Erratum: Reversal of P-glycoprotein-mediated multidrug resistance by cholesterol derived from low density lipoprotein in a vinblasine-resistant human lymphoblastic leukemia cell line

2008 ◽  
Vol 86 (1) ◽  
pp. 79-79
Author(s):  
Yu Shu ◽  
Hu Liu
Keyword(s):  
Multidrug Resistance ◽  
Cell Line ◽  
Lymphoblastic Leukemia ◽  
Low Density Lipoprotein ◽  
Leukemia Cell ◽  
Density Lipoprotein ◽  
Leukemia Cell Line ◽  
Low Density ◽  
P Glycoprotein ◽  
Lymphoblastic Leukemia Cell Line

Reversal of P-glycoprotein-mediated multidrug resistance by cholesterol derived from low density lipoprotein in a vinblastine-resistant human lymphoblastic leukemia cell line

2007 ◽  
Vol 85 (5) ◽  
pp. 638-646 ◽  
Author(s):  
Yu Shu ◽  
Hu Liu
Keyword(s):  
Multidrug Resistance ◽  
Lymphoblastic Leukemia ◽  
Low Density Lipoprotein ◽  
Leukemia Cell ◽  
Density Lipoprotein ◽  
Cytotoxic Agents ◽  
Leukemia Cell Line ◽  
Low Density ◽  
Glycoprotein P ◽  
P Glycoprotein

P-glycoprotein (P-gp) is believed to be one of the most common causes of multidrug resistance (MDR) in chemotherapy. Studies have shown that the biosynthesis of cholesterol and cholesterol esters interfere with the function of P-gp. Since low density lipoprotein (LDL) carries a large amount of cholesterol, we investigated the effect of cholesterol derived from LDL on a line of human lymphoblastic leukemia MDR cells, CEM/VLB. Our results demonstrated that, in addition to increased cytotoxicity, the uptake of vinblastine in CEM/VLB cells increased, and LDL subsequently increased the intracellular vinblastine concentrations retained by CEM/VLB cells. The cholesterol levels in the membrane of the MDR cells were restored, while LDL significantly decreased the P-gp-associated ATPase activity. Current studies have shown that LDL leads to the resensitization of CEM/VLB cells to cytotoxic agents, likely through the restoration of cholesterol and reduction of P-gp-associated ATPase in the cell membrane.

Activation ofHOX11L2 by juxtaposition with 3?-BCL11B in an acute lymphoblastic leukemia cell line (HPB-ALL) with t(5;14)(q35;q32.2)

2003 ◽  
Vol 37 (1) ◽  
pp. 84-91 ◽  
Author(s):  
Roderick A.F. MacLeod ◽  
Stefan Nagel ◽  
Maren Kaufmann ◽  
Johannes W.G. Janssen ◽  
Hans G. Drexler
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Cell Line ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Lymphoblastic Leukemia Cell Line

scholarly journals The oxidation of (−)-epigallocatechin-3-gallate inhibits T-cell acute lymphoblastic leukemia cell line HPB-ALL via the regulation of Notch1 expression

RSC Advances ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 1679-1684 ◽  
Author(s):  
Yu-Na Wang ◽  
Jing Wang ◽  
Hao-Nan Yang ◽  
Bang-Lei Zhang ◽  
Pan Zhang ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cell Line ◽  
Hematological Malignancy ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Activating Mutations ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Lymphoblastic Leukemia Cell Line

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy, and commonly associated with activating mutations in the Notch1 pathway.

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