Estrogen receptor beta (ER?) is expressed in brain astrocytic tumors and declines with dedifferentiation of the neoplasm

Batistatou, Anna; Stefanou, Dimitrios; Goussia, Anna; Arkoumani, Evdokia; Papavassiliou, Athanasios G.; Agnantis, Niki J.

doi:10.1007/s00432-004-0548-9

Cited by 66 publications

(64 citation statements)

References 33 publications

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“…[42][43][44] In the case of breast, colon and prostate cancer, as well as brain astrocytic tumors, ERb expression has been correlated to a higher tumor differentiation grade, in line with its antiproliferative and differentiating effects. [45][46][47][48] It is of interest that malignant lymphoid cells, as described for the cell lines used in this report, retain ERb expression. This may suggest that malignant transformation of cells of lymphoid origin is not generally associated with the loss of ERb expression and therefore remain as useful targets for therapy by ERb agonists.…”

Section: Discussionmentioning

confidence: 99%

Effect of ligand-activated estrogen receptor β on lymphoma growth in vitro and in vivo

et al. 2011

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Estrogen receptor b (ERb) is expressed in immune cells and studies have suggested an antiproliferative function of ERb. We detected ERb expression in murine T-and human B-cell lymphoma cell lines and analyzed the effects of estradiol and selective ERb agonists on lymphoma growth in culture and in vivo. Treating the cells with estradiol had minor effects on cell growth, whereas the selective ERb agonists diarylpropionitrile (DPN) and KB9520 showed a strong antiproliferative effect. When grafting mice with murine T-cell lymphoma cells, male mice developed larger tumors compared with female mice, a difference that was abolished following ovariectomy, showing estrogen-dependent growth in vivo. To investigate whether lymphoma growth may be inhibited in vivo by ERb agonist treatment, mice grafted with murine lymphoma cells were treated with DPN or KB9520. Both ERb-selective agonists strongly inhibited lymphoma growth. The reduced tumor size seen following either DPN or KB9520 treatment was due to reduced proliferation and increased apoptosis. Our results show an ERb ligand-dependent antiproliferative effect of lymphoma cells expressing endogenous ERb and that lymphoma cell growth in vivo can efficiently be inhibited by ERb agonists. This suggests that ERb agonists may be useful in the treatment of lymphomas.

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Section: Discussionmentioning

confidence: 99%

Effect of ligand-activated estrogen receptor β on lymphoma growth in vitro and in vivo

et al. 2011

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“…However, findings from these studies have also shed light on pathways involved in the development and progression of glioma in humans. This research has drawn upon knowledge of the role of endogenous and exogenous sex steroids in the etiology and pathogenesis of breast cancer and endometrial cancer and from an understanding of the tissue-specific nature of steroid hormone action (34)(35)(36). For example, selective estrogen receptor modulators (SERMs) may function as either estrogen antagonists or agonists, depending on the target tissue and on the estrogen receptor (ER) subtype mediating a specific response (34).…”

Section: Clinical and Experimental Studiesmentioning

confidence: 99%

“…Several studies reported finding either no detectable ERs or progestin receptors or very low levels in human gliomas/glioblastoma (43-47), whereas glucocorticoid and/or androgen receptors were detected in a higher proportion of gliomas (43,46,47). However, several more recent studies have documented ER expression in a substantial proportion of gliomas, glioblastomas, and astrocytomas (25,35,36,49,52,53).…”

Section: Steroid Receptors In Normal Glial Cells and Glioma Cellsmentioning

confidence: 99%

“…Although ERα has been detected in about one third of lower-grade tumors (52), it seems that most gliomas are ERα negative (36). Because many astrocytes express ERα in vivo (32,53), and there is also evidence that oligodendrocytes may express ERα (54,55), it is possible that ERα expression is reduced or lost during tumor development.…”

Section: Steroid Receptors In Normal Glial Cells and Glioma Cellsmentioning

confidence: 99%

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Do Steroid Hormones Play a Role in the Etiology of Glioma?

Kabat

Etgen

Rohan

2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Gliomas are the most common type of primary malignant brain tumor and have a very poor prognosis. Little is known, however, about the etiology of these tumors. Evidence from a number of sources suggests that endogenous steroid hormones may play a role in the development of gliomas. First, the descriptive epidemiology of glioma suggests a relative protection of females compared with males, particularly during the premenopausal years. Second, some gliomas and glioblastomas express estrogen receptors (ER), especially ERβ, as well as aromatase, the enzyme responsible for the conversion of testosterone to estradiol, and possibly other steroid hormone receptors. Third, experimental studies indicate that glioblastomas transplanted into animals grow at a slower rate in females compared with males. Finally, experimental studies show that estradiol, 2-methoxyestradiol, and a number of selective estrogen receptor modulators inhibit proliferation of gliomas and induce cell death. These hormonal agonists and antagonists may act either through classical steroid hormone receptors or independently of such receptors. In view of these findings, further clinical, experimental, and epidemiologic studies are needed to elucidate the role of steroid hormone agonists and antagonists in the development and proliferation of glioma. If hormonal pathways are involved in gliomagenesis, this could eventually lead to the design of preventive strategies. Cancer Epidemiol Biomarkers Prev; 19(10); 2421-7. ©2010 AACR.Little is known about the etiology of brain neoplasms, which in general are highly fatal (1). Gliomas, which include astrocytomas, oligodendrogliomas, and ependymomas, are the most common type of primary malignant brain tumor, accounting for approximately 80% of cases (2). Gliomas originate from glial cells (astrocytes or oligodendrocytes). Gliobastoma multiforme, the highest grade of glioma, is the most common and most aggressive type of malignant glioma. Most cases of glioblastoma multiforme (∼90%), referred to as "primary glioblastoma multiforme," develop rapidly without detectable evidence of a less malignant precursor tumor, whereas about 10% of glioblastomas, referred to as "secondary glioblastoma multiforme," develop slowly from low-grade astrocytomas (3). The only established risk factors for gliomas are high-dose ionizing radiation and certain rare genetic conditions, which together account for only a small proportion of cases (1, 4, 5). However, evidence from a number of sources suggests a possible role of endogenous ovarian steroid hormones in the development of glioma. Given that this topic has received little attention in major reviews on brain tumor epidemiology to date (1, 4-6), we review here findings from descriptive and analytic epidemiology, clinical studies, and experimental animal and cell culture studies pertinent to the potential role of steroid hormones in the development of glioma. Descriptive EpidemiologyThe incidence rate of glioma in adulthood is 50% greater in men than in women (5, 7). For example...

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“…The higher incidence in men becomes evident around the age of female menarche, reaching a maximum around the age of menopause and diminishing thereafter (6). Progesterone, estrogen, and androgen receptors are expressed in meningiomas (7)(8)(9) and gliomas (10,11) in various degrees. Use of exogenous female sex hormones has been reported in relation to meningioma and glioma risk with inconsistent results (12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Reproductive Factors and Risk of Meningioma and Glioma

Wigertz¹,

Lönn

Hall

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Female sex hormones have previously been suggested as possible risk factors for brain tumors, but published studies have reported conflicting results. We conducted a population-based case-control study of glioma (n = 626) and meningioma (n = 906) cases and randomly selected controls stratified on age and geographic region (n = 1,774) in Denmark, Finland, Norway, Sweden, and the United Kingdom. Unconditional logistic regression was used to estimate odds ratios (OR) for glioma and meningioma in relation to reproductive factors. A decreased glioma risk was associated with ever-pregnancy compared with neverpregnancy [OR, 0.8; 95% confidence interval (95% CI), 0.6-1.0]. Meningioma risk among women ages <50 years was increased in relation to number of pregnancies leading to a live birth (OR, 1.8; 95% CI: 1.1-2.8 for giving birth to 3 children compared with nulliparous women; P trend among parous women = 0.01). This relation was not found for older women. Breastfeeding among parous women increased the glioma risk (OR, 2.2; 95% CI, 1.3-3.9 for breast-feeding 36 months or more compared with breast-feeding 3 months or less). Menopausal status and age at menopause were not associated with meningioma or glioma risk. Our findings imply that reproductive hormones may influence the occurrence of meningioma and glioma.

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Estrogen receptor beta (ER?) is expressed in brain astrocytic tumors and declines with dedifferentiation of the neoplasm

Abstract: In as much as ERbeta is possibly the only ER expressed in astrocytes, its decreased expression may play an important role in astrocytic tumor initiation and in the potential response of glial neoplasms to tamoxifen.

Cited by 66 publications

References 33 publications

Effect of ligand-activated estrogen receptor β on lymphoma growth in vitro and in vivo

Effect of ligand-activated estrogen receptor β on lymphoma growth in vitro and in vivo

Do Steroid Hormones Play a Role in the Etiology of Glioma?

Reproductive Factors and Risk of Meningioma and Glioma

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