Article

Reproductive factors and risk of glioma in women.

National Institute for Occupational Safety and Health, 4676 Columbia Parkway, Cincinnati, OH 45226, USA.
Cancer Epidemiology Biomarkers &amp Prevention (Impact Factor: 4.56). 10/2004; 13(10):1583-8.
Source: PubMed

ABSTRACT Glioma is the most common primary malignant brain tumor in adults, responsible for 75% of adult primary malignant brain tumors, yet aside from its association with ionizing radiation, its etiology is poorly understood. Sex differences in brain tumor incidence suggest that hormonal factors may play a role in the etiology of these tumors, but few studies have examined this association in detail. The objective of this study was to explore the role of reproductive factors in the etiology of glioma in women.
As part of a population-based case-control study, histologically confirmed primary glioma cases (n = 341 women) diagnosed between January 1, 1995 and January 31, 1997 were identified through clinics and hospitals in four Midwest U.S. states. Controls (n = 527 women) were randomly selected from lists of licensed drivers and Health Care Finance Administration enrollees. In-person interviews with subjects (81%) or their proxies (19%) collected reproductive history and other exposure information.
Glioma risk increased with older age at menarche (P for trend = 0.009) but only among postmenopausal women. Compared with women who never breast-fed, women who breast-fed >18 months over their lifetime were at increased risk of glioma (odds ratio, 1.8; 95% confidence interval, 1.1-2.9). Women who reported using hormones for symptoms of menopause had a decreased risk of glioma compared with women who never used such hormones (odds ratio, 0.7; 95% confidence interval, 0.5-1.1).
These results support the hypothesis that reproductive hormones play a role in the etiology of glioma among women.

0 Bookmarks
 · 
83 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: To date, the etiology of primary tumors of the central nervous system (mainly gliomas and meningiomas) is poorly understood. The role of sex hormones has been suggested, based on clinical, experimental, biological, and epidemiological data. To review the epidemiological studies on the relation between hormonal factors and the occurrence of glioma and meningioma, in order to identify new research developments. Articles published until September 2010 were selected by considering exogenous and endogenous exposures and specific brain tumors. Standardized information was collected from 20 articles: 15 concerning gliomas and 13 meningiomas. An increased glioma risk was observed with later menarche and menopause, while a reduced glioma risk was observed with hormone replacement therapy (HRT) and oral contraceptive use, despite duration of use had no effect on risk. Meningioma risk increased after menopause and with HRT use. No clear association was found with pregnancy and breastfeeding. Results are globally concordant with the biologic hypothesis assuming that female sex hormones are protective against glioma and may increase the risk of meningioma. However, new epidemiological studies should be conducted in order to confirm these associations and to refine the role of hormonal factors in brain etiology.
    Cancer Causes and Control 02/2011; 22(5):697-714. · 3.20 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Spontaneous regression of pilocytic astrocytoma after incomplete resection is well recognized, especially for cerebellar and optic pathway tumors, and tumors associated with Neurofibromatosis type-1 (NF1). The purpose of this report is to document spontaneous regression of pilocytic astrocytomas of the septum pellucidum and to discuss the possible role of cannabis in promoting regression. We report two children with septum pellucidum/forniceal pilocytic astrocytoma (PA) tumors in the absence of NF-1, who underwent craniotomy and subtotal excision, leaving behind a small residual in each case. During Magnetic Resonance Imaging (MRI) surveillance in the first three years, one case was dormant and the other showed slight increase in size, followed by clear regression of both residual tumors over the following 3-year period. Neither patient received any conventional adjuvant treatment. The tumors regressed over the same period of time that cannabis was consumed via inhalation, raising the possibility that the cannabis played a role in the tumor regression. We advise caution against instituting adjuvant therapy or further aggressive surgery for small residual PAs, especially in eloquent locations, even if there appears to be slight progression, since regression may occur later. Further research may be appropriate to elucidate the increasingly recognized effect of cannabis/cannabinoids on gliomas.
    Child s Nervous System 02/2011; 27(4):671-9. · 1.24 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: PURPOSE: Emerging evidence suggests that primary and metastatic brain tumors may be sensitive to hormonal manipulations. However, the pharmacokinetics of compounds against such targets in the brain and, more importantly, in the brain tumor are not well characterized. Here, we investigated the pharmacokinetics of letrozole, a third-generation aromatase inhibitor, in the normal brain and in orthotopically implanted C6 glioma in Sprague-Dawley rats. METHODS: Intracerebral microdialysis was employed to determine the concentrations of unbound letrozole in the brain extracellular fluid (ECF) while simultaneously collecting blood samples (via jugular vein) to assess plasma levels of letrozole. Letrozole was administered intravenously at doses of 4, 6, 8 and 12 mg/kg, and ECF and blood samples were collected over 8 h. For assessing normal versus tumoral brain pharmacokinetics, letrozole (4 or 8 mg/Kg; i.v.) was administered 10 days after implantation of C6 glioma in the brain. Dual-probe intracerebral microdialysis was employed for assessing ECF samples from tumor-free and tumor-bearing regions of the brain. RESULTS: Normal brain ECF and plasma C max and AUC0-8h increased linearly with letrozole doses up to 8 mg/kg dose, but at 12 mg/kg, the pharmacokinetics were nonlinear. The relative brain distribution coefficients, AUCECF/AUCplasma (ub), were 0.3-0.98. The tumoral uptake of letrozole was 1.5- to 2-fold higher relative to tumor-free region. CONCLUSIONS: Thus, letrozole permeability across the blood brain barrier is high, and the exposure to the brain is dose dependent. Furthermore, the brain tumoral letrozole levels are markedly higher than those in the tumor-free regions, which underscore potential selectivity of its activity against tumor cells.
    Cancer Chemotherapy and Pharmacology 06/2013; · 2.80 Impact Factor