Epithelial–stromal interactions in the mouse and human mammary gland in vivo

Parmar, Hema; Cunha, Gerald R.

doi:10.1677/erc.1.00659

Cited by 165 publications

(151 citation statements)

References 103 publications

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“…However, in young adult (PND 60) mice, the number of TEBs was influenced by maternal separation events. By early adulthood, TEBs have guided the expansion of the ductal epithelial network to the distal boundaries of the fat pad and have begun to mature into morphologically distinct terminal LAUs (28,29). Relative to TR mice, those mice that experienced maternal separation events (BMS and LMS) had fewer immature TEB structures (Fig.…”

Section: Resultsmentioning

confidence: 99%

Neonatal Experiences Differentially Influence Mammary Gland Morphology, Estrogen Receptor α Protein Levels, and Carcinogenesis in BALB/c Mice

Boyd

Salleh

Humber

et al. 2010

Cancer Prevention Research

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Prevention of breast cancer can be achieved with a better understanding of the factors contributing to normal breast development. Because the breast develops postnatally, alterations in the development and lifetime activity of the neuroendocrine system may set up an environment that increases cancer risk. The present study examined how two neonatal experiences over the first 3 weeks of life influence normal and malignant mammary gland development in female BALB/c mice. Following puberty, both brief (15 minutes) and prolonged (4 hours) daily maternal separations of newborn mice accelerated mammary gland development relative to nonseparated mice. Despite similar mammary gland morphologies between mice exposed to these two neonatal separation experiences, only mice exposed to prolonged maternal separation bouts showed a higher incidence and faster onset of mammary tumorigenesis following adulthood carcinogen [7,12-dimethylbenz(a)anthracene] administration. Molecular analysis of estrogen receptor α (ERα) and p53, two proteins that have been implicated in breast cancer, revealed that for mice exposed to prolonged neonatal maternal separation bouts, mammary gland ERα protein levels were upregulated in a transcription-independent manner. On the other hand, p53 expression in mammary glands of adult mice was not differentially influenced by neonatal experiences. Our findings show that chronic, moderate psychosocial stress during the neonatal period increases the expression of ERα protein and promotes mammary tumorigenesis in adulthood. Cancer Prev Res; 3(11); 1398-408. ©2010 AACR.

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Section: Resultsmentioning

confidence: 99%

Neonatal Experiences Differentially Influence Mammary Gland Morphology, Estrogen Receptor α Protein Levels, and Carcinogenesis in BALB/c Mice

Boyd

Salleh

Humber

et al. 2010

Cancer Prevention Research

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“…A recently developed model has, for the first time, enabled examination of these interactions with human breast elements. Parmar and Cunha 34 implanted mammary fibroblasts together with mammary epithelial cells as xenografts under the renal capsules of female nude mice. These studies demonstrated the ability of stromal elements to interact with epithelial cells to enhance stimulation of mammary cell proliferation with estrogens.…”

Section: Discussionmentioning

confidence: 99%

Histologic changes in the breast with menopausal hormone therapy use

Harvey¹,

Santen²,

Petroni

et al. 2008

Menopause

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Objective-This retrospective study systematically compared mammographic density with histology in women receiving or not receiving menopausal hormone therapy (HT).Design-This study was approved by the institutional review board. Twenty-eight postmenopausal women using HT were matched with 28 postmenopausal women not using HT at the time of breast cancer diagnosis. Noncancerous tissue from mastectomy specimens was examined histologically to quantitate the content of fibrous stroma, ducts, and lobule types 1, 2, and 3. Tissue samples were also evaluated for estrogen receptor, progesterone receptor, and Ki67 activity in the ducts and lobules. Breast density was quantified by digitizing the contralateral mammogram and computer-assisted interactive thresholding.Results-High breast density in women using HT was correlated with greater fibrous stroma (P = 0.020) and lobule type 1 (P = 0.016). Breast density also correlated with Ki67 activity in the ducts (P = 0.031) and lobules (P = 0.023) for both groups combined. Estrogen and progesterone receptors did not correlate with either breast density or HT use.Conclusions-Increased fibrous stroma and lobule type 1 are associated with increasing mammographic density in women using HT, independent of estrogen and progesterone receptor up-regulation. These findings suggest that increased breast density may be mediated through a paracrine effect. The increase in breast cancer risk with HT use may be due to an increase in target lobule type 1 cells.

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“…The factors that regulate embryonic mammary gland development have been reviewed recently (Parmar & Cunha 2004, Hens & Wysolmerski 2005. In brief, the Wnt signaling pathway, fibroblast growth factor signaling pathway, the Msx1/2 homeobox transcription factors, and parathyroid hormone-related protein play major roles in embryonic development and initial ductal growth (van Genderen et al 1994, Satokata et al 2000, Foley et al 2001, Mailleux et al 2002.…”

Section: Hormonal Control Of Mammary Developmentmentioning

confidence: 99%

Pregnancy and the risk of breast cancer

Britt¹,

Ashworth²,

Smalley³

2007

Endocrine Related Cancer

197

175

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It is well established that childless women and women having children later in life are at an increased risk of developing breast cancer. In particular, women having a first child before 20 years of age have a 50% reduction in lifetime breast cancer risk when compared with women who do not have children. This protective effect is specific for estrogen receptor positive breast cancer. Nevertheless, it remains unclear how parity decreases breast cancer risk. Possible mechanisms of action include changes to the hormonal profile of parous women, a more differentiated and so less susceptible mammary gland or changes within specific epithelial cell subpopulations. In this review, we discuss the epidemiological evidence for the protective effects of parity on breast cancer. We also explore the mechanisms by which parity protects, with a particular emphasis on the role of stem cells and the interactions between stem cells and estrogen.

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Epithelial–stromal interactions in the mouse and human mammary gland in vivo

Cited by 165 publications

References 103 publications

Neonatal Experiences Differentially Influence Mammary Gland Morphology, Estrogen Receptor α Protein Levels, and Carcinogenesis in BALB/c Mice

Neonatal Experiences Differentially Influence Mammary Gland Morphology, Estrogen Receptor α Protein Levels, and Carcinogenesis in BALB/c Mice

Histologic changes in the breast with menopausal hormone therapy use

Pregnancy and the risk of breast cancer

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