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Methylation Status of Epstein-Barr Virus Major Latent Promoter C in NK/T-cell Lymphoma and Peripheral T-cell Lymphoma.
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Original Article Methylation Status of Epstein-Barr Virus Major Latent Promoter C in NK/T-cell Lymphoma and Peripheral T-cell Lymphoma.
Ji Eun Kim, Young A Kim, Sung Shin Park, Yoon Kyoun Jeon, Seung Sook Lee, Chul Woo Kim
Journal of Pathology and Translational Medicine 2003;37(3):174-179
DOI: https://doi.org/
1Department of Pathology, Seoul Municipal Boramae Hospital, Seoul, Korea.
2Tumor Immunity Medical Research Center and Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
3Department of Pathology, Korea Cancer Center Hospi, Korea.
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BACKGROUND
Both the Natural killer/T-cell lymphoma (NKTL) and the peripheral T-cell lymphoma (PTCL) are relatively prevalent in the Asian population, and they are strongly associated with the Epstein-Barr virus (EBV). These two diseases have several common pathologic features, but show somewhat different clinical presentations. The critical point in terms of differentiating of these disease groups might be the impact of EBV in pathogenesis, and the variable gene expression of EBV regulated by a major latent C promoter (Cp).
METHODS
We investigated 43 cases of NKTL and 30 cases of PTCL to evaluate EBV associated characteristics. EBV in situ hybridization was performed in all of the submitted cases. In the EBV positive cases, the methylation status of Cp which drives the expression of immunodominant viral nuclear protein, was examined by sensitive methylation specific PCR using paraffin embedded tissue.
RESULTS
EBV was found in 70% (30/43) of NKTL and 43% (13/30) of PTCL. Nasal and gastrointestinal lymphomas were predominantly NKTL. All of the successfully amplified cases of EBV positive NKTL and PTCL were of methylated Cp status.
CONCLUSIONS
The detection rate of EBV is high in NKTL, especially in the nasal area. The constantly methylated EBV Cp reflects the major role of Cp in regulating the EBV latency pattern and in helping EBV to avoid host immune system in both NKTL and PTCL.

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