Nilotinib concentration in cell lines and primary CD34(+) chronic myeloid leukemia cells is not mediated by active uptake or efflux by major drug transporters.
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Management of Chronic Myeloid Leukemia Patients Resistant to Tyrosine Kinase Inhibitors TreatmentPharmacogenetics of BCR/ABL Inhibitors in Chronic Myeloid LeukemiaIntracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cellsNilotinib counteracts P-glycoprotein-mediated multidrug resistance and synergizes the antitumoral effect of doxorubicin in soft tissue sarcomasPTEN regulates BCRP/ABCG2 and the side population through the PI3K/Akt pathway in chronic myeloid leukemiaComparison of ATP-binding cassette transporter interactions with the tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib.Practical advice for determining the role of BCR-ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia.Metabolism considerations for kinase inhibitors in cancer treatmentNCCN Task Force report: tyrosine kinase inhibitor therapy selection in the management of patients with chronic myelogenous leukemiaInteractions of tyrosine kinase inhibitors with organic cation transporters and multidrug and toxic compound extrusion proteinsSynthesis and characterization of a BODIPY conjugate of the BCR-ABL kinase inhibitor Tasigna (nilotinib): evidence for transport of Tasigna and its fluorescent derivative by ABC drug transporters.Interaction of innovative small molecule drugs used for cancer therapy with drug transporters.In vitro and in vivo identification of ABCB1 as an efflux transporter of bosutinib.Tyrosine kinase inhibitors as modulators of ABC transporter-mediated drug resistance.Drug Resistance Mechanisms in Non-Small Cell Lung Carcinoma.Mechanisms of resistance to BCR-ABL kinase inhibitors.Evolving treatment strategies for patients newly diagnosed with chronic myeloid leukemia: the role of second-generation BCR-ABL inhibitors as first-line therapy.Selection of therapy: rational decisions based on molecular events.Breast cancer resistance protein (BCRP/ABCG2): its role in multidrug resistance and regulation of its gene expression.Targeted therapy for patients with chronic myeloid leukemia: clinical trial experience and challenges in inter-trial comparisons.BCR-ABL1 kinase domain mutations: methodology and clinical evaluation.Interaction of the efflux transporters ABCB1 and ABCG2 with imatinib, nilotinib, and dasatinib.Kinase-inhibitor-insensitive cancer stem cells in chronic myeloid leukemia.Physicochemical properties of novel protein kinase inhibitors in relation to their substrate specificity for drug transporters.OCT1 and imatinib transport in CML: is it clinically relevant?Misoprostol-induced fever and genetic polymorphisms in drug transporters SLCO1B1 and ABCC4 in women of Latin American and European ancestry.Effect of bosutinib on the absorption of dabigatran etexilate mesylate, a P-glycoprotein substrate, in healthy subjects.Nilotinib alone or in combination with selumetinib is a drug candidate for neurofibromatosis type 2.BCR-ABL1-independent PI3Kinase activation causing imatinib-resistance.Nilotinib: evaluation and analysis of its role in chronic myeloid leukemia.Dasatinib targets chronic myeloid leukemia-CD34+ progenitors as effectively as it targets mature cells.Population pharmacokinetic and exposure-response analysis of nilotinib in patients with newly diagnosed Ph+ chronic myeloid leukemia in chronic phase.Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis.Nilotinib does not significantly reduce imatinib OCT-1 activity in either cell lines or primary CML cells.Chronic myeloid leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 activity.Nilotinib-mediated inhibition of ABCB1 increases intracellular concentration of dasatinib in CML cells: implications for combination TKI therapy.Degree of kinase inhibition achieved in vitro by imatinib and nilotinib is decreased by high levels of ABCB1 but not ABCG2.Tyrosinekinase inhibition facilitates cooperation of transcription factor SALL4 and ABC transporter A3 towards intrinsic CML cell drug resistance.Chronic myeloid leukemia: the paradigm of targeting oncogenic tyrosine kinase signaling and counteracting resistance for successful cancer therapy.Effects of rifampin and ketoconazole on the pharmacokinetics of nilotinib in healthy participants.
P2860
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P2860
Nilotinib concentration in cell lines and primary CD34(+) chronic myeloid leukemia cells is not mediated by active uptake or efflux by major drug transporters.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
@zh
2009年學術文章
@zh-hant
name
Nilotinib concentration in cell lines and primary CD34
@nl
Nilotinib concentration in cel ...... ux by major drug transporters.
@en
type
label
Nilotinib concentration in cell lines and primary CD34
@nl
Nilotinib concentration in cel ...... ux by major drug transporters.
@en
altLabel
Nilotinib concentration in cel ...... lux by major drug transporters
@en
prefLabel
Nilotinib concentration in cell lines and primary CD34
@nl
Nilotinib concentration in cel ...... ux by major drug transporters.
@en
P2093
P2860
P50
P356
P1433
P1476
Nilotinib concentration in cel ...... lux by major drug transporters
@en
P2093
N E Jordanides
R J Harris
S Hatziieremia
P2860
P2888
P304
P356
10.1038/LEU.2009.166
P50
P577
2009-08-27T00:00:00Z