A Comparative Study of the Effect of Oestrogen Substitution Therapy on Breast Development in Girls With Hypo—and Hypergonadotrophic Hypogonadism

Pertzelan, A; Yalon, L.; Kauli, Rivka; Laron, Zvi

doi:10.1111/j.1365-2265.1982.tb00728.x

Cited by 25 publications

(13 citation statements)

References 19 publications

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“…Even gonadotropin, not usually considered as a mammogenic hormone, has been reported to be involved in normal breast development. There has been a report of the effect of estrogen substitution therapy on breast development in girls with hypo-and hyper-gonadotropic hypogonadism (Pertzelan et al 1982). In the patients with gonadal dysgenesis, in whom the hypothalamic-pituitary function was normal, treatment led to full breast development.…”

Section: Discussionmentioning

confidence: 99%

Reconstituted normal human breast in nude mice: effect of host pregnancy environment and human chorionic gonadotropin on proliferation

Popnikolov

Yang²,

Liu³

et al. 2001

Journal of Endocrinology

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The proliferation of normal human breast epithelial cells in women is highest during the first trimester of pregnancy.In an attempt to analyze this hormonal environment in a model system, the effect of host mouse pregnancy and the administration of human chorionic gonadotropin (hCG) were assessed in normal human breast epithelial cells transplanted into athymic nude mice. Human breast epithelial cells, dissociated from reduction mammoplasty specimens and embedded inside the extracellular matrices comprised of collagen gel and Matrigel, were transplanted into nude mice. Proliferation was measured in vivo by BrdU labeling followed by immunostaining of sections from recovered gels in response to an altered hormonal environment of the host animal. The host animal was mated to undergo pregnancy and the complex hormonal environment of the host animal pregnancy stimulated growth of transplanted human cells. This effect increased with progression of pregnancy and reached the maximum during late pregnancy prior to parturition. In order to determine whether additional stimulation could be achieved, the transplanted human cells were exposed to a second cycle of host mouse pregnancy by immediately mating the animal after parturition. This additional exposure of host mouse pregnancy did not result in further increase of proliferation. The effect of hCG administration on transplanted human cells was also tested, since hCG level is highest during the first trimester of human pregnancy and coincides with the maximal breast cell proliferation. Administration of hCG alone stimulated proliferation of human cells in a dose-dependent manner, and could further enhance stimulation achieved with estrogen. The host mouse mammary gland also responded to hCG treatment resulting in increased branching and lobulo-alveolar development. However, the hCG effect on both human and mouse cells was dependent on intact ovary since the stimulation did not occur in ovariectomized animals. Although hCG receptor transcripts were detected in human breast epithelial cells, raising the possibility of a direct mitogenic action, the hCG effect observed in this study may have been mediated via the ovary by increased secretion of ovarian steroids. In summary, using our in vivo nude mice system, the proliferation of normal human breast epithelial cells could be stimulated by host mouse pregnancy and by administration of hCG.

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Section: Discussionmentioning

confidence: 99%

Reconstituted normal human breast in nude mice: effect of host pregnancy environment and human chorionic gonadotropin on proliferation

Popnikolov

Yang²,

Liu³

et al. 2001

Journal of Endocrinology

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“…Stromal Gli2 activity coordinates a niche signaling program for mammary epithelial stem cells Chen Zhao, 1,2 * † Shang Cai, 1 * Kunyoo Shin, 1,2,3 Agnes Lim, 1,4 Tomer Kalisky, 5 Wan-Jin Lu, 1,2 Michael F. Clarke, 1 Philip A. Beachy 1,2,4,6 ‡ The stem cell niche is a complex local signaling microenvironment that sustains stem cell activity during organ maintenance and regeneration. The mammary gland niche must support its associated stem cells while also responding to systemic hormonal regulation that triggers pubertal changes.…”

Section: Stem Cell Nichementioning

confidence: 99%

Stromal Gli2 activity coordinates a niche signaling program for mammary epithelial stem cells

Zhao

Cai

Shin

et al. 2017

Science

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The stem cell niche is a complex local signaling microenvironment that sustains stem cell activity during organ maintenance and regeneration. The mammary gland niche must support its associated stem cells while also responding to systemic hormonal regulation that triggers pubertal changes. We find that , the major Hedgehog pathway transcriptional effector, acts within mouse mammary stromal cells to direct a hormone-responsive niche signaling program by activating expression of factors that regulate epithelial stem cells as well as receptors for the mammatrophic hormones estrogen and growth hormone. Whereas prior studies implicate stem cell defects in human disease, this work shows that niche dysfunction may also cause disease, with possible relevance for human disorders and in particular the breast growth pathogenesis associated with combined pituitary hormone deficiency.

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“…Clinical studies on estrogen deficiency syndromes in humans (Pertzelan et al 1982) have implicated estrogen in the normal development of the breast. Definitive evidence for the importance of estrogen signaling in normal mammary gland development has been obtained from experiments in mice.…”

Section: Estrogen Signaling In Breast Cancermentioning

confidence: 99%

Interactions between estrogen and insulin-like growth factor signaling pathways in human breast tumor cells.

Hamelers

Steenbergh

2003

Endocrine-Related Cancer

107

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Estrogens and insulin-like growth factors (IGFs) act as mitogens promoting cell proliferation in normal breast tissue as well as in breast carcinomas. Both hormones have been shown to play a role in the development of breast cancer and were found to activate multiple signaling pathways leading to proliferation of human breast cancer cell lines in vitro. Originally, it was considered that these agents manifest their mitogenic actions through separate pathways, but a growing body of evidence suggests that the IGF-and estrogen-mediated signaling pathways are intertwined. 17β-Estradiol (E2) has been shown to enhance IGF signaling at multiple levels. E2 treatment of breast cancer cells alters expression of nearly all of the IGF family members including IGF-I, IGF-II, IGF-binding proteins, IGF type I receptor (IGF-RI), and insulin receptor substrate 1. The ligand-bound estrogen receptor has been reported to bind to and to activate the IGF-RI directly. Vice versa, IGF signaling has been reported to enhance estrogen receptor activation in human breast cancer cells by inducing phosphorylation of the estrogen receptor. Finally, several groups have described synergistic effects of the combination of E2 and IGF-I on S phase entry in breast tumor cell lines. Here, we review recent, often contradictory, reports describing the effects of E2 and IGFs on the proliferation of breast tumor cells, with special emphasis on the synergistic effects of the two hormones.

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A Comparative Study of the Effect of Oestrogen Substitution Therapy on Breast Development in Girls With Hypo—and Hypergonadotrophic Hypogonadism

Cited by 25 publications

References 19 publications

Reconstituted normal human breast in nude mice: effect of host pregnancy environment and human chorionic gonadotropin on proliferation

Reconstituted normal human breast in nude mice: effect of host pregnancy environment and human chorionic gonadotropin on proliferation

Stromal Gli2 activity coordinates a niche signaling program for mammary epithelial stem cells

Interactions between estrogen and insulin-like growth factor signaling pathways in human breast tumor cells.

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