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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: engler j. 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: engler j. 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.
Mechanisms of Resistance to EGFR Inhibition Reveal Metabolic Vulnerabilities in Human GBM.
McKinney A, Lindberg OR, Engler JR, Chen KY, Kumar A, Gong H, Lu KV, Simonds EF, Cloughesy TF, Liau LM, Prados M, Bollen AW, Berger MS, Shieh JTC, James CD, Nicolaides TP, Yong WH, Lai A, Hegi ME, Weiss WA, Phillips JJ. McKinney A, et al. Among authors: engler jr. Mol Cancer Ther. 2019 Sep;18(9):1565-1576. doi: 10.1158/1535-7163.MCT-18-1330. Epub 2019 Jul 3. Mol Cancer Ther. 2019. PMID: 31270152 Free PMC article.
266 results