Erman L, Baruchel A, Goekbuget N, Schrappe M, Pui CH. L-asparaginase
Erman L, Baruchel A, Goekbuget N, Schrappe M, Pui CH. L-asparaginase therapy in acute lymphoblastic leukemia: a concentrate on Erwinia asparaginase. Cancer. 2011; 117: 23849. eight. Verma N, Kumar K, Kaur G, Anand S. L-asparaginase: a promising chemotherapeutic agent. Crit Rev Biotechnol. 2007; 27:452. 9. Stams WA, den Boer ML, Holleman A, Appel IM, Beverloo HB, van Wering ER, Janka-Schaub GE, Evans WE, Pieters R. Asparagine synthetase expression is linked with L-asparaginase resistance in TEL-AML1-negative but not TEL-AML1-positive pediatric acute lymphoblastic leukemia. Blood. 2005; 105:4223225. ten. Covini D, Tardito S, Bussolati O, Chiarelli LR, Pasquetto MV, Digilio R, Valentini G, Scotti C. Expanding targets for a metabolic therapy of cancer: L-asparaginase. Current Pat Anticancer Drug Discov. 2012; 7:43. 11. Iwamoto S, Mihara K, Downing JR, Pui CH, Campana D. Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase. J Clin Invest. 2007; 117:1049057. 12. Douer D, Aldoss I, Lunning MA, Burke PW, Ramezani L, Mark L, Vrona J, Park JH, Tallman MS, Avramis VI, Pullarkat V, Mohrbacher AM. Pharmacokinetics-based integration of IL-13 Protein custom synthesis several doses of intravenous pegaspargase in a pediatric regimen for adults with newly diagnosed acute lymphoblastic leukemia. J Clin Oncol. 2014; 32:90511. 13. Kobrinsky NL, Sposto R, Shah NR, Anderson JR, DeLaat C, Morse M, Warkentin P, Gilchrist GS, Cohen MD, 3871 OncotargetConfocal microscopyK562 and KU812 cells were seeded into 6-well plates at a density of 1 105mL after which treated with 0.five IUmL of asparaginase. After 24 h of incubation, cells were stained with Cyto-IDGreen dye and Hoechst 33342 at 37 for 30 min according to the manufacturer’s protocol. Then the cells have been washed and re-suspended with PBS. A drop on the cell suspension had been taken to a glass microscope slide and overlaid having a coverslip and promptly analyzed by confocal microscopy. Good controls had been treated with all the autophagy inducer Rapamycin at 50 nM for 12 h, and disposed with same measures. All of the procedures have been accomplished inside the dark location.Statistical analysisData from this study have been presented as imply values with standard deviations (SD). The statistical significance of the variations among groups was evaluated by Student t test. , , and indicated P 0.05, P 0.01 and P 0.001, respectively.ACKNOWLEDGMENTSThis study was supported by National Essential Simple Analysis System of China (2013CB932502, 2015CB931800) and Shanghai Science and Technology Funds (14431900200, 13431900303, 11431920104).
Chronic myeloid leukemia (CML) is often a hematopoietic stem cell illness integrated within the broader diagnostic category of myeloproliferative neoplasms [1] that may be characterized by neoplastic overproduction of mainly granulocytes. CML is consistently linked with fusion by chromosome translocation from the breakpoint cluster area gene (BCR) at chromosome 22q11 towards the Abelson gene (ABL1) at chromosome 9q34. This fusion gene BCRABL1 encodes for an oncoprotein (P210, additional hardly ever P190 or P230) using a robust constitutive activated tyrosine kinase activity inducing many downstream signals causing the transformation of hemopoietic stem cells [2]. The translocation t(9;22) may very well be detected by routine karyotype as Philadelphia (Ph) chromosome, while in 20 from the situations, the fusion gene arises from a variant translocation [3]. Two variant subgroups have been recognized: the easy variant group with the 22q IL-3 Protein Biological Activity segment translocated onch.