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Total 75 results found since Jan 2013.

Expression of inducible NOS is indispensable for the antiproliferative and proapoptotic effect of imatinib in BCR-ABL positive cells.
Abstract Chronic myeloid leukemia (CML) is characterized by constitutive BCR-ABL kinase activity, an aggressive proliferation of immature cells, and reduced differentiation. Targeting tyrosine kinase activity of BCR-ABL with imatinib is an effective therapy for the newly diagnosed CML patients; however, 20%-30% of the patients initially treated with imatinib eventually experience treatment failure. Therefore, early identification of these patients is of high clinical relevance. In the present study, we by undertaking a direct comparison of inducible NOS (iNOS) status in neutrophils from healthy volunteers, newly d...
Source: Journal of Leukocyte Biology - February 2, 2021 Category: Hematology Authors: Singh AK, Awasthi D, Dubey M, Nagarkoti S, Chandra T, Barthwal MK, Tripathi AK, Dikshit M Tags: J Leukoc Biol Source Type: research

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

Melanoma Cancer Immunotherapy Using PD-L1 siRNA and Imatinib Promotes Cancer-Immunity Cycle
ConclusionOverall, results revealed that the tumors treated with siPDIN restored the immunity of CTLs by potentially inhibiting the immune checkpoint interactions, suppressed the mTOR signaling pathway and exhibited an enhanced anticancer efficacy in melanoma.
Source: Pharmaceutical Research - May 30, 2020 Category: Drugs & Pharmacology Source Type: research

Arg mediates LPS-induced disruption of the pulmonary endothelial barrier.
Abstract Acute Respiratory Distress Syndrome (ARDS) is a devastating disease process that involves dysregulated inflammation and decreased alveolar-capillary barrier function. Despite increased understanding of the pathophysiology, no effective targeted therapies exist to treat ARDS. Recent preclinical studies suggest that the multi-tyrosine kinase inhibitor, imatinib, which targets the Abl kinases c-Abl and Arg, has the potential to restore endothelial dysfunction caused by inflammatory agonists. Prior work demonstrates that imatinib attenuates LPS (lipopolysaccharide)-induced vascular leak and inflammation; howe...
Source: Vascular Pharmacology - March 29, 2020 Category: Drugs & Pharmacology Authors: Rizzo AN, Belvitch P, Demeritte R, Garcia JGN, Letsiou E, Dudek SM Tags: Vascul Pharmacol Source Type: research

Inhibition of the Nrf2-TrxR Axis Sensitizes the Drug-Resistant Chronic Myelogenous Leukemia Cell Line K562/G01 to Imatinib Treatments.
Abstract Nuclear factor erythroid 2-related factor 2 (Nrf2) is involved in tumor drug resistance, but its role in imatinib resistance of chronic myeloid leukemia (CML) remains elusive. We aimed to investigate the effects of Nrf2 on drug sensitivity, thioredoxin reductase (TrxR) expression, reactive oxygen species (ROS) production, and apoptosis induction in imatinib-resistant CML K562/G01 cells and explored their potential mechanisms. Stable K562/G01 cells with knockdown of Nrf2 were established by infection of siRNA-expressing lentivirus. The mRNA and protein expression levels of Nrf2 and TrxR were determined by ...
Source: Biomed Res - December 14, 2019 Category: Research Authors: Xu L, Zhao Y, Pan F, Zhu M, Yao L, Liu Y, Feng J, Xiong J, Chen X, Ren F, Tan Y, Wang H Tags: Biomed Res Int Source Type: research

Naked antisense double-stranded DNA oligonucleotide efficiently suppresses BCR-ABL positive leukemic cells
In conclusion, ADO technology is an attractive method for therapeutic application.
Source: Investigational New Drugs - October 23, 2019 Category: Drugs & Pharmacology Source Type: research

Simvastatin preparations promote PDGF-BB secretion to repair LPS-induced endothelial injury through the PDGFR β/PI3K/Akt/IQGAP1 signalling pathway.
Simvastatin preparations promote PDGF-BB secretion to repair LPS-induced endothelial injury through the PDGFRβ/PI3K/Akt/IQGAP1 signalling pathway. J Cell Mol Med. 2019 Oct 01;: Authors: Zheng X, Zhang W, Wang Z Abstract Endothelial barrier dysfunction is a critical pathophysiological process of sepsis. Impaired endothelial cell migration is one of the main reasons for endothelial dysfunction. Statins may have a protective effect on endothelial barrier function. However, the effect and mechanism of statins on lipopolysaccharide (LPS)-induced endothelial barrier dysfunction remain unclear. Simvastatin ...
Source: J Cell Mol Med - September 30, 2019 Category: Molecular Biology Authors: Zheng X, Zhang W, Wang Z Tags: J Cell Mol Med 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

Functional interaction between PDGF and GluN2B-containing NMDA receptors in smooth muscle cell proliferation and migration in pulmonary arterial hypertension.
In this study, we explored the complex interactions between platelet-derived growth factor (PDGF) and N-methyl D-aspartate receptor (NMDAR), and their effect on the excessive proliferation and migration of smooth muscle cells leading to obstructed arteries in Pulmonary Arterial Hypertension (PAH). We report lower expression of GluN2B, a subunit composing NMDARs expected to affect cell survival/proliferation of pulmonary artery smooth muscle cells (PASMCs), in PAH patients' lungs. PASMCs exposure to PDGF-BB, stimulated immediate increased levels of phosphorylated Src family kinases (SFKs) together with increased phosphoryla...
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - December 13, 2018 Category: Cytology Authors: Quatredeniers M, Nakhleh MK, Dumas SJ, Courboulin A, Vinhas MC, Antigny F, Phan C, Guignabert C, Bendifallah I, Vocelle M, Fadel E, Dorfmüller P, Humbert M, Cohen-Kaminsky S Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

PKM2 Mediates Chronic Myeloid Leukemia Imatinib Resistance By Regulating Glycolysis Energy Metabolism
Conclusion: Pyruvate kinase M2 (PKM2) acts as an important rate-limiting enzyme in the aerobic glycolytic pathway, and mediates abnormal metabolic pathways which promote tumor cell proliferation, invasion and drug resistance. Compared to the TKI-sensitive primary cell and cell line, PKM2 was increased in the TKI-resistant primary cell and cell line and related to glycolytic level. PKM2 inhibitor can inhibit CML cells growth, induce cell apoptosis, and combined with IM at a low dose can exhibited a synergistic anti-leukemia effect on TKI-resistant cells. Low dose PKM2 inhibitor combined with IM can enhance targeted killing ...
Source: Blood - November 21, 2018 Category: Hematology Authors: Tong, L., Xu, N., Zhou, X., Huang, J., wan-Er, W., Chen, C., Liang, L., Liu, Q., Xiaoli, L. Tags: 631. Chronic Myeloid Leukemia: Biology and Pathophysiology, excluding Therapy: Poster I Source Type: research

Aurora Kinase a/MDM2-Mediated SETD2 Loss of Function in Chronic Myeloid Leukemia Patients in Blast Crisis Induces Genetic Instability and Can be Therapeutically Targeted
In conclusion, phosphorylation by Aurora Kinase A and ubiquitination by MDM2 contribute to SETD2 non-genomic loss of function in advanced-phase CML. Loss of SETD2/H3K36me3 is associated with increased DNA damage and impaired HR repair. Restoring physiological H3K36me3 levels may help improve the outcome of this critical subset of pts.Acknowledgments: study supported by AIRC (project code 16996) and AIL (Associazione Italiana contro le Leucemia, Linfomi e Mieloma).Figure 1.DisclosuresCastagnetti: Incyte: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; Bristol Meyers Squibb: Consultancy, Honoraria; Novartis: Consulta...
Source: Blood - November 21, 2018 Category: Hematology Authors: Mancini, M., De Santis, S., Monaldi, C., Bavaro, L., Martelli, M., Castagnetti, F., Gugliotta, G., Rosti, G., Fontana, M. C., Dan, E., Sinigaglia, B., Iurlo, A., Orofino, N., Abruzzese, E., Salvucci, M., Pregno, P., Gozzini, A., Crugnola, M., Albano, F., Tags: 631. Chronic Myeloid Leukemia: Biology and Pathophysiology, excluding Therapy: Poster I Source Type: research

Concomitant Targeting of FLT3 and BTK with CG'806 Overcomes FLT3-Inhibitor Resistance through Inhibition of Autophagy
Fms-like tyrosine kinase 3 (FLT3)-targeted therapy represents an important paradigm in the management of patients with highly aggressive FLT3 mutated acute myeloid leukemia (AML). However, clinical efficacy is usually transient and followed by emergence of resistance to FLT3-inhibitors (Borthakur et al., 2011; Cortes et al., 2013; Zhang et al., 2008). Such resistance often results from acquired mutations of TKD, which are frequently identified in D835, Y842 and F691 residues (Smith et al., 2015; Smith et al., 2012; Zhang et al., 2014). It was reported that the FLT3-ITD-targeting drug sorafenib can induce autophagy in human...
Source: Blood - November 21, 2018 Category: Hematology Authors: Zhang, W., Yu, G., Zhang, H., Ly, C., Yuan, B., Ruvolo, V., Piya, S., Bhattacharya, S., Zhang, Q., Borthakur, G., Battula, V. L., Konopleva, M. Y., Rice, W. G., Andreeff, M. Tags: 604. Molecular Pharmacology and Drug Resistance in Myeloid Diseases: Poster II Source Type: research

c-Abl phosphorylation of Yin Yang 1's conserved tyrosine 254 in the spacer region modulates its transcriptional activity
In conclusion, we demonstrate the novel role of c-Abl kinase in regulation of YY1's transcriptional activity, linking YY1 regulation with c-Abl tyrosine kinase signaling pathways.Graphical abstract
Source: Biochimica et Biophysica Acta (BBA) Molecular Cell Research - July 11, 2018 Category: Molecular Biology Source Type: research

Montelukast, a cysteinyl leukotriene receptor antagonist, inhibits the growth of chronic myeloid leukemia cells through apoptosis.
Authors: Zovko A, Yektaei-Karin E, Salamon D, Nilsson A, Wallvik J, Stenke L Abstract The clinical outcome for patients with chronic myeloid leukemia (CML) has improved significantly with the introduction of tyrosine kinase inhibitors (TKIs). However, their curative potential appears limited, probably as a consequence of TKI-resistant leukemic stem cells (LSCs) that persist as a result of aberrant pathways independent of the well-established oncoprotein Bcr-Abl. One such pathway involves signaling through leukotrienes (LTs), bioactive compounds that have been suggested to play a role in several other malignancies. ...
Source: Oncology Reports - June 1, 2018 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research