Mechanisms of Cancer Drug Resistance

Annual Review of Medicine - Tập 53 Số 1 - Trang 615-627 - 2002
Michael M. Gottesman1
1Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4255;

Tóm tắt

▪ Abstract  The design of cancer chemotherapy has become increasingly sophisticated, yet there is no cancer treatment that is 100% effective against disseminated cancer. Resistance to treatment with anticancer drugs results from a variety of factors including individual variations in patients and somatic cell genetic differences in tumors, even those from the same tissue of origin. Frequently resistance is intrinsic to the cancer, but as therapy becomes more and more effective, acquired resistance has also become common. The most common reason for acquisition of resistance to a broad range of anticancer drugs is expression of one or more energy-dependent transporters that detect and eject anticancer drugs from cells, but other mechanisms of resistance including insensitivity to drug-induced apoptosis and induction of drug-detoxifying mechanisms probably play an important role in acquired anticancer drug resistance. Studies on mechanisms of cancer drug resistance have yielded important information about how to circumvent this resistance to improve cancer chemotherapy and have implications for pharmacokinetics of many commonly used drugs.

Từ khóa


Tài liệu tham khảo

10.1126/science.278.5340.1036

10.1053/sonc.2001.22811

10.1016/S0169-409X(97)00094-X

10.1056/NEJM200104053441402

10.1073/pnas.081626898

Green SK, 1999, Anticancer-Drug Designs, 14, 153

Longo-Sorbello GS, 2001, Haematologica, 86, 121

10.1101/SQB.1994.059.01.078

10.1096/fj.00-0223com

10.1016/0092-8674(93)90719-7

10.1038/87912

10.1093/jnci/91.19.1604

10.1093/jnci/92.16.1295

10.1146/annurev.pharmtox.39.1.361

10.1016/0005-2736(76)90160-7

10.1073/pnas.84.9.3004

10.1016/0092-8674(86)90595-7

10.1128/MCB.9.3.1346

Lothstein L, 1989, J. Biol. Chem., 264, 16054, 10.1016/S0021-9258(18)71586-X

10.1146/annurev.cb.08.110192.000435

10.1093/jnci/81.2.116

10.1073/pnas.95.1.282

10.1038/sj.bjp.0703920

10.1172/JCI2575

10.1021/bi973045u

10.1073/pnas.97.6.2515

10.1074/jbc.M011294200

10.1126/science.1360704

10.1093/jnci/90.22.1735

Loe DW, 1998, Cancer Res., 58, 5130

10.1016/S0005-2736(99)00167-4

10.1073/pnas.96.12.6914

10.1073/pnas.120159197

10.1073/pnas.95.26.15665

Allikmets R, 1998, Cancer Res., 58, 5337

Miyake K, 1999, Cancer Res., 59, 8

Komatani H, 2001, Cancer Res., 61, 2827

10.1016/S1388-1981(00)00053-6

Childs S, 1998, Cancer Res., 58, 4160

Laing NM, 1998, Cancer Res., 58, 1332

Lyall RM, 1987, Cancer Res., 47, 2961

10.1038/bjc.1993.221

Shen D-W, 1998, Cancer Res., 58, 268

10.1002/(SICI)1097-4652(200004)183:1<108::AID-JCP13>3.0.CO;2-4

10.1182/blood.V91.5.1749

Abolhoda A, 1999, Clin. Cancer Res., 5, 3352

10.1200/JCO.1993.11.9.1652

Marie J-P, 1993, Leukemia, 7, 821

10.1056/NEJM199112053252304

10.1200/JCO.1998.16.11.3674

10.1182/blood.V93.3.787

Crankshaw CL, 1998, J. Nucl. Med., 39, 77

10.1073/pnas.94.8.4028

Allen JD, 2000, Cancer Res., 60, 5761

Johnson DR, 2001, Cancer Res., 61, 1469

10.1038/85115

10.1073/pnas.050585397

10.1146/annurev.ge.29.120195.003135

Gottesman MM, Licht T, Zhou Y, et al. 2000. Selectable markers for gene therapy. InGene Therapy: Therapeutic Mechanisms and Strategies, ed. D Lasic, N Templeton, 16:333–52. New York: Marcel Dekker

10.1126/science.1352414

10.1182/blood.V94.1.52.413k35_52_61

10.1182/blood.V92.7.2269

Thông tin
Thông tin xuất bản

Annual Review of Medicine

Tập 53 Số 1

615-627

Thông tin tác giả