This Article Full Text Full Text (PDF) Supplementary Data Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hong, C. Articles by Costello, J. F. Search for Related Content PubMed PubMed Citation Articles by Hong, C. Articles by Costello, J. F.

The Contribution of Genetic and Epigenetic Mechanisms to Gene Silencing in Oligodendrogliomas

¹ Department of Neurological Surgery, The Brain Tumor Research Center,
² Department of Pathology,
³ Comprehensive Cancer Center, University of California, San Francisco

Very little is known of the genes and mechanisms contributing to the genesis of oligodendrogliomas, a subtype of primary brain tumors. Using an integrated genetic and epigenetic analysis of oligodendrogliomas, we show that aberrant CpG island methylation is the most prevalent alteration in these tumors, and the majority of methylated genes are independent of regions affected by deletion. In contrast, a subset of the gene-associated CpG islands are preferentially affected by converging methylation and deletion, including a putative zinc finger gene, ZNF342, located in a commonly deleted region at chromosome 19q13. ZNF342 expression is specifically decreased in primary oligodendrogliomas and up-regulated in glioma cell lines treated with a demethylating agent, whereas the expression level of the adjacent gene, Gemin7, is not consistently altered in these samples. This initial integrated approach identifies novel targets of gene silencing, and provides a more comprehensive view of the genes and mechanisms underlying oligodendrogliomas.

This article has been cited by other articles:

				P. Jun, C. Hong, A. Lal, J. M. Wong, M. W. McDermott, A. W. Bollen, C. Plass, W. A. Held, D. J. Smiraglia, and J. F. Costello Epigenetic silencing of the kinase tumor suppressor WNK2 is tumor-type and tumor-grade specific Neuro-oncol, January 1, 2009; 11(4): 414 - 422. [Abstract] [Full Text] [PDF]

				R. M. Brena and J. F. Costello Genome-epigenome interactions in cancer Hum. Mol. Genet., April 15, 2007; 16(R1): R96 - R105. [Abstract] [Full Text] [PDF]

				C. Hong, A. Maunakea, P. Jun, A. W. Bollen, J. G. Hodgson, D. D. Goldenberg, W. A. Weiss, and J. F. Costello Shared Epigenetic Mechanisms in Human and Mouse Gliomas Inactivate Expression of the Growth Suppressor SLC5A8 Cancer Res., May 1, 2005; 65(9): 3617 - 3623. [Abstract] [Full Text] [PDF]

				M. Alaminos, V. Davalos, S. Ropero, F. Setien, M. F. Paz, M. Herranz, M. F. Fraga, J. Mora, N.-K. V. Cheung, W. L. Gerald, et al. EMP3, a Myelin-Related Gene Located in the Critical 19q13.3 Region, Is Epigenetically Silenced and Exhibits Features of a Candidate Tumor Suppressor in Glioma and Neuroblastoma Cancer Res., April 1, 2005; 65(7): 2565 - 2571. [Abstract] [Full Text] [PDF]

				S. Bai, K. Ghoshal, J. Datta, S. Majumder, S. O. Yoon, and S. T. Jacob DNA Methyltransferase 3b Regulates Nerve Growth Factor-Induced Differentiation of PC12 Cells by Recruiting Histone Deacetylase 2 Mol. Cell. Biol., January 15, 2005; 25(2): 751 - 766. [Abstract] [Full Text] [PDF]