Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity
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Pharmacogenetics of BCR/ABL Inhibitors in Chronic Myeloid LeukemiaTyrosine kinase inhibitors in chronic myeloid leukaemia: which, when, for whom?MATE1 regulates cellular uptake and sensitivity to imatinib in CML patientsImatinib plasma trough concentration and its correlation with characteristics and response in Chinese CML patients.Genotypes of SLC22A4 and SLC22A5 regulatory loci are predictive of the response of chronic myeloid leukemia patients to imatinib treatment.Selecting 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.Using functional genomics to overcome therapeutic resistance in hematological malignancies.The choice of first-line chronic myelogenous leukemia treatment.Modelling Predictors of Molecular Response to Frontline Imatinib for Patients with Chronic Myeloid Leukaemia.Comparison of mutated ABL1 and JAK2 as oncogenes and drug targets in myeloproliferative disordersDo we have to kill the last CML cell?Targeting the BCR-ABL tyrosine kinase in chronic myeloid leukemia as a model of rational drug design in cancer.Evolving treatment strategies for patients newly diagnosed with chronic myeloid leukemia: the role of second-generation BCR-ABL inhibitors as first-line therapy.Targeted therapy for patients with chronic myeloid leukemia: clinical trial experience and challenges in inter-trial comparisons.Mechanisms and novel approaches in overriding tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Advances in treatment of chronic myeloid leukemia with tyrosine kinase inhibitors: the evolving role of Bcr-Abl mutations and mutational analysis.Prognostic Significance of Treatment Response in CML in View of Current Recommendations for Treatment and Monitoring.The EUTOS prognostic score: review and validation in 1288 patients with CML treated frontline with imatinib.Which tyrosine-kinase inhibitor to use first in chronic phase chronic myelogenous leukemia?OCT1 and imatinib transport in CML: is it clinically relevant?Chronic myeloid leukemia: First-line drug of choice.Current trends in molecular diagnostics of chronic myeloid leukemia.Dynamics of Expression of Drug Transporters: Methods for Appraisal.Chronic Myeloid Leukemia in the Era of Tyrosine Kinase Inhibitors: An Evolving Paradigm of Molecularly Targeted Therapy.hOCT1 gene expression predict for optimal response to Imatinib in Tunisian patients with chronic myeloid leukemia.Evidence that the pregnane X and retinoid receptors PXR, RAR and RXR may regulate transcription of the transporter hOCT1 in chronic myeloid leukaemia cells.Pharmacogenetics of drug transporters in modulating imatinib disposition and treatment outcomes in chronic myeloid leukemia & gastrointestinal stromal tumor patients.Dasatinib rapidly induces deep molecular response in chronic-phase chronic myeloid leukemia patients who achieved major molecular response with detectable levels of BCR-ABL1 transcripts by imatinib therapy.Intelligent Techniques Using Molecular Data Analysis in Leukaemia: An Opportunity for Personalized Medicine Support System.Chronic myeloid leukemia 2011: successes, challenges, and strategies--proceedings of the 5th annual BCR-ABL1 positive and BCR-ABL1 negative myeloproliferative neoplasms workshop.The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia.OCT-1 activity measurement provides a superior imatinib response predictor than screening for single-nucleotide polymorphisms of OCT-1.Synergistic activity of the Src/Abl inhibitor bosutinib in combination with imatinib.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.BCR-ABL1-induced downregulation of WASP in chronic myeloid leukemia involves epigenetic modification and contributes to malignancy.OCT1 (SLC22A1) R61C polymorphism and response to imatinib treatment in chronic myeloid leukemia patients.Reduced ABCG2 and increased SLC22A1 mRNA expression are associated with imatinib response in chronic myeloid leukemia.
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Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity
description
article
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im Dezember 2007 veröffentlichter wissenschaftlicher Artikel
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wetenschappelijk artikel
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наукова стаття, опублікована в грудні 2007
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name
Most CML patients who have a s ...... e impact of low OCT-1 activity
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Most CML patients who have a s ...... e impact of low OCT-1 activity
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type
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Most CML patients who have a s ...... e impact of low OCT-1 activity
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Most CML patients who have a s ...... e impact of low OCT-1 activity
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Most CML patients who have a s ...... e impact of low OCT-1 activity
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Most CML patients who have a s ...... e impact of low OCT-1 activity
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P2093
P1433
P1476
Most CML patients who have a s ...... e impact of low OCT-1 activity
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Amity Venables
Jane Engler
Kevin Lynch
Paul W Manley
Phuong Dang
Stephanie Zrim
Timothy Hughes
Verity A Saunders
P304
P356
10.1182/BLOOD-2007-06-093617
P407
P577
2007-08-30T00:00:00Z