Think globally, act locally: the making of a mouse mammary gland

Hennighausen, Lothar; Robinson, Gertraud W.

doi:10.1101/gad.12.4.449

Cited by 247 publications

(173 citation statements)

References 38 publications

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“…The human mammary gland undergoes several major developmental changes involving cell proliferation, morphogenesis, differentiation, and apoptosis in conjunction with the influence of endocrine and paracrine factors [26]. Female reproductive hormones such as E2 and progesterone are key regulators of postnatal development of the mammary gland as determined by endocrine disruption and replacement studies in rodents [27].…”

Section: E2 Signaling In Mammary Gland Developmentmentioning

confidence: 99%

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

Zhou

Qiao

Shetty

et al. 2013

Cell. Mol. Life Sci.

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Estrogen and estrogen receptors (ERs) are critical regulators of breast epithelial cell proliferation, differentiation, and apoptosis. Compromised signaling vis-à-vis the estrogen receptor is believed © Springer Basel 2013 yow4@pitt.edu. ), which predicts for response to endocrine-based therapy; however, innate or acquired resistance to endocrinebased drugs remains a serious challenge. The complexity of regulation for estrogen signaling coupled with the crosstalk of other oncogenic signaling pathways is a reason for endocrine therapy resistance. Alternative strategies that target novel molecular mechanisms are necessary to overcome this current and urgent gap in therapy. A thorough analysis of estrogen-signaling regulation is critical. In this review article, we will summarize current insights into the regulation of estrogen signaling as related to breast carcinogenesis and breast cancer therapy. NIH Public Access

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Section: E2 Signaling In Mammary Gland Developmentmentioning

confidence: 99%

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

Zhou

Qiao

Shetty

et al. 2013

Cell. Mol. Life Sci.

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“…A reduction in epithelial apoptosis was seen previously in other models of TGF-␣ transgenic mice 12,13 and in bitransgenic c-myc-TGF-␣ 14 and prolactin-TGF-␣ mice 15 compared with the single transgenic c-myc-or prolactin-overexpressing mice. Reduced apoptosis coupled with augmented cell proliferation can promote an environment in which defective cells normally destined for programmed cell death remain alive.…”

Section: Discussionmentioning

confidence: 50%

Mammary Carcinogenesis Is Preceded by Altered Epithelial Cell Turnover in Transforming Growth Factor-α and c-myc Transgenic Mice

Rose-Hellekant

Wentworth

Nikolai

et al. 2006

The American Journal of Pathology

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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 ␣ (TGF-␣) 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-␣ mice, indicating that some growth and death regulatory mechanisms remain intact in TGF-␣ 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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“…During pregnancy, glandular expansion and hyperplasia prepares the mammae for functional lactation (Hennighausen and Robinson, 1998;Fenton, 2006). After pups are weaned, the entire alveolar compartment regresses to a quiescent, prepregnancy state (Hennighausen and Robinson, 1998). Studies have documented the necessity of ovarian steroid hormones, pituitary peptide hormones, and estrogen receptor-a on mammary development (Tekmal et al, 2005).…”

mentioning

confidence: 99%

“…The rapid increase in hormone production during the peripubertal period results in marked ductal outgrowth and alveolar proliferation. During pregnancy, glandular expansion and hyperplasia prepares the mammae for functional lactation (Hennighausen and Robinson, 1998;Fenton, 2006). After pups are weaned, the entire alveolar compartment regresses to a quiescent, prepregnancy state (Hennighausen and Robinson, 1998).…”

mentioning

confidence: 99%

Presence of Hyperplastic Pectoral Mammary Glands in a White-footed Mouse (Peromyscus leucopus) from a Superfund Site in Oklahoma, USA

Hays

Breshears²

2011

Journal of Wildlife Diseases

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Think globally, act locally: the making of a mouse mammary gland

Cited by 247 publications

References 38 publications

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

Mammary Carcinogenesis Is Preceded by Altered Epithelial Cell Turnover in Transforming Growth Factor-α and c-myc Transgenic Mice

Presence of Hyperplastic Pectoral Mammary Glands in a White-footed Mouse (Peromyscus leucopus) from a Superfund Site in Oklahoma, USA

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