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Inhibition of ABL1 tyrosine kinase reduces HTLV-1 proviral loads in peripheral blood mononuclear cells from patients with HTLV-1-associated myelopathy/tropical spastic paraparesis
by Daisuke Kodama, Masakazu Tanaka, Toshio Matsuzaki, Kimiko Izumo, Nobuaki Nakano, Eiji Matsuura, Mineki Saito, Masahiro Nagai, Masahisa Horiuchi, Atae Utsunomiya, Hiroshi Takashima, Ryuji Kubota, Shuji Izumo Human T-cell leukemia virus type 1 (HTLV-1) causes incurable adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Patients with HAM/TSP have increased levels of HTLV-1-infected cells compared with asymptomatic HTLV-1 carriers. However, the roles of cellula r genes in HTLV-1-infected CD4+ T cells await discovery. We performed microarray analysis of CD4+ T cells from HAM/TSP p...
Source: PLoS Neglected Tropical Diseases - July 14, 2020 Category: Tropical Medicine Authors: Daisuke Kodama Source Type: research

Novel Application of Radotinib for the Treatment of Solid Tumors via Natural Killer Cell Activation.
This study provides the first evidence that radotinib could be used as an effective and strong therapeutic to treat solid tumors via upregulation of NK cell cytotoxicity, suggesting that radotinib has indirect killing mechanisms via upregulation of antitumor innate immune responses as well as direct killing activities for CML cells. PMID: 30687767 [PubMed - in process]
Source: Journal of Immunology Research - January 29, 2019 Category: Allergy & Immunology Tags: J Immunol Res Source Type: research

Caspase-Independent Pathway is Related to Nilotinib Cytotoxicity in Cultured Cardiomyocytes
Conclusion: Our findings demonstrate that nilotinib increases autophagy and cathepsin B activity, leading to mitochondrial AIF release and nuclear translocation, which is responsible for p53 and apoptosis induction in H9C2 cells.Cell Physiol Biochem 2017;42:2182 –2193
Source: Cellular Physiology and Biochemistry - August 16, 2017 Category: Cytology Source Type: research

Imatinib and Nilotinib inhibit Bcr–Abl-induced ROS through targeted degradation of the NADPH oxidase subunit p22phox
In this study, using the K562 CML cell line we showed that inhibition of Bcr–Abl signalling, by either Imatinib or Nilotinib, led to a significant reduction in ROS levels which was concurrent with the GSK-3β dependent, post-translational down-regulation of the small membrane-bound protein p22phox, an essential component of the Nox complex. Furthermore, siRNA knockdown of p22phox in these cells established its importance in ROS production and proliferation. Taken together we believe our results provide a possible link between Bcr–Abl signalling and ROS production through Nox activity and demonstrate a novel mechanism o...
Source: Leukemia Research - December 5, 2012 Category: Hematology Authors: William D. Landry, John F. Woolley, Thomas G. Cotter Tags: Laboratory Studies Source Type: research