Abstract：
:Imatinib mesylate (STI571), a potent tyrosine kinase inhibitor, is successfully used in the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumors. However, the intended chronic oral administration of imatinib may lead to development of cellular resistance and subsequent treatment failure. Indeed, several molecular mechanisms leading to imatinib resistance have already been reported, including overexpression of the MDR1/ABCB1 drug pump. We examined whether imatinib is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump that is frequently overexpressed in human tumors. Using a panel of well-defined BCRP-overexpressing cell lines, we provide the first evidence that imatinib is a substrate for BCRP, that it competes with mitoxantrone for drug export, and that BCRP-mediated efflux can be reversed by the fumitremorgin C analog Ko-143. Since BCRP is highly expressed in the gastrointestinal tract, BCRP might not only play a role in cellular resistance of tumor cells but also influence the gastrointestinal absorption of imatinib.
journal_name
Bloodjournal_title
Bloodauthors
Burger H,van Tol H,Boersma AW,Brok M,Wiemer EA,Stoter G,Nooter Kdoi
10.1182/blood-2004-04-1398subject
Has Abstractpub_date
2004-11-01 00:00:00pages
2940-2issue
9eissn
0006-4971issn
1528-0020pii
2004-04-1398journal_volume
104pub_type
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