2001
DOI: 10.1590/s0001-37652001000100007
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Abstract: Multidrug resistance to chemotherapy is a major obstacle in the treatment of cancer patients. The best characterised mechanism responsible for multidrug resistance involves the expression of the MDR-1 gene product, P-glycoprotein. However, the resistance process is multifactorial. Studies of multidrug resistance mechanisms have relied on the analysis of cancer cell lines that have been selected and present cross-reactivity to a broad range of anticancer agents. This work characterises a multidrug resistant cel… Show more

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Cited by 111 publications
(83 citation statements)
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“…Sensitivity to chemotherapeutic drugs of K562 and Lucena-1 cells Studying therapy-induced drug resistance in vitro remains a challenge, but Lucena-1 cells have previously been described as vincristine-resistant leukemia cells derived from vincristine-sensitive K562 parental cells (Rumjanek et al, 2001) ( Figure 1); indeed, in our hands, the microtubule polymerization inhibitor vincristine, as well as other therapeutically important drugs such as the DNA intercalating mitoxantrone and doxorubicin, efficiently kills K562 cells, whereas these drugs only minimally affect Lucena-1 survival ( Figure 1a). Chemoresistance of Lucena-1 was accompanied by upregulation of drug transporters P-gp and MRP-1, (Figure 1b) whereas the P-gp inhibitor verapamil partially reverted drug resistance.…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…Sensitivity to chemotherapeutic drugs of K562 and Lucena-1 cells Studying therapy-induced drug resistance in vitro remains a challenge, but Lucena-1 cells have previously been described as vincristine-resistant leukemia cells derived from vincristine-sensitive K562 parental cells (Rumjanek et al, 2001) ( Figure 1); indeed, in our hands, the microtubule polymerization inhibitor vincristine, as well as other therapeutically important drugs such as the DNA intercalating mitoxantrone and doxorubicin, efficiently kills K562 cells, whereas these drugs only minimally affect Lucena-1 survival ( Figure 1a). Chemoresistance of Lucena-1 was accompanied by upregulation of drug transporters P-gp and MRP-1, (Figure 1b) whereas the P-gp inhibitor verapamil partially reverted drug resistance.…”
Section: Resultsmentioning
confidence: 99%
“…Whether the Hh pathway has a similar role in leukemia remains elusive, and this study therefore aimed at deciphering the potential role of Hh in chemotherapy resistance in leukemia. To this end, we compared Hh pathway activity in chemotherapy-sensitive parental K562 cells and in MDR-resistant Lucena-1 daughter cells (Rumjanek et al, 2001). We established that Hh signaling maintains the chemoresistant phenotype in an apparently P-gpdependent manner and propose that Hh inhibition might be an attractive treatment strategy to revert (or prevent) chemoresistance in myeloid leukemia.…”
Section: Introductionmentioning
confidence: 99%
“…The human tumor cell lines Raji and Namalwa (Burkitt's lymphoma), HT-29 (Colon adenocarcinoma), and GLC-4 (small cell lung carcinoma), which express mutant p53 protein and the cell lines MT2 and C91pl (adult T-cell leukemia/lymphoma), MCF-7 (breast carcinoma), and H460 (lung carcinoma), which express wild-type p53 protein were used as positive controls. The human cell lines K562 (CML), K562-Lucena (CML), Jurkat (T-cell lymphoblastic leukemia), Daudi (Burkitt's lymphoma), and HL-60 (acute promyelocytic leukemia), which do not express p53 protein were used as negative controls (20)(21)(22).…”
Section: Controlsmentioning
confidence: 99%
“…The human chronic myelogenous leukemia (CML) cell line K562, and its vincristine-resistant, derived cell line K562-Lucena (29), were used as negative and positive controls of Pgp expression, respectively. The Raji, Burkittcell line was used as positive control of p53 expression (30) and GLC-4 and GLC-4 ADR cell lines (human smalllung cell carcinoma) were used for negative and positive controls of MRP expression, respectively.…”
Section: Controlsmentioning
confidence: 99%