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Carcinoma Gene in Nasopharyngeal p 16 Hypermethylation of the Updated Version

We have recently reported that inactivation of the pi6 gene by mutation and deletion is common in nasopharyngeal carcinoma (NPC). The present study demonstrates that hypermethylation of the 5' CpG island can serve as an alternative mechanism for inactivation of the pi6 gene in this tumor. Using Southern blotting analysis and multiplex PCR, aberrant methylation of the 5' CpG island of the pI6 gene was found in a NPC xenograft (xeno-666) and 6 (22%) of 27 primary tumors, but not in normal tissues of the nasopharynx. In the NPC xenograft (xeno-666) and its newly derived cell line (cell-666), both showing hypermethylation of the pl6 gene, no piÃ2 gene expression was found. After treatment with 5-aza-2'deoxycytidine, reexpression of the piÃ2 gene was detected in the cell line cell-666. These findings suggest that aberrant methylation of the 5' CpG island may participate in the transcriptional inactivation of the piÃ2 gene in NPC. The present results further support that the piÃ2 gene is the critical target on chromosome 9p21 for inactivation during the develop ment of this disease.