Identification of ATLL-associated genes in Rapid ATLL model mouse

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K14388
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: National Institute of Infectious Diseases
• Principal Investigator: Saito Masumichi 国立感染症研究所, 血液・安全性研究部, 主任研究官 (20571045)
• Co-Investigator(Kenkyū-buntansha): 日吉 真照 国立感染症研究所, 血液・安全性研究部, 主任研究官 (40448519)
• Co-Investigator(Renkei-kenkyūsha): HIDEKATSU Iha 大分大学, 医学部, 准教授 (50242631) ; HIROO Hasegawa 長崎大学, 医学部, 准教授 (00398166)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 実験動物モデル

Outline of Final Research Achievements

In ATLL model mouse, we found that point mutations and 5’deletions of HTLV-1 induce HBZ activation. Furthermore, the HBZ activation mechanism on HTLV-1 carrying the deletion was due to disruption of mir-324-3P mediated HBZ repression. Interestingly, we also found that mir-324-3P was deleted in about 40% of ATLL cases. This result strongly suggests that mir-324-3P might function as a tumor suppressor gene in the process of ATLL development

Free Research Field

総合生物、腫瘍学