Patients with low OCT-1 activity and high ABCB1 fold rise have poor long-term outcomes in response to tyrosine kinase inhibitor therapy
Author:
Publisher
Springer Science and Business Media LLC
Subject
Oncology,Cancer Research,Hematology
Link
http://www.nature.com/articles/s41375-018-0101-5.pdf
Reference10 articles.
1. Eadie LN, Dang P, Saunders VA, Yeung DT, Osborn MP, Grigg AP, et al. The clinical significance of ABCB1 overexpression in predicting outcome of CML patients undergoing first-line imatinib treatment. Leukemia. 2017;31:75–82.
2. White DL, Dang P, Engler J, Frede A, Zrim S, Osborn M, et al. Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib. J Clin Oncol. 2010;28:2761–7.
3. White DL, Radich J, Soverini S, Saunders VA, Frede AK, Dang P, et al. 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. Haematologica. 2012;97:907–14.
4. White DL, Saunders VA, Dang P, Engler J, Venables A, Zrim S, et al. 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. Blood. 2007;110:4064–72.
5. White DL, Saunders VA, Dang P, Engler J, Zannettino AC, Cambareri AC, et al. 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. Blood. 2006;108:697–704.
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