Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells

被引:0
作者
Ramon C Sun
Philip G Board
Anneke C Blackburn
机构
[1] Australian National University,Molecular Genetics Group, Department of Translational Biosciences, John Curtin School of Medical Research
[2] Stanford School of Medicine,Department of Radiation Oncology
来源
Molecular Cancer | / 10卷
关键词
Dichloroacetate; breast cancer; electron transport chain; mitochondria; arsenic trioxide;
D O I
暂无
中图分类号
学科分类号
摘要
引用
收藏
相关论文
共 272 条
[1]  
Antman KH(2001)Introduction: the history of arsenic trioxide in cancer therapy Oncologist 6 1-2
[2]  
Emadi A(2010)Arsenic trioxide - An old drug rediscovered Blood Rev 24 191-199
[3]  
Gore SD(2010)Arsenic trioxide improves event-free and overall survival for adults with acute promyelocytic leukemia: North American Leukemia Intergroup Study C9710 Blood 116 3751-3757
[4]  
Powell BL(2008)Acute promyelocytic leukemia: from highly fatal to highly curable Blood 111 2505-2515
[5]  
Moser B(2007)Arsenical-based cancer drugs Cancer Treat Rev 33 542-564
[6]  
Stock W(2003)Induction of autophagic cell death in malignant glioma cells by arsenic trioxide Cancer Res 63 2103-2108
[7]  
Gallagher RE(2002)Arsenic trioxide-induced apoptosis through oxidative stress in cells of colon cancer cell lines Life Sciences 70 2253-2269
[8]  
Willman CL(2008)Arsenic-based antineoplastic drugs and their mechanisms of action Met Based Drugs 2008 260146-270
[9]  
Stone RM(2000)Arsenic trioxide-induced apoptosis and differentiation are associated respectively with mitochondrial transmembrane potential collapse and retinoic acid signaling pathways in acute promyelocytic leukemia Leukemia 14 262-1247
[10]  
Rowe JM(2004)Essential role of the voltage-dependent anion channel (VDAC) in mitochondrial permeability transition pore opening and cytochrome c release induced by arsenic trioxide Oncogene 23 1239-42