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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.
White DL, Saunders VA, Dang P, Engler J, Zannettino AC, Cambareri AC, Quinn SR, Manley PW, Hughes TP. White DL, et al. Among authors: manley pw. Blood. 2006 Jul 15;108(2):697-704. doi: 10.1182/blood-2005-11-4687. Epub 2006 Apr 4. Blood. 2006. PMID: 16597591 Free article.
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.
White DL, Saunders VA, Dang P, Engler J, Venables A, Zrim S, Zannettino A, Lynch K, Manley PW, Hughes T. White DL, et al. Among authors: manley pw. Blood. 2007 Dec 1;110(12):4064-72. doi: 10.1182/blood-2007-06-093617. Epub 2007 Aug 30. Blood. 2007. PMID: 17761829 Free article. Clinical Trial.
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.
White DL, Radich J, Soverini S, Saunders VA, Frede AK, Dang P, Cilloni D, Lin P, Mongay L, Woodman R, Manley P, Slader C, Kim DW, Pane F, Martinelli G, Saglio G, Hughes TP. White DL, et al. Haematologica. 2012 Jun;97(6):907-14. doi: 10.3324/haematol.2011.056457. Epub 2011 Dec 29. Haematologica. 2012. PMID: 22207690 Free PMC article. Clinical Trial.
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