pathways, we assessed the effects of treating ovx rats for 3 days with E2 and 3-MC, alone or in combination, on the number of TEBs in whole-mount preparations of the mammary gland (Figure 1A).
The inhibition of E2-induced development of TEBs, cell proliferation, up-regulation of the cell cycle, and proliferation-related pathways that we observed in response to 3-MC treatment suggests that these effects are independent of the specific AHR ligand and could therefore also be caused by the much more abundant PAHs.
A common measurement in mammary whole mounts is the number of TEBs.
Some agents alter the pace at which differentiation occurs, leading to an increased or decreased number of TEBs depending on timing of assessment.
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We used analysis of variance to evaluate the fixed effects of HFD and maternal TCDD exposure and their interaction on branch elongation, fat pad length, number of TEBs
in PND35 and PND49 mammary glands, and Comt, Ccdn1, Cypla1, Cyp1a1, Cyp1a2, Cyp1b1, Insig1.
The LOEL for the number and area of TEBs
occurred at a lower dose than in CD-1 females.
The expansion of TEBs
represents an opportunity for malignant transformation because they contain pluripotent mammary stem cells.
68) suggested that TCDD treatment in utero potentiates the carcinogenic effects of DMBA by increasing the number of terminal end buds (TEBs
) at the time of the DMBA injection at 50 days of age; the TEBs
are suggested to be the target sites for the carcinogenic effects of chemical initiators (102).
are composed of three to six layers of medium-sized epithelial cells.
With maturation, TEBs
either differentiate into alveolar buds (which comprise type I and II lobules) or regress to terminal ducts.
had differentiated and lobules were regressing in control animals at PND60 (maturity), differentiation within the fat pad of exposed animals was hindered as treatment dose was increased.