Cancer drug pan-resistance: pumps, cancer stem cells, quiescence, epithelial to mesenchymal transition, blocked cell death pathways, persisters or what?

Open Biology - Tập 2 Số 5 - Trang 120066 - 2012
Piet Borst1,2,3,4
1Find this author on PubMed
2Google Scholar
3Molecular Oncology, NKI-AVL, Plesmanlaan 121, Amsterdam, The Netherlands
4Piet Borst

Tóm tắt

Although chemotherapy of tumours has scored successes, drug resistance remains the major cause of death of cancer patients. Initial treatment often leaves residual disease, from which the tumour regrows. Eventually, most tumours become resistant to all available chemotherapy. I call this pan-resistance to distinguish it from multi-drug resistance, usually describing resistance caused by upregulation of drug transporters, such as P-glycoprotein. In this review, I discuss mechanisms proposed to explain both residual disease and pan-resistance. Although plausible explanations are at hand for residual disease, pan-resistance is still a mystery. My conclusion is that it is time for a major effort to solve this mystery using the new genetically modified mouse tumour models that produce real tumours resembling cancer in human patients.

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Tài liệu tham khảo

10.4161/cc.6.16.4538

10.1086/528867

Harris AL, 1985, DNA repair and resistance to chemotherapy, Cancer Surv., 4, 601

10.1038/nrc1691

10.1038/nrd3374

10.2325/jbcs.14.420

10.1002/cncr.11436

10.1126/science.1171362

10.1038/471316a

10.1126/science.1208347

10.1038/nm.2652

10.1016/0005-2736(76)90160-7

10.1038/nrd1984

10.1146/annurev.biochem.71.102301.093055

10.1152/physrev.00035.2005

10.1016/j.febslet.2004.03.123

10.2174/1389200043489199

10.1111/j.1742-4658.2011.08235.x

10.1158/0008-5472.CAN-09-0041

10.1158/0008-5472.CAN-09-3367

10.1038/sj.onc.1206951

10.1002/0470846356.ch7

10.1074/jbc.M602998200

10.1200/JCO.2005.09.077

10.1158/1078-0432.CCR-09-2247

10.1200/JCO.2010.31.2231

10.1073/pnas.0702955104

10.1016/j.ctrv.2006.12.002

10.1093/nar/24.17.3370

10.1126/science.1062538

10.1073/pnas.0504952102

10.1172/JCI30890

10.1126/science.331.6024.1542

10.1038/nrc1044

10.1038/nature09883

10.1038/nature07815

10.1016/j.molonc.2010.06.001

10.1038/nbt.1607

10.1016/j.stem.2010.03.008

10.1038/sj.leu.2404609

10.1016/j.cell.2010.04.020

10.1016/j.cell.2010.02.027

10.1073/pnas.1109632108

10.1073/pnas.0800939105

10.1056/NEJMra072067

10.1016/j.ccr.2011.12.029

10.1158/1078-0432.CCR-08-2048

10.1038/nm.2304

10.1007/s10911-009-9109-9

Curtin JC, 2010, Drug discovery approaches to target Wnt signaling in cancer stem cells, Oncotarget, 1, 563, 10.18632/oncotarget.191

10.1038/nrd2137

10.1016/j.stem.2009.02.003

10.1038/nature10212

10.1016/j.ccr.2010.10.012

10.1038/nature04372

10.1038/nrc2499

10.1053/j.gastro.2011.03.052

10.1038/nature05236

10.1038/nature07733

10.1073/pnas.1118857109

10.1038/ncb2059

10.1038/nrc3007

10.1038/nrc2256

10.1007/s12033-010-9321-2

10.1038/onc.2010.215

10.4161/cc.9.18.13002

10.1016/j.cell.2009.06.034

10.1172/JCI41004

10.1200/JCO.2010.27.9943

10.4161/cc.7.10.5930

10.1158/0008-5472.CAN-09-2422

10.1054/drup.2001.0188

10.1054/drup.2001.0187

10.1038/nrc1560

10.4161/cc.4.12.2259

10.1073/pnas.0803513105

10.4161/cc.6.22.4936

10.1038/ni.2159

10.1038/cdd.2011.164

Speirs CK, 2011, Harnessing the cell death pathway for targeted cancer treatment, Am. J. Cancer Res., 1, 43

10.1073/pnas.1018867108

10.1186/bcr3037

10.1038/sj.onc.1209871

10.1073/pnas.1111840108

Goldie JH, 1979, A mathematic model for relating the drug sensitivity of tumors to their spontaneous mutation rate, Cancer Treat Rep., 63, 1727

Goldie JH, 1984, The genetic origin of drug resistance in neoplasms: implications for systemic therapy, Cancer Res., 44, 3643

10.1038/483544a

10.1007/s10911-011-9199-z

10.1016/j.drup.2012.01.001

10.1038/483546a

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Open Biology

Tập 2 Số 5

120066

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