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Here, by serial transplantation in NOG mice, we established two highly tumorigenic adult T\u2010cell leukemia\u2010derived cell lines, ST1\u2010N6 and TL\u2010Om1\u2010N8. When transplanted s.c., these cells formed tumors significantly earlier and from fewer initial cells than their parental lines ST1 and TL\u2010Om1. We found that protein kinase B (AKT) signaling was upregulated in ST1\u2010N6 and TL\u2010Om1\u2010N8 cells, and that this upregulation was due to the decreased expression of a negative regulator, INPP5D. Furthermore, the introduction of a constitutively active AKT mutant expression vector into ST1 cells augmented the tumorigenicity of the cells, whereas treatment with the AKT inhibitor MK\u20102206 attenuated the progression of tumors induced by ST1\u2010N6 cells. Collectively, our results reveal that the AKT signaling pathway plays a critical role in the malignancy of adult T\u2010cell leukemia\u2010derived cells.<\/jats:p>","DOI":"10.1111\/cas.12921","type":"journal-article","created":{"date-parts":[[2016,2,29]],"date-time":"2016-02-29T15:40:05Z","timestamp":1456760405000},"page":"638-643","source":"Crossref","is-referenced-by-count":2,"title":["Xenotransplantation elicits salient tumorigenicity of adult T\u2010cell leukemia\u2010derived cells via aberrant AKT activation"],"prefix":"10.1111","volume":"107","author":[{"given":"Kazunori","family":"Yamaguchi","sequence":"first","affiliation":[{"name":"Division of Molecular and Cellular Oncology Miyagi Cancer Center Research Institute Natori Japan"},{"name":"Department of Cancer Science Tohoku University Graduate School of Medicine Sendai Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomoka","family":"Takanashi","sequence":"additional","affiliation":[{"name":"Division of 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