Data/hora: 06/06/2024 03:03:59

Provedor de dados: 	42	
País: 	Brazil	
Título: 	Multidrug resistance in tumour cells: characterisation of the multidrug resistant cell line K562-Lucena 1	
Autores: 	RUMJANEK,VIVIAN M.; TRINDADE,GILMA S.; WAGNER-SOUZA,KAREN; MELETTI-DE-OLIVEIRA,MICHELE C.; MARQUES-SANTOS,LUIS F.; MAIA,RAQUEL C.; CAPELLA,MÁRCIA A. M.	
Data: 	2001-03-01	
Ano: 	2001	
Palavras-chave: 	Multidrug resistance; Leukaemia; P-glycoprotein; Chemosensitisers.	
Resumo: 	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 cell line, originally selected for resistance to the Vinca alkaloid vincristine and derived from the human erythroleukaemia cell K562. This cell line, named Lucena 1, overexpresses P-glycoprotein and have its resistance reversed by the chemosensitisers verapamil, trifluoperazine and cyclosporins A, D and G. Furthermore, we demonstrated that methylene blue was capable of partially reversing the resistance in this cell line. On the contrary, the use of 5-fluorouracil increased the resistance of Lucena 1. In addition to chemotherapics, Lucena 1 cells were resistant to ultraviolet A radiation and hydrogen peroxide and failed to mobilise intracellular calcium when thapsigargin was used. Changes in the cytoskeleton of this cell line were also observed.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652001000100007	
Editor: 	Academia Brasileira de Ciências	
Relação: 	10.1590/S0001-37652001000100007	
Formato: 	text/html	
Fonte: 	Anais da Academia Brasileira de Ciências  v.73 n.1 2001	
Fonte: 	info:eu-repo/semantics/openAccess