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Hovey, Russell C.; Trott, Josephine F.; Vonderhaar, Barbara K.

doi:10.1023/a:1015766322258

Cited by 259 publications

(90 citation statements)

References 153 publications

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“…Yet another school of thought maintains that progesterone, not E 2 , is the proliferative hormone in the mammary epithelium (16)(17)(18)(19)(20). The strongest support for this idea is that proliferation in the mammary gland occurs during the luteal phase of the estrus cycle when progesterone levels are high (17).…”

mentioning

confidence: 99%

Estrogen receptors ERα and ERβ in proliferation in the rodent mammary gland

Cheng

Zhang

Warner

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

128

111

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Most evidence supports the view that ERα is responsible for estrogen (ovarian estradiol, E 2 )-induced proliferation in the epithelial cells of the mammary gland, but despite this, proliferating epithelial cells do not express ERα. We have examined this apparent paradox by studying the role of ERα and ERβ in E 2 -induced proliferation in mammary glands (measured by BrdUrd incorporation into DNA) in mice with intact ERβ (WT mice) and those in which the ERβ gene has been inactivated (ERβ -/- mice). On treatment of ERβ -/- mice with E 2 or ovariectomized WT mice with E 2 , tamoxifen, or a specific ERβ agonist (BAG), the number of BrdUrd-labeled cells in mammary glands increased from 3.4% in controls to 28-38% in the treated mice. This indicates that both ERα and ERβ can mediate E 2 -induced proliferation independently of each other. With specific antibodies, ERβ was found in both epithelial and stromal cells, whereas ERα was strictly epithelial. Within 4 h of a single dose of E 2 , ERα was lost from the nuclei of epithelial cells. In WT mice, ERα reappeared by 24 h, but in ERβ -/- mice, return to the nucleus was delayed by 24 h. At 4 h after E 2 , neither ERα nor progesterone receptor was detectable in BrdUrd-labeled nuclei but by 48 h after E 2 , 29% of the BrdUrd-labeled cells expressed ERα, and 21-38% expressed progesterone receptor. During 3 weeks of continuous E 2 treatment, ERβ remained in the nucleus, but there was no detectable ERα. With tamoxifen treatment, ERα remained in the nucleus, but ERβ was lost. From these results, we conclude that ERα receives the proliferation signal from E 2 , initiates DNA synthesis, and is then lost from cells. The subsequent steps in proliferation can proceed in the absence of either ERα or ERβ. ERβ facilitates the return of ERα to the nucleus and restores responsiveness to E 2 . By down-regulating ERβ, tamoxifen may prolong refractoriness to E 2 in mammary epithelium.

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mentioning

confidence: 99%

Estrogen receptors ERα and ERβ in proliferation in the rodent mammary gland

Cheng

Zhang

Warner

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

128

111

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“…1B), as reviewed in refs. [22][23][24]. The mammary gland undergoes a cycle of cell proliferation, followed by cell differentiation, and finally an involution phase that involves programmed cell death at the end of the cycle.…”

Section: Tissues As Dynamic Systemsmentioning

confidence: 99%

Eavesdropping on altered cell-to-cell signaling in cancer by secretome profiling

Klinke

2015

Molecular & Cellular Oncology

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In the past decade, cumulative clinical experiences with molecular targeted therapies and immunotherapies for cancer have promoted a shift in our conceptual understanding of cancer. This view shifted from viewing solid tumors as a homogeneous mass of malignant cells to viewing tumors as heterogeneous structures that are dynamically shaped by intercellular interactions among the variety of stromal, immune, and malignant cells present within the tumor microenvironment. As in any dynamic system, identifying how cells communicate to maintain homeostasis and how this communication is altered during oncogenesis are key hurdles for developing therapies to restore normal tissue homeostasis. Here, I discuss tissues as dynamic systems, using the mammary gland as an example, and the evolutionary concepts applied to oncogenesis. Drawing from these concepts, I present 2 competing hypotheses for how intercellular communication might be altered during oncogenesis. As an initial test of these competing hypotheses, a recent secretome comparison between normal human mammary and HER2C breast cancer cell lines suggested that the particular proteins secreted by the malignant cells reflect a convergent evolutionary path associated with oncogenesis in a specific anatomical niche, despite arising in different individuals. Overall, this study illustrates the emerging power of secretome proteomics to probe, in an unbiased way, how intercellular communication changes during oncogenesis.

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“…The hormones that regulate breast development have been known since the 1930s [24] and the involvement of THs in the development and differentiation of normal breast tissue has been established [25][26][27] . Breast growth and development require the coordinated action of many hormones, such as prolactin, estrogen, progesterone, adrenal steroids, insulin, growth hormone, and THs [28,29] .…”

Section: Triiodothyronine Effect In the Mammary Glandmentioning

confidence: 99%

“…This development includes various stages of proliferation and morphogenesis, which are largely driven by simultaneous changes in the main hormones and growth factors in various reproductive states. Ductal extension is driven by estrogen, growth hormone, growth factor similar to insulin I, and epidermal growth factor; however, ductal branching and alveolar budding are influenced by additional factors, such as progesterone, prolactin, and THs [27] . THs are not essential for the development of the breast ducts; however, they appear to stimulate the development of the lobules of these glands [25] .…”

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confidence: 99%

Triiodothyronine and breast cancer

Síbio¹,

Oliveira²,

Moretto³

et al. 2014

WJCO

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The thyroid hormones (THs), triiodothyronine (T3) and thyroxine (T4), are essential for survival; they are involved in the processes of development, growth, and metabolism. In addition to hyperthyroidism or hypothyroidism, THs are involved in other diseases. The role of THs in the development and differentiation of mammary epithelium is well established; however, their specific role in the pathogenesis of breast cancer (BC) is controversial. Steroid hormones affect many human cancers and the abnormal responsiveness of the mammary epithelial cells to estradiol (E2) in particular is known to be an important cause for the development and progression of BC. The proliferative effect of T3 has been demonstrated in various types of cancer. In BC cell lines, T3 may foster the conditions for tumor proliferation and increase the effect of cell proliferation by E2; thus, T3 may play a role in the development and progression of BC. Studies show that T3 has effects similar to E2 in BC cell lines. Despite controversy regarding the relationship between thyroid disturbances and the incidence of BC, studies show that thyroid status may influence the development of tumor, proliferation and metastasis.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Thyroid hormone; Triiodothyronine; Breast cancer; Mammary gland and metabolism Core tip: Breast cancer (BC) is a malignant tumor occurring much more frequently in women than in men; worldwide, the incidence of BC has increased markedly in recent years. It is estimated that 1.7 million women will be diagnosed with BC in 2020, marking an increase of 26%, compared to the current incidence: 1.35 million new cases annually. Countless environmental risk factors, pathological conditions, and physiological agents, as well as thyroid hormones (THs), have been involved in the development of BC. Various lines of evidence suggest tumor-promoting effects of THs. The literature contains controversial reports regarding the relationship between thyroid diseases and BC; furthermore, studies reporting both an excess of and a lack of THs may affect breast development and progression to cancer. Epidemiologically, many studies suggest that hyperthyroidism is a factor in the development of BC. Furthermore, experimental studies have shown that high levels of THs reduce the interval of multiplication of BC cell lines. Therefore, the influence of THs on BC is unclear. However, the majority of BC research suggests a relationship, primarily, when the molecular aspects of these hormones are considered in the progression of this type of tumor.De Sibio MT, de Oliveira M, Moretto FCF, Olimpio RMC, Conde SJ, Luvizon AC, Nogueira CR. Triiodothyronine and breast TOPIC HIGHLIGHT Triiodothyronine and breast cancer INTRODUCTIONThyroid hormones (THs), 3,5,3′,-triiodothyronine (T3) and thyroxine (T4), play critical roles in the differentiation, growth, metabolism, and physiological function of nearly all mammalian tissues [1,2] ; in addition, they are required for amphibian metamorphosis [3] ....

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Untitled

Cited by 259 publications

References 153 publications

Estrogen receptors ERα and ERβ in proliferation in the rodent mammary gland

Estrogen receptors ERα and ERβ in proliferation in the rodent mammary gland

Eavesdropping on altered cell-to-cell signaling in cancer by secretome profiling

Triiodothyronine and breast cancer

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