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Ann Thorac Surg 2005;79:1180-1188
© 2005 The Society of Thoracic Surgeons
Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, Cancer Research Institute, Xenotransplantation Research Center, Seoul National University College of Medicine, Seoul, Korea
Accepted for publication September 21, 2004.
* Address reprint requests to Dr Y. T. Kim, Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, 28 Yongon-Dong, Chongno-Gu, Seoul, 110–744, Republic of Korea (E-mail: ytkim{at}snu.ac.kr).
Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.
BACKGROUND: Aberrant methylation of CpG islands acquired in tumor cells in promoter regions is one cause for the loss of gene function. We examined whether aberrant DNA hypermethylation could be used to predict the clinical outcomes of patients with primary nonsmall cell lung cancer (NSCLC) after curative resection.
METHODS: We tested 61 patients with NSCLC using methylation-specific polymerase chain reaction (MSP) and searched for promoter hypermethylation of the genes p16INK4a, retinoic acid receptor ß-promoter (RARßP2), death-associated protein kinase (DAPK), and O6-methylguanine-DNA-methyltransferase (MGMT). The clinical data, the presence of DNA hypermethylation, and clinical outcomes were analyzed.
RESULTS: Hypermethylation in the tumor samples was detected in 67% (41 of 61) for p16INK4a, 49% (30 of 61) for RARßP2, 30% (18 of 61) for DAPK, and 62% (38 of 61) for MGMT. Thirty patients (49%) developed recurrence within 33 months; 16 in the remaining lung, 10 in other organs, and 4 in both. We found no correlation between the specific DNA hypermethylation and any of the clinicopathological characteristics of the patients. DNA hypermethylation was not associated with a different survival or recurrence rate. However, the aberrant hypermethylation of RARßP2 seemed to be related to the location of cancer recurrence. Although advanced T stage and preoperative chemotherapy were statistically significant in univariate analysis, unmethylation of DAPK (p = 0.030) and hypermethylation of RARßP2 (p = 0.014), as well as advanced T stage (p = 0.075) and preoperative chemotherapy (p = 0.025), were significant risk factors in multivariate analysis for early recurrence in the remaining lung.
CONCLUSIONS: The P2 hypermethylation of the RARß gene and unmethylation of DAPK seem to be important factors in predicting early cancer recurrence in the remaining lung and could be used as a prognostic marker in NSCLC. However, the clinical implications of this finding need further investigation.
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