About: 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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About: 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 Goto Sponge NotDistinct Permalink

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scientific article published on 04 April 2006

Attributes	Values
rdf:type	Item
description	wetenschappelijk artikel (nl) article scientifique publié en 2006 (fr) наукова стаття, опублікована в липні 2006 (uk) im Juli 2006 veröffentlichter wissenschaftlicher Artikel (de) artículu científicu espublizáu n'abril de 2006 (ast) scientific article published on 04 April 2006 (en)
publication date	wds:Q59236733-81E02056-0495-4BFE-9180-FD172CCC8C13
publication date	2006-04-04 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q59236733-436B016B-656D-4109-9D69-F2F25845C487
language of work or name	English
author name string	wds:Q59236733-00821201-5AED-48B9-80E8-DE05FB819870 wds:Q59236733-7B312FA1-0058-46C8-B7E8-819CB1F27FC5 wds:Q59236733-8ABFAE69-916B-46D2-9E53-9EF150119183 wds:Q59236733-AD8EC816-4796-4060-8342-0C2E11C5E690 wds:Q59236733-C4144525-FDF0-4F98-BD5F-752257CEC229 wds:Q59236733-D7249ED9-5801-4594-9D4A-6D12854BB768 wds:Q59236733-DAC2A17F-54AA-4459-9D14-CC1B2164A4EB
author name string	Phuong Dang Timothy P Hughes Verity A Saunders Paul W Manley Jane Engler Antony C Cambareri Steven R Quinn
rdfs:label	OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (nl) 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 (en)
skos:prefLabel	OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (nl) 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 (en)
name	OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (nl) 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 (en)
author	wds:Q59236733-3F23AF3F-EC3C-4A24-BDCB-AECFC20B2A84 wds:Q59236733-41C72083-B710-4719-B03E-5A602CF92817
author	Deborah L. White Andrew Zannettino
title	wds:Q59236733-D568F97A-860B-430E-AACA-6A826E55DCFD
title	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 (en)
page(s)	wds:Q59236733-52D06AD2-800D-4CC2-A859-9ED5B3F02D44
page(s)	697-704
instance of	wds:Q59236733-166CA10A-E910-4DBC-A551-7D53AA21D88C
instance of	scholarly article
main subject	wds:Q59236733-4D2EFC36-960F-486F-8D1B-4356D89658D6
main subject	wd:Q177094
PubMed ID	wds:Q59236733-F30C1F8D-F8E0-4F9B-A4EA-746791322550
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/16597591
PubMed ID	16597591
published in	wds:Q59236733-AE1BD629-35B9-4B0C-9CDC-3D6BA195DA1F
published in	Blood
issue	wds:Q59236733-D80DE06C-3AE2-4A29-B29C-0BB18A518993
volume	wds:Q59236733-E1054BBA-69DA-4B73-9ECE-969A3AB305B2
issue	2
volume	108
number of pages	wds:Q59236733-02A23553-FE46-4907-8C08-2E0C181CBB2A
number of pages	8 (xsd:decimal)
DOI	wds:Q59236733-0E753E43-984F-48CC-B92B-79F2658FDEF9
DOI	http://dx.doi.org/10.1182/BLOOD-2005-11-4687
DOI	10.1182/BLOOD-2005-11-4687
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q59236733
is cites work of	Endoplasmic reticulum stress-mediated apoptosis in imatinib-resistant leukemic K562-r cells triggered by AMN107 combined with arsenic trioxide Development and validation of a sensitive assay for the quantification of imatinib using LC/LC-MS/MS in human whole blood and cell culture Recent advances in cancer stem/progenitor cell research: therapeutic implications for overcoming resistance to the most aggressive cancers Final report of a phase II study of imatinib mesylate with hyper-CVAD for the front-line treatment of adult patients with Philadelphia chromosome-positive acute lymphoblastic leukemia Adherence is the critical factor for achieving molecular responses in patients with chronic myeloid leukemia who achieve complete cytogenetic responses on imatinib. Pharmacokinetic impact of SLCO1A2 polymorphisms on imatinib disposition in patients with chronic myeloid leukemia Expression of the uptake drug transporter hOCT1 is an important clinical determinant of the response to imatinib in chronic myeloid leukemia Seeking the causes and solutions to imatinib-resistance in chronic myeloid leukemia Multidrug resistance in chronic myeloid leukaemia: how much can we learn from MDR-CML cell lines? Plasma exposure of imatinib and its correlation with clinical response in the Tyrosine Kinase Inhibitor Optimization and Selectivity Trial A phase I/II study of imatinib plus reinduction therapy for c-kit-positive relapsed/refractory acute myeloid leukemia: inhibition of Akt activation correlates with complete response Bortezomib induces apoptosis in primitive chronic myeloid leukemia cells including LTC-IC and NOD/SCID repopulating cells. Membrane transporters in drug development The bone marrow microenvironment as a sanctuary for minimal residual disease in CML. Recent advances on the molecular mechanisms involved in the drug resistance of cancer cells and novel targeting therapies Beneficial effects of combining nilotinib and imatinib in preclinical models of BCR-ABL+ leukemias Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia Secondary mutations as mediators of resistance to targeted therapy in leukemia AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL Properties of CD34+ CML stem/progenitor cells that correlate with different clinical responses to imatinib mesylate Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival Nilotinib counteracts P-glycoprotein-mediated multidrug resistance and synergizes the antitumoral effect of doxorubicin in soft tissue sarcomas Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells. Interaction of nilotinib, dasatinib and bosutinib with ABCB1 and ABCG2: implications for altered anti-cancer effects and pharmacological properties Influence of CYP3A5 and drug transporter polymorphisms on imatinib trough concentration and clinical response among patients with chronic phase chronic myeloid leukemia Nilotinib: a novel, selective tyrosine kinase inhibitor Part II: management of resistance to imatinib in chronic myeloid leukaemia NCCN Task Force report: tyrosine kinase inhibitor therapy selection in the management of patients with chronic myelogenous leukemia Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase Tyrosine kinase inhibitor resistance in chronic myeloid leukemia cell lines: investigating resistance pathways Tyrosine kinase inhibitors in chronic myeloid leukaemia: which, when, for whom? Effects of PKC412, nilotinib, and imatinib against GIST-associated PDGFRA mutants with differential imatinib sensitivity Insights into the stem cells of chronic myeloid leukemia Selecting the best frontline treatment in chronic myeloid leukemia Chronic phase chronic myeloid leukemia patients with low OCT-1 activity randomized to high-dose imatinib achieve better responses and have lower failure rates than those randomized to standard-dose imatinib Targeting the BCR-ABL tyrosine kinase in chronic myeloid leukemia as a model of rational drug design in cancer Molecular resistance: an early indicator for treatment change? Chronic myeloid leukemia stem cells possess multiple unique features of resistance to BCR-ABL targeted therapies Chronic myeloid leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 activity 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. Phase 2 study of nilotinib as third-line therapy for patients with gastrointestinal stromal tumor. Lyn regulates BCR-ABL and Gab2 tyrosine phosphorylation and c-Cbl protein stability in imatinib-resistant chronic myelogenous leukemia cells

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