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Specific Genes Expressed in Association with Progesterone Receptors in Meningioma

Departments of ¹ Neurosurgery and ² Pathology, Brigham and Women's Hospital; ³ Children's Hospital Informatics Program and Harvard-Partners Center for Genetics and Genomics, Boston, Massachusetts; and ⁴ Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut

Requests for reprints: Elizabeth B. Claus, Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College Street, P.O. Box 208034, New Haven, CT 06520-8034. E-mail: elizabeth.claus{at}yale.edu.

An association between hormones and meningioma has been postulated. No data exist that examine gene expression in meningioma by hormone receptor status. The data are surgical specimens from 31 meningioma patients undergoing neurosurgical resection at Brigham and Women's Hospital from March 15, 2004 to May 10, 2005. Progesterone and estrogen hormone receptors (PR and ER, respectively) were measured via immunohistochemistry and compared with gene expression profiling results. The sample is 77% female with a mean age of 55.7 years. Eighty percent were grade 1 and the mean MIB was 6.2, whereas 33% and 84% were ER+ and PR+, respectively. Gene expression seemed more strongly associated with PR status than with ER status. Genes on the long arm of chromosome 22 and near the neurofibromatosis type 2 (NF2) gene (22q12) were most frequently noted to have expression variation, with significant up-regulation in PR+ versus PR– lesions, suggesting a higher rate of 22q loss in PR– lesions. Pathway analyses indicated that genes in collagen and extracellular matrix pathways were most likely to be differentially expressed by PR status. These data, although preliminary, are the first to examine gene expression for meningioma cases by hormone receptor status and indicate a stronger association with PR than with ER status. PR status is related to the expression of genes near the NF2 gene, mutations in which have been identified as the initial event in many meningiomas. These findings suggest that PR status may be a clinical marker for genetic subgroups of meningioma and warrant further examination in a larger data set. [Cancer Res 2008;68(1):314–22]

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