Grant-in-Aid for Scientific Research on Priority Areas.
|Research Institution||Tottori University Faculty of Medicine|
SAIRENJI Takeshi Tottori University Faculty of Medicine, Department of Biosignaling, Professor, 医学部, 教授 (10117351)
YANAI Hideo Yamaguchi University School of Medicine, Department of Internal Medicine, Instructor, 医学部, 講師 (60220175)
FUKAYAMA Masashi Graduate School of Medicine, Tokyo University, Department of Pathology, Professor, 医学部, 教授 (70281293)
AOZASA Katsuyuki Osaka University Medical School, Department of Pathology, Professor, 医学部, 教授 (30115985)
徳永 正義 鹿児島大学, 医学部, 講師 (80041317)
HIRAI Kanji Medical Research Institute, Tokyo Medical and Dental University, Department of Tumor Virology, Professor, 難治疾患研究所, 教授 (00100991)
EIZURU Yoshito Kagoshima University School of Medicine, Division of Persisten and Oncogenic Viruses, Professor, 医学部, 教授 (00041351)
|Project Fiscal Year
1999 – 2000
Completed(Fiscal Year 2000)
|Budget Amount *help
¥105,000,000 (Direct Cost : ¥105,000,000)
Fiscal Year 1999 : ¥35,000,000 (Direct Cost : ¥35,000,000)
Fiscal Year 1998 : ¥35,000,000 (Direct Cost : ¥35,000,000)
Fiscal Year 1997 : ¥35,000,000 (Direct Cost : ¥35,000,000)
|Keywords||Epstein-Barr virus (EBV) / EBV associated gastric cancer / EBV associated malignant lymphoma / NK lymphoma / LMP1 / tumorigenesis / EBV positive cell lines / apoptosis / EBウイルス(EBV) / EBV関連胃癌 / EBV関連悪性リンパ腫 / EBV発がん / EBV感染細胞株 / NKリンパ腫 / EBNA-LP / アポトーシス / EBV関連悪性りンパ腫 / SCIDマウス / LMPl / 腫瘍形成 / EBV感染 / 胃癌 / 悪性リンパ腫 / SCIPマウス / 腫瘍発生 / EBV細胞株|
(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.