Chronic myeloid leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 activity (Q43165899)

15 November 2017

Chronic myeloid leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 activity (English)

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15 November 2017

chronic myeloid leukemia

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T P Hughes

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15 November 2017

J R Engler

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A Frede

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V A Saunders

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A C W Zannettino

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15 November 2017

11 February 2010

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24

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765-770

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https://scigraph.springernature.com/pub.10.1038/leu.2010.16

15 November 2017

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Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction

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Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate

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Active transport of imatinib into and out of cells: implications for drug resistance

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The SLC22 drug transporter family

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hOCT 1 and resistance to imatinib

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Expression of the uptake drug transporter hOCT1 is an important clinical determinant of the response to imatinib in chronic myeloid leukemia

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Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump

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Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro

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Loss of P-glycoprotein expression in hematopoietic stem cells does not improve responses to imatinib in a murine model of chronic myelogenous leukemia

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Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells.

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Regulation of organic cation transport.

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Regulation of the human organic cation transporter hOCT1.

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Identification of genetic variations of the human organic cation transporter hOCT1 and their functional consequences

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Evolutionary conservation predicts function of variants of the human organic cation transporter, OCT1

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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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BCR/ABL kinase inhibition by imatinib mesylate enhances MAP kinase activity in chronic myelogenous leukemia CD34+ cells

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CD34+/Ph+ cells are still detectable in chronic myeloid leukemia patients with sustained and prolonged complete cytogenetic remission during treatment with imatinib mesylate

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A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia

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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

21 January 2018

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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

21 January 2018

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https://api.crossref.org/works/10.1038%2FLEU.2010.16

Organic cation transporters

21 January 2018

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https://api.crossref.org/works/10.1038%2FLEU.2010.16

inferred from DOI database lookup

7 January 2021

based on heuristic

Nilotinib exerts equipotent antiproliferative effects to imatinib and does not induce apoptosis in CD34+ CML cells

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.16

inferred from DOI database lookup

7 January 2021

based on heuristic

Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.16

inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1038/LEU.2010.16

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Dimensions Publication ID

15 November 2017

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