Bone mineral density in breast cancer patients with positive estrogen receptor tumor status

Douchi, Tsutomu; Yonehara, Yukie; Kosha, Shoichiro; Iwamoto, Ichiro; Rai, Yoshiaki; Sagara, Yoshiatsu; Umekita, Yoshihisa

doi:10.1016/j.maturitas.2006.11.012

Cited by 7 publications

(2 citation statements)

References 26 publications

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“…During the last few years, an increasing number of studies have reported that xenobiotic compounds from different sources are able to mimic the natural estrogens, thus exerting comparable effects by activating gene transcription through ERα and/or ERβ ( Effenberger et al , 2005 ; Escande et al , 2006 ; Gutendorf and Westendorf, 2001 ; Sonneveld et al , 2006 ; ter Veld et al , 2006 ; van der Woude et al , 2005 ). Estrogens stimulate cell proliferation in normal developing breast tissues and may prevent osteoporosis by increasing bone mineral density ( Douchi et al , 2007 ). However, several studies also suggest that estrogens may stimulate the growth of a large proportion of ERα-positive breast cancers ( Hartman et al , 2006 ; Lazennec, 2006 ; Monroe et al , 2005 ; Pedram et al , 2006 ; Weitzmann and Pacifici, 2006 ).…”

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confidence: 99%

Influence of Cellular ERα/ERβ Ratio on the ERα-Agonist Induced Proliferation of Human T47D Breast Cancer Cells

Covaleda

Berg

Vervoort

et al. 2008

Toxicological Sciences

108

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Breast cancer cells show overexpression of estrogen receptor (ER) α relative to ERβ compared to normal breast tissues. This observation has lead to the hypothesis that ERβ may modulate the proliferative effect of ERα. This study investigated how variable cellular expression ratios of the ERα and ERβ modulate the effects on cell proliferation induced by ERα or ERβ agonists, respectively. Using human osteosarcoma (U2OS) ERα or ERβ reporter cells, propyl-pyrazole-triol (PPT) was shown to be a selective ERα and diarylpropionitrile (DPN) a preferential ERβ modulator. The effects of these selective estrogen receptor modulators (SERMs) and of the model compound E2 on the proliferation of T47D human breast cancer cells with tetracycline-dependent expression of ERβ (T47D-ERβ) were characterized. E2-induced cell proliferation of cells in which ERβ expression was inhibited was similar to that of the T47D wild-type cells, whereas this E2-induced cell proliferation was no longer observed when ERβ expression in the T47D-ERβ cells was increased. In the T47D-ERβ cell line, DPN also appeared to be able to suppress cell proliferation when levels of ERβ expression were high. In the T47D-ERβ cell line, PPT was unable to suppress cell proliferation at all ratios of ERα/ERβ expression, reflecting its ability to activate only ERα and not ERβ. It is concluded that effects of estrogen-like compounds on cell proliferation are dependent on the actual ERα/ERβ expression levels in these cells or tissues and the potential of the estrogen agonists to activate ERα and/or ERβ.

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mentioning

confidence: 99%

Influence of Cellular ERα/ERβ Ratio on the ERα-Agonist Induced Proliferation of Human T47D Breast Cancer Cells

Covaleda

Berg

Vervoort

et al. 2008

Toxicological Sciences

108

View full text Add to dashboard Cite

show abstract

“…Cell proliferation in normal developing breast tissue is stimulated by estrogens and estrogens may prevent osteoporosis by increasing bone mineral density (Douchi et al, 2007). However, as cells can have their own set of ER splice variants that varies in time and abundance the estrogen receptor proteins can be expected to have a role in developmental regulation depending on splice variant and ligand present.…”

Section: Discussionmentioning

confidence: 99%

Human ERα and ERβ Splice Variants: Understanding Their Domain Structure in Relation to Their Biological Roles in Breast Cancer Cell Proliferation

Covaleda¹,

Vervoort²,

Rietjens³

et al. 2012

Biochemistry

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Bisphosphonates: Prevention of Bone Metastases in Breast Cancer

Gnant

Dubsky

Hadji

2012

Prevention of Bone Metastases

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Disease recurrence and distant metastases remain challenging for patients with breast cancer despite advances in early diagnosis, surgical expertise, and adjuvant therapy. Bone is the most common site for breast cancer metastasis, and the bone microenvironment plays a crucial role in harboring disseminated tumor cells (DTCs), a putative source of late relapse in and outside bone. Therefore, agents that affect bone metabolism might not only prevent the development of bone lesions but also provide meaningful reductions in the risk of relapse both in bone and beyond. Bisphosphonates bind to mineralized bone surfaces and are ingested by osteoclasts, wherein they inhibit osteolysis, thereby preventing the release of growth factors from the bone matrix. Therefore, the bone microenvironment becomes less conducive to survival and growth of DTCs and bone lesion formation. Recent trials of zoledronic acid in the adjuvant setting in breast cancer have demonstrated reduced disease recurrence in bone and other sites in premenopausal and postmenopausal women with early breast cancer. Based on the proven effect of bone protection during adjuvant endocrine therapy, new treatment guidelines recommend the routine use of bisphosphonates to prevent bone loss during adjuvant therapy, which may likely become the standard practice.

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Bone mineral density in breast cancer patients with positive estrogen receptor tumor status

Cited by 7 publications

References 26 publications

Influence of Cellular ERα/ERβ Ratio on the ERα-Agonist Induced Proliferation of Human T47D Breast Cancer Cells

Influence of Cellular ERα/ERβ Ratio on the ERα-Agonist Induced Proliferation of Human T47D Breast Cancer Cells

Human ERα and ERβ Splice Variants: Understanding Their Domain Structure in Relation to Their Biological Roles in Breast Cancer Cell Proliferation

Bisphosphonates: Prevention of Bone Metastases in Breast Cancer

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