The oestrogen receptor and its selective modulators in gynaecological and breast cancer

Vergote, Ignace; Neven, Patrick; Dam, P Van; Serreyn, Rudolphe; Prins, F. De; Sutter, Petra De; Albertyn, G.

doi:10.1016/s0959-8049(00)00203-3

Cited by 11 publications

(9 citation statements)

References 65 publications

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“…estrogenic action at low concentrations (<10 −6 M) and antiestrogenic action at high concentrations (>10 −6 M), at which they exert antiestrogenic-cytotoxic activity [11,23,24]. The preferential binding of the known phytoestrogens to ER␤ may be important in their antiestrogenic effect in suppressing breast tumor growth, since ER␣ is mainly involved in promoting cell proliferation, whereas ER␤ has a counterproliferative, protective effect [25][26][27]. In this study, however, the new phytoestrogens acteoside and martynoside demonstrate antiestrogenic effects, mainly via the ER␣ pathway, at low concentrations at which most of the known phytoestrogens exhibit estrogenic effects.…”

Section: Discussionmentioning

confidence: 99%

Acteoside and martynoside exhibit estrogenic/antiestrogenic properties

Papoutsi

Kassi

Mitakou

et al. 2006

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Discussionmentioning

confidence: 99%

Acteoside and martynoside exhibit estrogenic/antiestrogenic properties

Papoutsi

Kassi

Mitakou

et al. 2006

The Journal of Steroid Biochemistry and Molecular Biology

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“…In general, the protein expression of ERα in BCs correlates with low tumor grade and negative lymph node status (no metastasis) [20–22]. While ER-positive tumors are less invasive and respond well to endocrine therapy [23], ER-negative BC is less responsive to endocrine treatment and presents with a more aggressive progression [24, 25]. However, the correlation of ERβ expression with invasiveness is less clear.…”

Section: Introductionmentioning

confidence: 99%

Estradiol increases ER-negative breast cancer metastasis in an experimental model

Yang

Belosay

et al. 2013

Clin Exp Metastasis

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Breast cancer (BC) is the most common cancer affecting women in the United States and metastatic breast cancer is the leading cause of death. The role estradiol plays in ER-positive BC is well-documented, but the way it contributes to ER-negative BC remains unclear. In the present study, we utilized an experimental model of BC metastasis into lung by injecting ER-negative murine 4T1 cells into mice via the lateral tail vein. A 56 % metastasis occurrence rate following the injection of 5 × 103 cells was observed, thus this cell number was selected to study the potential stimulatory effect of estradiol on ER-negative BC metastasis. Female ovariectomized mice were randomized into estradiol and control groups with 16 mice per group, and estradiol pellets were implanted subcutaneously in the estradiol group. Results demonstrated that estradiol accelerated BC metastasis as indicated by bioluminescent imaging. In addition, estradiol enhanced metastatic tumor colony formation and increased the size of tumor nodules in the lungs, which were due, in part, to the increase in proliferative cells in the metastatic tumors. In vitro, estradiol increased the motility and invasion of 4T1 cells, and the stimulatory effect on cell motility was not blocked by ICI 182, 780, confirming that ER was not involved in the process. Results from the present study suggest that estradiol plays a role in ER-negative BC metastasis in whole animals.

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“…Estrogen action promotes cell proliferation, suppresses apoptosis, and, therefore, has been an important target in the diagnosis and treatment of estrogen-dependent breast tumors. However, estrogen-nonresponsive tumor cells are associated with more advanced breast cancer progression, an important variable in tailoring endocrine treatments in a clinical setting (1)(2)(3). Circulating levels of 17h-estradiol (E 2 ) have been shown to affect tumor growth; however, the role of circulating E 2 in modulating mechanisms of metastasis and signaling in the host compartment has received less attention (4,5).…”

Section: Introductionmentioning

confidence: 99%

Estrogen Induces Lung Metastasis through a Host Compartment–Specific Response

et al. 2006

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Direct proliferative effects of estrogen (E 2 ) on estrogen receptor-positive tumors are well documented; however, the potential for E 2 to mediate effects selective for the host (i.e., angiogenesis, vascular permeability, or stromal effects), which influence tumor growth and/or metastasis, has received less attention. In this study, we examine the capacity for E 2 to promote tumor growth and/or metastasis independent of direct effects on tumor cells. In these studies, we distinguish host versus tumor compartment components of E 2 action in tumor growth and metastasis by analysis of E 2 -nonresponsive tumor cells implanted in ovariectomized (OVX) mice that contain s.c. implants of placebo (OVX) or E 2 -containing slowrelease pellets (OVX + E 2 ). We show that the D121 lung carcinoma cell line is E 2 -nonresponsive, and following s.c. implantation in OVX versus OVX + E 2 mice, E 2 action on the host compartment leads to an increase in spontaneous metastasis but not primary tumor growth or neovascularization. Similarly, experimental lung metastasis of E 2 -nonresponsive 4T1 mammary carcinoma cells also leads to increased tumor burden in the lungs of OVX + E 2 mice. These results suggest that the E 2 status of the host compartment influences late steps in tumor cell metastasis that can provide important insights into the role of E 2 in the tumor versus host compartments. (Cancer Res 2006; 66(7): 3667-72)

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The oestrogen receptor and its selective modulators in gynaecological and breast cancer

Cited by 11 publications

References 65 publications

Acteoside and martynoside exhibit estrogenic/antiestrogenic properties

Acteoside and martynoside exhibit estrogenic/antiestrogenic properties

Estradiol increases ER-negative breast cancer metastasis in an experimental model

Estrogen Induces Lung Metastasis through a Host Compartment–Specific Response

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