Loss of heterozygosity of TRIM3 in malignant gliomas

• Main Authors: Dolder Béatrice, Taylor Elisabeth, Stiefel Urs, Boulay Jean-Louis, Merlo Adrian, Hirth Frank
• Format: Article
• Language: English
• Published: BMC 2009-02-01
• Series: BMC Cancer
• Online Access: http://www.biomedcentral.com/1471-2407/9/71

<p>Abstract</p> <p>Background</p> <p>Malignant gliomas are frequent primary brain tumors associated with poor prognosis and very limited response to conventional chemo- and radio-therapies. Besides sharing common growth features with other types of solid tumors, gliomas are highly invasive into adjacent brain tissue, which renders them particularly aggressive and their surgical resection inefficient. Therefore, insights into glioma formation are of fundamental interest in order to provide novel molecular targets for diagnostic purposes and potential anti-cancer drugs. Human <it>Tripartite motif protein 3 </it>(<it>TRIM3</it>) encodes a structural homolog of <it>Drosophila brain tumor </it>(<it>brat</it>) implicated in progenitor cell proliferation control and cancer stem cell suppression. <it>TRIM3 </it>is located within the loss of allelic heterozygosity (LOH) hotspot of chromosome segment 11p15.5, indicating a potential role in tumor suppression. ...</p> <p>Methods</p> <p>Here we analyze 70 primary human gliomas of all types and grades and report somatic deletion mapping as well as single nucleotide polymorphism analysis together with quantitative real-time PCR of chromosome segment 11p15.5.</p> <p>Results</p> <p>Our analysis identifies LOH in 17 cases (24%) of primary human glioma which defines a common 130 kb-wide interval within the <it>TRIM3 </it>locus as a minimal area of loss. We further detect altered genomic dosage of <it>TRIM3 </it>in two glioma cases with LOH at 11p15.5, indicating homozygous deletions of <it>TRIM3</it>.</p> <p>Conclusion</p> <p>Loss of heterozygosity of chromosome segment 11p15.5 in malignant gliomas suggests <it>TRIM3 </it>as a candidate brain tumor suppressor gene.</p>