Journal articles on the topic 'Multidrug resistance'

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1

Sodani, Kamlesh, Atish Patel, Rishil J. Kathawala, and Zhe-Sheng Chen. "Multidrug resistance associated proteins in multidrug resistance." Chinese Journal of Cancer 31, no. 2 (February 5, 2012): 58–72. http://dx.doi.org/10.5732/cjc.011.10329.

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2

Pastan, I., and M. M. Gottesman. "Multidrug Resistance." Annual Review of Medicine 42, no. 1 (February 1991): 277–84. http://dx.doi.org/10.1146/annurev.me.42.020191.001425.

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3

Tsuruo, Takashi, and Akihiro Tomida. "Multidrug resistance." Anti-Cancer Drugs 6, no. 2 (April 1995): 213–18. http://dx.doi.org/10.1097/00001813-199504000-00003.

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4

Tiirikainen, Maarit I., and Tom Krusius. "Multidrug Resistance." Annals of Medicine 23, no. 5 (January 1991): 509–20. http://dx.doi.org/10.3109/07853899109150511.

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5

Mickisch, G. H. "Multidrug Resistance." Der Urologe A 35, no. 5 (September 1996): 370–77. http://dx.doi.org/10.1007/s001200050038.

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6

Persidis, Aris. "Cancer multidrug resistance." Nature Biotechnology 17, no. 1 (January 1999): 94–95. http://dx.doi.org/10.1038/5289.

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7

Gao, Mian, Masayo Yamazaki, Douglas W. Loe, Christopher J. Westlake, Caroline E. Grant, Susan P. C. Cole, and Roger G. Deeley. "Multidrug Resistance Protein." Journal of Biological Chemistry 273, no. 17 (April 24, 1998): 10733–40. http://dx.doi.org/10.1074/jbc.273.17.10733.

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8

Levy, Stuart B. "Confronting Multidrug Resistance." JAMA 269, no. 14 (April 14, 1993): 1840. http://dx.doi.org/10.1001/jama.1993.03500140092042.

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9

Brennan, Richard G. "Introduction: multidrug resistance." Seminars in Cell & Developmental Biology 12, no. 3 (June 2001): 201–4. http://dx.doi.org/10.1006/scdb.2000.0245.

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10

Ouellette, Marc, and Christoph Kündig. "Microbial multidrug resistance." International Journal of Antimicrobial Agents 8, no. 3 (January 1997): 179–87. http://dx.doi.org/10.1016/s0924-8579(96)00370-6.

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11

KUWANO, MICHIHIKO. "Transporter; 7. Multidrug Resistance Transporters: Multidrug Resistance to Anticancer Agents." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 35, no. 2 (2004): 89–96. http://dx.doi.org/10.3999/jscpt.35.2_89.

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12

Lautier, Dominique, Yvan Canitrot, Roger G. Deeley, and Susan P. C. Cole. "Multidrug resistance mediated by the multidrug resistance protein (MRP) gene." Biochemical Pharmacology 52, no. 7 (October 1996): 967–77. http://dx.doi.org/10.1016/0006-2952(96)00450-9.

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13

Çelik, Cem. "Increasing antimicrobial resistance in nosocomial pathogens; multidrug-resistant extensively drug-resistant and pandrug-resistant Acinetobacter baumannii." Journal of Microbiology and Infectious Diseases 4, no. 1 (March 1, 2014): 7–12. http://dx.doi.org/10.5799/ahinjs.02.2014.01.0116.

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14

Boyanova, Lyudmila, Rumyana Markovska, and Ivan Mitov. "Multidrug resistance in anaerobes." Future Microbiology 14, no. 12 (August 2019): 1055–64. http://dx.doi.org/10.2217/fmb-2019-0132.

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Multidrug resistance (MDR) in anaerobes is not a well-known topic. Bacteroides fragilis group isolates have numerous resistance determinants such as multidrug efflux pumps, cfiA and nimB genes and activating insertion sequences, and some isolates exhibited extensive drug-resistant patterns. MDR rates in B. fragilis group were from 1.5 to >18% and up to >71% in cfiA and nimB positive isolates carrying insertion sequences. MDR was present in >1/2 of Clostridioides difficile isolates, most often in epidemic/hypervirulent strains and unusually high metronidazole or vancomycin resistance has been reported in single studies. MDR was found in Prevotella spp. (in ≤10% of isolates), Finegoldia magna, Veillonella spp. and Cutibacterium acnes. Resistance in the anaerobes tends to be less predictable and anaerobic microbiology is required in more laboratories. New hopes may be new antibiotics such as eravacycline, cadazolid, surotomycin, ridinilazol or C. difficile toxoid vaccines; however, more efforts are needed to track the MDR in anaerobes.
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15

Kruh, Gary D., and Lori J. Goldstein. "Doxorubicin and multidrug resistance." Current Opinion in Oncology 5, no. 6 (November 1993): 1029–34. http://dx.doi.org/10.1097/00001622-199311000-00014.

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16

Sonneveld, Pieter, and Erik Wiemer. "Inhibitors of multidrug resistance." Current Opinion in Oncology 9, no. 6 (November 1997): 543–48. http://dx.doi.org/10.1097/00001622-199711000-00009.

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17

Holmes, Jon A. "Multidrug Resistance in Leukaemia." Leukemia & Lymphoma 1, no. 3-4 (January 1990): 163–68. http://dx.doi.org/10.3109/10428199009042475.

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18

Nikaido, Hiroshi. "Multidrug Resistance in Bacteria." Annual Review of Biochemistry 78, no. 1 (June 2009): 119–46. http://dx.doi.org/10.1146/annurev.biochem.78.082907.145923.

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19

MCKENNA, SHARON L., and ROSE ANN PADUA. "MULTIDRUG RESISTANCE IN LEUKAEMIA." British Journal of Haematology 96, no. 4 (March 1997): 659–74. http://dx.doi.org/10.1046/j.1365-2141.1997.d01-2095.x.

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20

Emini, Emilio A., Donald J. Graham, Leah Gotlib, Jon H. Condra, and Vera W. Byrnes. "HIV and multidrug resistance." Nature 364, no. 6439 (August 1993): 679. http://dx.doi.org/10.1038/364679b0.

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21

BATES, S. E., Z. ZHAN, B. DICKSTEIN, J. S. LEE, S. SCALA, A. T. FOJO, K. PAULL, and W. WILSON. "Reversal of Multidrug Resistance." Journal of Hematotherapy 3, no. 3 (January 1994): 219–23. http://dx.doi.org/10.1089/scd.1.1994.3.219.

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22

Mickisch, G. "Multidrug Resistance des Nierenzellkarzinoms." Aktuelle Urologie 25, no. 06 (November 1994): 327–37. http://dx.doi.org/10.1055/s-2008-1058250.

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23

TWENTYMAN, PETER R. "MODIFIERS OF MULTIDRUG RESISTANCE." British Journal of Haematology 90, no. 4 (August 1995): 735–37. http://dx.doi.org/10.1111/j.1365-2141.1995.tb05189.x.

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24

Dennis, David T., and James M. Hughes. "Multidrug Resistance in Plague." New England Journal of Medicine 337, no. 10 (September 4, 1997): 702–4. http://dx.doi.org/10.1056/nejm199709043371010.

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25

Baik, Seung, and Dong Hoon Lim. "Multidrug Resistance inNeisseria gonorrhoeae." Korean Journal of Urogenital Tract Infection and Inflammation 8, no. 2 (2013): 90. http://dx.doi.org/10.14777/kjutii.2013.8.2.90.

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26

Hall, Andrea M., and C. J. Chang. "Multidrug-Resistance Modulators fromStephaniajaponica." Journal of Natural Products 60, no. 11 (November 1997): 1193–95. http://dx.doi.org/10.1021/np9702042.

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27

Gulshan, Kailash, and W. Scott Moye-Rowley. "Multidrug Resistance in Fungi." Eukaryotic Cell 6, no. 11 (September 14, 2007): 1933–42. http://dx.doi.org/10.1128/ec.00254-07.

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28

Leweke, F., M. S. Damian, C. Schindler, and W. Schachenmayr. "Multidrug Resistance in Glioblastoma." Pathology - Research and Practice 194, no. 3 (January 1998): 149–55. http://dx.doi.org/10.1016/s0344-0338(98)80015-0.

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29

Robert, Jacques, and Christian Jarry. "Multidrug Resistance Reversal Agents." Journal of Medicinal Chemistry 46, no. 23 (November 2003): 4805–17. http://dx.doi.org/10.1021/jm030183a.

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30

Chang, Geoffrey. "Multidrug resistance ABC transporters." FEBS Letters 555, no. 1 (October 2, 2003): 102–5. http://dx.doi.org/10.1016/s0014-5793(03)01085-8.

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31

Baines, Paul, Peter Cumber, and Rose Ann Padua. "Multidrug resistance in leukaemia." Baillière's Clinical Haematology 5, no. 4 (October 1992): 943–60. http://dx.doi.org/10.1016/s0950-3536(11)80053-3.

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32

Ferry, D. R., and D. J. Kerr. "Multidrug resistance in cancer." BMJ 308, no. 6922 (January 15, 1994): 148–49. http://dx.doi.org/10.1136/bmj.308.6922.148.

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33

Kaye, SB. "The multidrug resistance phenotype." British Journal of Cancer 58, no. 6 (December 1988): 691–94. http://dx.doi.org/10.1038/bjc.1988.291.

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34

Nash, Kevin A. "Multidrug Resistance in Mycobacteria." Current Clinical Microbiology Reports 3, no. 1 (February 13, 2016): 53–61. http://dx.doi.org/10.1007/s40588-016-0032-8.

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35

Warris, Adilia, Corry M. Weemaes, and Paul E. Verweij. "Multidrug Resistance inAspergillus fumigatus." New England Journal of Medicine 347, no. 26 (December 26, 2002): 2173–74. http://dx.doi.org/10.1056/nejm200212263472618.

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36

Rout, Subhashree, and Rajani Kanta Mahapatra. "Plasmodium falciparum: Multidrug resistance." Chemical Biology & Drug Design 93, no. 5 (February 12, 2019): 737–59. http://dx.doi.org/10.1111/cbdd.13484.

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37

Leith, Catherine. "Multidrug resistance in leukemia." Current Opinion in Hematology 5, no. 4 (1998): 287–91. http://dx.doi.org/10.1097/00062752-199807000-00008.

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38

Croop, J. M., P. Gros, and D. E. Housman. "Genetics of multidrug resistance." Journal of Clinical Investigation 81, no. 5 (May 1, 1988): 1303–9. http://dx.doi.org/10.1172/jci113455.

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39

Chabner, B. A., and W. Wilson. "Reversal of multidrug resistance." Journal of Clinical Oncology 9, no. 1 (January 1991): 4–6. http://dx.doi.org/10.1200/jco.1991.9.1.4.

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40

Yuen, A. R., and B. I. Sikic. "Multidrug resistance in lymphomas." Journal of Clinical Oncology 12, no. 11 (November 1994): 2453–59. http://dx.doi.org/10.1200/jco.1994.12.11.2453.

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PURPOSE To discuss the significance of multidrug resistance (MDR) in human lymphomas and to review recent and ongoing clinical trials using MDR modulators. DESIGN A medical literature search was used to identify articles that reported results on the expression or modulation of MDR in human lymphomas. This review summarizes the various methods for detecting expression of the mdr1 gene in tumor specimens, the patterns of expression in lymphomas, and recent and upcoming clinical trials using modulating agents to reverse MDR. RESULTS There is considerable variation in the assays used to evaluate the expression of mdr1 in lymphomas. Current methodology includes reverse transcriptase polymerase chain reaction (rt-PCR) for assay of mdr1 mRNA, and immunohistochemistry or flow cytometry for detection of the multidrug transporter, P-glycoprotein (P-gp). The preponderance of evidence suggests that mdr1 expression is relatively low in untreated patients (10% to 20% of lymphomas positive), but increases in patients with recurrent disease (50% to 70% positive). Some evidence suggests that mdr1 expression is a prognostic factor for response to chemotherapy, as well as for subsequent survival. Verapamil and cyclosporine (CsA) have been used as competitive inhibitors of the multidrug transporter P-gp in early clinical trials. Although these studies show some activity in modulating clinical MDR, both verapamil and CsA manifest considerable toxicities at doses below those required for complete inhibition of P-gp function. CONCLUSION MDR due to the expression of the mdr1 gene is an important factor in the course of patients with lymphomas. Continued clinical trials with more potent and less toxic modulators are needed to define the ultimate benefit of modulating MDR in lymphomas.
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41

Kartner, Norbert, and Victor Ling. "Multidrug Resistance in Cancer." Scientific American 260, no. 3 (March 1989): 44–51. http://dx.doi.org/10.1038/scientificamerican0389-44.

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42

Bradley, Grace, Peter F. Juranka, and Victor Ling. "Mechanism of multidrug resistance." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 948, no. 1 (August 1988): 87–128. http://dx.doi.org/10.1016/0304-419x(88)90006-6.

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43

Ferguson, Lynnette R., and Bruce C. Baguley. "Multidrug resistance and mutagenesis." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 285, no. 1 (January 1993): 79–90. http://dx.doi.org/10.1016/0027-5107(93)90054-j.

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44

Kaye, S. B. "Reversal of multidrug resistance." Cancer Treatment Reviews 17 (December 1990): 37–43. http://dx.doi.org/10.1016/0305-7372(90)90014-7.

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45

Kavallaris, Maria. "The role of multidrug resistance-associated protein (MRP) expression in multidrug resistance." Anti-Cancer Drugs 8, no. 1 (January 1997): 17–25. http://dx.doi.org/10.1097/00001813-199701000-00002.

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46

Ibrahim, Doa’a Anwar, Al-Akhali A. Al-Akhali A, and Farouk A. Al-Qadasi. "The Prevalence of Antituberculosis Multidrug Resistance in Yemen 2013." International Journal of Scientific Research 3, no. 7 (June 1, 2012): 450–53. http://dx.doi.org/10.15373/22778179/july2014/142.

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47

Gottesman, Michael M., Robert W. Robey, and Suresh V. Ambudkar. "New mechanisms of multidrug resistance: an introduction to the Cancer Drug Resistance special collection." Cancer Drug Resistance 6, no. 3 (2023): 590–5. http://dx.doi.org/10.20517/cdr.2023.86.

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Cancer Drug Resistance publishes contributions to understanding the biology and consequences of mechanisms that interfere with successful treatment of cancer. Since virtually all patients who die of metastatic cancer have multidrug-resistant tumors, improved treatment will require an understanding of the mechanisms of resistance to design therapies that circumvent these mechanisms, exploit these mechanisms, or inactivate these multidrug resistance mechanisms. One example of a resistance mechanism is the expression of ATP-binding cassette efflux pumps, but unfortunately, inhibition of these transporters has not proved to be the solution to overcome multidrug resistance in cancer. Other mechanisms that confer multidrug resistance, and the confluence of multiple different mechanisms (multifactorial multidrug resistance) have been identified, and it is the goal of this Special Collection to expand this catalog of potential multidrug resistance mechanisms, to explore novel ways to overcome resistance, and to present thoughtful reviews on the problem of multidrug resistance in cancer.
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48

Weisburg, J. H., M. Curcio, P. C. Caron, G. Raghu, E. B. Mechetner, P. D. Roepe, and D. A. Scheinberg. "The multidrug resistance phenotype confers immunological resistance." Journal of Experimental Medicine 183, no. 6 (June 1, 1996): 2699–704. http://dx.doi.org/10.1084/jem.183.6.2699.

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Multidrug resistance (MDR), which is due, in part, to the overexpression of P-glycoprotein, confers resistance to a variety of natural product chemotherapeutic agents such as daunorubicin, vincristine, and colchicine. RV+ cells are a P-glycoprotein overexpressing variant of the HL60 myeloid leukemia cell line. In addition to classic MDR, RV+ cells displayed relative resistance to complement-mediated cytotoxicity with both immunoglobulin G and M antibodies against different cell surface antigens, but not to antibody-dependent cellular cytotoxicity and lymphokine-activated killing. Complement resistance was reversed both by treatment with verapamil and with specific monoclonal antibodies (mAbs) capable of binding to P-glycoprotein and blocking its function. To further confirm that the resistance of RV+ cells was not a consequence of the selection of the cells on vincristine, a second system involving P-glycoprotein infectants was also investigated. K562 cells infected with the MDR1 gene, which were never selected on chemotherapeutic drugs, also displayed relative resistance to complement-mediated cytotoxicity. This MDR1 infection-induced resistance was also reversed by mAbs that bind to P-glycoprotein. Therefore, the MDR phenotype as mediated by P-glycoprotein provides resistance to complement-mediated cytotoxicity. The increased intracellular pH and the decreased membrane potential due to the MDR phenotype may result in abnormal membrane attack complex function. This observation may have implications for the possible mechanisms of action of P-glycoprotein and for a possible physiologic role for P-glycoprotein in protection against complement-mediated autolysis.
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49

Wang, Jing-Quan, Yuqi Yang, Chao-Yun Cai, Qiu-Xu Teng, Qingbin Cui, Jun Lin, Yehuda G. Assaraf, and Zhe-Sheng Chen. "Multidrug resistance proteins (MRPs): Structure, function and the overcoming of cancer multidrug resistance." Drug Resistance Updates 54 (January 2021): 100743. http://dx.doi.org/10.1016/j.drup.2021.100743.

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50

Zhao, Lihua, Yanhui Sun, Xiaoqing Li, Xianqing Jin, Youhua Xu, Zhenhua Guo, Rui Liang, Xionghui Ding, Tingfu Chen, and Siqi Wang. "Multidrug resistance strength of the novel multidrug resistance gene HA117: compared with MRP1." Medical Oncology 28, no. 4 (July 16, 2010): 1188–95. http://dx.doi.org/10.1007/s12032-010-9624-y.

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