Clinical usefulness of serum EBV DNA levels of BamHI W and LMP1 for Nasal NK/T-cell lymphoma
✍ Scribed by Hideyuki Ishii; Takeshi Ogino; Christoph Berger; Nicole Köchli-Schmitz; Toshihiro Nagato; Miki Takahara; David Nadal; Yasuaki Harabuchi
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 239 KB
- Volume
- 79
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
Quantitative real‐time polymerase chain reaction (PCR) was utilized to measure serum EBV DNA levels of BamHI W fragment and latent membrane protein 1 (LMP1) in 20 nasal natural killer (NK)/T‐cell lymphoma patients. Both serum EBV DNAs were detected at high levels in all patients, but the levels were below the limit of detection in all healthy controls. The BamHI Z fragment, Epstein–Barr‐replication activator (ZEBRA) expression was detected in a small proportion (0.1–3%) of lymphoma cells from 10 (50%) of the patients. Patients with ZEBRA expression showed significantly higher DNA levels of BamHI W and LMP1 (P = 0.0081, P = 0.004), suggesting that EBV DNA may be caused by EBV replication from lymphoma cells. Kaplan–Meier and univariate analyses revealed that high DNA levels of BamHI W and LMP1 at pre‐treatment and high BamHI W DNA level at post‐treatment were associated with short disease‐free survival and overall survival (P < 0.05, each). Although the DNA levels of BamHI W and LMP1 correlated significantly, their dynamics were not always parallel. Patients with low pre‐treatment level of both EBV DNAs showed a favorable course, in contrast to patients with high pre‐treatment level of both EBV DNAs who showed an aggressive course (P = 0.0085). More importantly, the high pre‐treatment level of both EBV DNAs was determined as the only independent prognostic factor among various prognostic factors. These data suggest that simultaneous measurement of serum levels of both BamHI W and LMP1 DNAs may be useful for diagnosis, disease monitoring, and prediction of prognosis for nasal NK/T‐cell lymphoma patients. J. Med. Virol. 79:562–572, 2007. © 2007 Wiley‐Liss, Inc.