Steroid Receptors in Intracranial Tumors

Brentani, Maria M.C.; Lopes, Míriam Teresa Paz; Martins, Vilma R.; Plese, José Píndaro Pereira

doi:10.1097/00002826-198412000-00013

Cited by 45 publications

(18 citation statements)

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“…[5][6][7][8][9] Functional GR also occurs in meningiomas at a rate of 70-100%. [10][11][12][13] The results of our experiments were in accordance with other research. The GRa-positive rate of 58 meningiomas was as high as 84.5%, and the strong positive rate was 36.2%.…”

Section: Discussionsupporting

confidence: 90%

Expression and significance of glucocorticoid receptor α in meningiomas

Zhao

Teng

Wang

et al. 2007

Journal of Clinical Neuroscience

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Section: Discussionsupporting

confidence: 90%

Expression and significance of glucocorticoid receptor α in meningiomas

Zhao

Teng

Wang

et al. 2007

Journal of Clinical Neuroscience

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“…Since the 1980s, several investigators have attempted to identify steroid hormone receptors in normal human brain cells and in human glioma and glioblastoma cells, as well as in rat glial and glioma cell lines (42)(43)(44)(45)(46)(47)(48)(49)(50)(51). Classical ERs and/or progestin, glucocorticoid, and androgen receptors are expressed in normal rat glial cells (26,42).…”

Section: Steroid Receptors In Normal Glial Cells and Glioma Cellsmentioning

confidence: 99%

“…Findings concerning the presence of ERs and other steroid hormone receptors in human and rat glioma and glioblastoma cell lines are varied and inconsistent. 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%

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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“…This is in large part because corticosteroids can affect many cellular processes, both within normal brain tissue and brain tumors. These are glucocortieoid receptors in botch normal brain [2] and brain tumors [3,4]. Among the published effects o f corticosteroids on brain tumors must be listed changes in cellular proliferation [5], tumor blood flow [6], tumor capillary permeability [7] and energy metabolism [6,8], besides the well known reduction of tumor-associated brain edema [1].…”

Section: Tnlroauctlonmentioning

confidence: 99%

Dexamethasone effects on vascular volume and tissue hematocrit in experimental RG-2 gliomas and adjacent brain

et al. 1988

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We have studied the effects of dexamethasone, a corticosteroid commonly used to treat brain tumors, on vascular volume and tissue hematocrit in RG-2 experimental rat gliomas. 125I-RISA (radioiodinated serum albumin) was used to measure tissue plasma vascular volume (Vp) and 51Cr labeled red cells were used to measure tissue red cell volume (Vrbc). Quantitative autoradiography was used to obtain local measurements of Vp and Vrbc in different brain and tumor regions. From these experimentally measured values, we calculated the tissue vascular volume (Vv), tissue hematocrit (THct) and systemic arterial hematocrit (AHct). The value reported primarily reflect capillary and small vessel volumes since blood drained from larger vessels during tissue processing and large vascular structures were avoided during analysis of the autoradiographic images. A total of 110 tumors were studied in 29 animals. There was a consistent trend for Vp and Vv to be reduced in all tumor regions after dexamethasone treatment, although a significant decrease was seen only in tumor center. Dexamethasone did not affect Vp or Vv in tumor-free brain regions. Dexamethasone appeared to have little effect on Vrbc in any brain or tumor region. THct was consistently, although not significantly, higher in tumors after treatment with dexamethasone; THct in tumor-free brain regions was unaffected by dexamethasone treatment.

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Steroid Receptors in Intracranial Tumors

Cited by 45 publications

References 0 publications

Expression and significance of glucocorticoid receptor α in meningiomas

Expression and significance of glucocorticoid receptor α in meningiomas

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

Dexamethasone effects on vascular volume and tissue hematocrit in experimental RG-2 gliomas and adjacent brain

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