OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib
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AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABLPharmacogenetics of BCR/ABL Inhibitors in Chronic Myeloid LeukemiaIntracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cellsApplication of multiplexed kinase inhibitor beads to study kinome adaptations in drug-resistant leukemiaEsters of Bendamustine Are by Far More Potent Cytotoxic Agents than the Parent Compound against Human Sarcoma and Carcinoma CellsTyrosine kinase inhibitors in chronic myeloid leukaemia: which, when, for whom?Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells.Combination of low-dose imatinib plus nilotinib for the treatment of chronic-phase chronic myeloid leukaemia after imatinib failure.Importance of Drug Pharmacokinetics at the Site of ActionSelecting the best frontline treatment in chronic myeloid leukemiaMetabolism considerations for kinase inhibitors in cancer treatmentDownregulation of organic cation transporters OCT1 (SLC22A1) and OCT3 (SLC22A3) in human hepatocellular carcinoma and their prognostic significance.Phase III study of nilotinib versus best supportive care with or without a TKI in patients with gastrointestinal stromal tumors resistant to or intolerant of imatinib and sunitinib.In vitro and in vivo identification of ABCB1 as an efflux transporter of bosutinib.Modelling Predictors of Molecular Response to Frontline Imatinib for Patients with Chronic Myeloid Leukaemia.Treatment of human pre-B acute lymphoblastic leukemia with the Aurora kinase inhibitor PHA-739358 (Danusertib)Management of imatinib-resistant patients with chronic myeloid leukemia.Tailoring tyrosine kinase inhibitor therapy in chronic myeloid leukemia.Interaction of nilotinib, dasatinib and bosutinib with ABCB1 and ABCG2: implications for altered anti-cancer effects and pharmacological propertiesAdvances in treatment of chronic myelogenous leukemia--new treatment options with tyrosine kinase inhibitors.Insights into the stem cells of chronic myeloid leukemia.Targeting the BCR-ABL tyrosine kinase in chronic myeloid leukemia as a model of rational drug design in cancer.Tyrosine kinase inhibitors as modulators of ATP binding cassette multidrug transporters: substrates, chemosensitizers or inducers of acquired multidrug resistance?Evolving treatment strategies for patients newly diagnosed with chronic myeloid leukemia: the role of second-generation BCR-ABL inhibitors as first-line therapy.Prognostic Significance of Treatment Response in CML in View of Current Recommendations for Treatment and Monitoring.Multidrug resistance in chronic myeloid leukaemia: how much can we learn from MDR-CML cell lines?Individualizing kinase-targeted cancer therapy: the paradigm of chronic myeloid leukemia.Combination therapy with nilotinib for drug-sensitive and drug-resistant BCR-ABL-positive leukemia and other malignancies.Physicochemical properties of novel protein kinase inhibitors in relation to their substrate specificity for drug transporters.Transporter-Mediated Disposition of Opioids: Implications for Clinical Drug Interactions.OCT1 and imatinib transport in CML: is it clinically relevant?Role of SLC22A1 polymorphic variants in drug disposition, therapeutic responses, and drug-drug interactions.Considering baseline factors and early response rates to optimize therapy for chronic myeloid leukemia in chronic phase.Treatment of chronic myeloid leukemia: assessing risk, monitoring response, and optimizing outcome.The Role of Transporters in the Toxicity of Chemotherapeutic Drugs: Focus on Transporters for Organic Cations.hOCT1 gene expression predict for optimal response to Imatinib in Tunisian patients with chronic myeloid leukemia.A preclinical study demonstrating the efficacy of nilotinib in inhibiting the growth of pediatric high-grade glioma.Advances and challenges in hereditary cancer pharmacogenetics.Pharmacogenetics of drug transporters in modulating imatinib disposition and treatment outcomes in chronic myeloid leukemia & gastrointestinal stromal tumor patients.Endoplasmic reticulum stress-mediated apoptosis in imatinib-resistant leukemic K562-r cells triggered by AMN107 combined with arsenic trioxide.
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OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib
description
im Juli 2006 veröffentlichter wissenschaftlicher Artikel
@de
scientific article published on 04 April 2006
@en
wetenschappelijk artikel
@nl
наукова стаття, опублікована в липні 2006
@uk
name
OCT-1-mediated influx is a key ...... vitro sensitivity to imatinib
@en
OCT-1-mediated influx is a key ...... of imatinib but not nilotinib
@nl
type
label
OCT-1-mediated influx is a key ...... vitro sensitivity to imatinib
@en
OCT-1-mediated influx is a key ...... of imatinib but not nilotinib
@nl
prefLabel
OCT-1-mediated influx is a key ...... vitro sensitivity to imatinib
@en
OCT-1-mediated influx is a key ...... of imatinib but not nilotinib
@nl
P2093
P1433
P1476
OCT-1-mediated influx is a key ...... vitro sensitivity to imatinib
@en
P2093
Antony C Cambareri
Jane Engler
Paul W Manley
Phuong Dang
Steven R Quinn
Timothy P Hughes
Verity A Saunders
P304
P356
10.1182/BLOOD-2005-11-4687
P407
P577
2006-04-04T00:00:00Z