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EBV Conference 2008 Guangzhou - Baylor College of Medicine

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20 (RegID: 1132)<br />

Qian Tao<br />

Institution: Chinese University <strong>of</strong> Hong Kong<br />

e-mail: qtao@clo.cuhk.edu.hk<br />

EPIGENETIC ETIOLOGY OF NASOPHARYNGEAL CARCINOMA<br />

Qian Tao<br />

Oralabstract:<br />

Carcinogenesis is a multi-step process, involving multiple genetic and epigenetic alterations including the<br />

epigenetic disruption <strong>of</strong> tumor suppressor genes (TSGs) through promoter CpG methylation. The frequent<br />

presence <strong>of</strong> epigenetic abnormalities in tumor cells provides us with potential epigenetic biomarkers for<br />

molecular cancer diagnosis and also a novel way <strong>of</strong> identifying new TSGs. Using DNA methyltransferase<br />

inhibitors as demethylation agents, epigenetic inactivation <strong>of</strong> TSGs can also be reversed and exploited as a<br />

cancer therapeutic strategy. Using nasopharyngeal carcinoma (NPC) as a tumor model which is prevalent<br />

in southern China, I attempted to identify epigenetically inactivated novel TSGs, by employing integrative<br />

epigenetic/genomic approaches such as methylation subtraction, array-CGH, high-throughput expression<br />

pr<strong>of</strong>iling coupled with methylation analysis, and functional studies. A few novel candidate TSGs have<br />

been identified, including cell signaling-related and transcriptional regulatory genes. These genes are<br />

frequently methylated and downregulated in common tumors including NPC. Functional analyses showed<br />

that these candidate genes could induce apoptosis <strong>of</strong> tumor cells and suppress tumor cell growth, are thus<br />

functional TSGs. The epigenetic silencing <strong>of</strong> these TSGs would disrupt normal cell signaling control and<br />

contribute to NPC pathogenesis.<br />

<strong>EBV</strong> <strong>Conference</strong> <strong>2008</strong> <strong>Guangzhou</strong><br />

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