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. 2003 Nov 1;9(14):5171-7.

The role of breast cancer resistance protein in acute lymphoblastic leukemia

Sabine L A Plasschaert  1 , Dorina M van der Kolk, Eveline S J M de Bont, Willem A Kamps, Kuniaki Morisaki, Susan E Bates, George L Scheffer, Rik J Scheper, Edo Vellenga, Elisabeth G E de Vries
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  • PMID: 14613996

The role of breast cancer resistance protein in acute lymphoblastic leukemia

Sabine L A Plasschaert et al. Clin Cancer Res. .

Abstract

Purpose: Overexpression of the transporter ABCG2, also known as breast cancer resistance protein and mitoxantrone resistance protein, can confer resistance to a variety of cytostatic drugs, such as mitoxantrone, topotecan, doxorubicin, and daunorubicin VSports手机版. This study analyzes the ABCG2 expression and activity in 46 human de novo acute lymphoblastic leukemia B- and T-lineage (ALL) samples. .

Experimental design: ABCG2 expression was measured flow cytometrically with the BXP-34 monoclonal antibody. ABCG2 functional activity was determined flow cytometrically by measuring mitoxantrone accumulation in combination with the ABCG2 inhibitor fumitremorgin C (FTC) V体育安卓版. To determine a possible effect of the transporters P-glycoprotein and multidrug resistance-associated protein (MRP1 and MRP2) on mitoxantrone accumulation, the accumulation was investigated in the presence of the P-glycoprotein inhibitor PSC 833 and MRP inhibitor MK-571. The ABCG2 gene was sequenced to investigate the amino acid at position 482. .

Results: In B-lineage ALL (n = 23), the median BXP-34:IgG1 ratio was higher, namely 2. 4 (range, 1. 7-3. 7), than in T-lineage ALL (n = 23; 1. 9; range, 1. 2-6. 6; P = 0. 003). The addition of FTC to mitoxantrone treatment caused a median increase in mitoxantrone accumulation of 21% (range, 0-140%) in B-lineage ALL. In T-lineage ALL, this FTC effect was less pronounced (5%; range, 0-256%; P = 0. 013). The influence of FTC on mitoxantrone accumulation correlated with ABCG2 protein expression (r = 0. 52; P < 0. 001; n = 43). The increase in mitoxantrone accumulation, when FTC was added to cells treated with both PSC 833 and MK-571, correlated with the ABCG2 expression in B-lineage ALL but not in T-lineage ALL. Sequencing the ABCG2 gene revealed no ABCG2 mutation at position 482 in patients who accumulated more rhodamine after FTC V体育ios版. .

Conclusions: This study shows that ABCG2 is expressed higher and functionally more active in B-lineage than in T-lineage ALL VSports最新版本. .

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