N	Concordance
1	ilure of therapy, relapse, and acquired multidrug resistance during the initial 
2	r investigated the relationship between multidrug resistance (MDR) mediated by P
3	ting ATPase has been termed canalicular multidrug resistance protein (cMRP) beca
4	microfilament compounds that circumvent multidrug resistance mediated by overexp
5	f MDR protein overexpression but higher multidrug resistance due to selection wi
6	ycoprotein (P-gp), encoded by the human multidrug resistance gene MDR1, plays a 
7	ive. Conventional chemotherapies induce multidrug resistance rapidly. Just as in
8	closporin) is a P-glycoprotein-mediated multidrug resistance modulator currently
9	chromosome abnormality, the presence of multidrug resistance characteristics, th
10	lated with the functional expression of multidrug resistance (MDR-1) at diagnosi
11	 and MDR1, a marker associated with the multidrug resistance phenotype, confer a
12	rations in haematological patients with multidrug resistance by means of total, 
13	A subline with the drug does not induce multidrug resistance, indicating that il
14	 human lung cancer cells expressing the multidrug resistance-associated protein 
15	pharmacologic agents aimed at reversing multidrug resistance. This followed the