| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
Human retrovirus HTLV-1 is an etiological agent for Adult T-cell leukemia/lymphoma (ATL), but additional cellular events such as aberrant modulation of signal transduction taking place for several decades after the initial HTLV-1 infection are totally unveiled. Previously we obtained highly tumorigenic populations of ATL-derived ST1 and TL-Om1 cells and found these cell populations exhibited an activated AKT signaling pathway, which may contribute to the malignancy observed in the ATL-derived cells. In this study we analyzed molecular mechanism underlying upregulation of AKT signaling in the highly tumorigenic ATL cells and found that PIK3IP1 and INPP5D, negative regulators for AKT signaling, are both inactivated in these cells. In addition, our observations suggest that activating phosphorylation of AKT might be accomplished by atypical kinase(s) in ATL cells.
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