Epstein-Barr Virus and Human Cancer

(l)我们证明EBV相关胃癌（EBV aGC）在发展的早期阶段甚至在胃粘膜中表现出克隆增殖。癌伴多癌感染EBV。(2)我们确定EBV aGC发生在慢性萎缩性胃炎前，与胃粘膜边界密切相关，是胃管结构重塑的地方。(3)我们发现了一种新的EBV aGC， EBV感染在一小部分癌中受到限制。从癌变部分和非癌变部分分别建立了2株EBV感染细胞株。(4)我们重新评估了鼻T/NK细胞淋巴瘤起源于NK细胞，并确定了细胞中EBV潜伏期2型感染。(5)我们证实了致死性中线肉芽肿（进行性坏疽性鼻炎）起源于NK细胞或T细胞，并建立了具有淋巴瘤特征的细胞系。所有细胞系均为EBV阳性NK细胞，6号染色体异常伴长臂缺失。(6)我们定义了脓胸相关淋巴瘤和鼻自然杀伤细胞淋巴瘤逃避细胞毒性t细胞介导的免疫监视机制的差异。(7)我们对ena - lp进行了表征，并确定了ena - lp在细胞质中的表达、与细胞调节因子HAX-1的共定位和同质二聚化。(8)我们分析了LMP-l的c端区域对细胞凋亡的调控至关重要，bhrb通过抑制caspase 8活性抑制TRAIL细胞凋亡。

(l) We demonstrated that EBV associated gastric carcinomas (EBV aGC) represent a clonal proliferation even in gastric mucosa at very early stages of the development. The carcinomas accompany with multiple carcinomas infected with EBV.(2) We defined that EBV aGC develops in front of chronic atrophic gastritis and associates closely with the gastric mucosa border which is the place for remodel of tubular structures.(3) We found a new type of EBV aGC which EBV infection is restricted in a small portion of the carcinoma. Two EBV infected cell lines were established from the cancerous and non-cancerous portions, respectively.(4) We re-evaluated that nasal T/NK cell lymphomas were originated from NK cells and defined the EBV latency type 2 infection in the cells.(5) We demonstrated that lethal midline granuloma (rhintis gangrenosa progressiva) is originated from NK or T cells and established the cell lines which have the characters of the lymphoma. The all cell lines were EBV positive NK cells and had the abnormality of chromosom 6 accompanied with a deletion of the long arm.(6) We defined the difference of escaping to cytotoxic T-cell mediated immune surveillance mechanisms between pyothorax-associated lymphoma and nasal natural killer-cell lymphoma.(7) We characterized EBNA-LP and defined the expression in cytoplasm and the co-localization with a cellular regulating factor HAX-1 and homo-dimelization of EBNA-LP.(8) We analyzed that the C-terminal regions of LMP-l is critical for the regulation of apoptosis and BHRFinhibits the apoptosis with TRAIL by suppression of caspase 8 activity.