Relevant bibliographies by topics / Multidrug resistance

Academic literature on the topic 'Multidrug resistance'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Multidrug resistance"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Multidrug resistance"

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Bolhuis, Hendrik. "Multidrug resistance in Lactococcus lactis." [S.l. : [Groningen] : s.n.] ; [University Library Groningen] [Host], 1996. http://irs.ub.rug.nl/ppn/153237724.

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Di, Nicolantonio Federica. "Multidrug resistance in solid tumours." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1354622/.

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Introduction: Most cancers show heterogeneity of response to chemotherapy. This may be due in part to the differential expression of drug resistance proteins and the molecular targets of the drugs concerned. Methods: An ex vivo ATP-based Tumour Chemosensitivity Assay (ATP-TCA), immunohistochemistry and quantitative RT-PCR have been used to assess the chemosensitivity and resistance of a variety of solid tumours and cell lines. Results: (a) Melanoma cell lines showed higher chemosensitivity than tumour-derived cells, partially reversible by lowering the serum concentration, and hence the proliferation rate of the cells. (b) Studies of retinoblastoma samples confirmed that this malignancy is susceptible to cytotoxic drugs of all types, though multidrug resistance may occur in some cases. (c) The ATP-TCA was used to study the activity of high-dose doxorubicin in combination with other cytotoxic agents in ovarian adenocarcinoma samples. The combination of liposomal doxorubicin + vinorelbine was selected for further development. (d) A number of experimental drugs with varying sensitivity to resistance mechanisms were also assessed. One drug, XR5944, has entered phase I/II clinical trials during the course of this project, and the data have provided clinical indications. (e) An inhibitor of multi-drug resistance, tariquidar, has been tested in combination with doxorubicin, vinorelbine or paclitaxel, and has been shown to reverse this resistance. (f) Molecular studies have determined the expression of topoisomerases and drug transporters in tumour cells before and after exposure to chemotherapeutic agents. P-gp expression has been found to be a determinant of sensitivity to a certain number of drugs. Conclusion: The results suggest that drug resistance contributes to heterogeneity of chemosensitivity in many solid tumour types, as well as other mechanisms. Reversal of such resistance may benefit a subset of patients undergoing chemotherapy.
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Clark, Fiona S. "Multidrug resistance in Candida albicans." Thesis, University of Aberdeen, 1994. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU073141.

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Azole-resistance in Candida albicans is becoming common and is associated with the widespread prophylactic use of azoles. Resistance to one azole is usually associated with resistance to other structurally dissimilar azoles. C.albicans is also inherently resistant to a wide range of eukaryotic inhibitors such as cycloheximide and gentamycin. Certain studies have shown that azole-resistance in some strains of C.albicans is associated with alterations in the cell membrane. This project has sought to determine whether azole-resistance in C.albicans strain 3302 was due, at least in part, to a multidrug resistance mechanism. An assay was developed using the fluorescent dye Rh123 to measure P-glycoprotein like activity. Active efflux of Rh123 has been shown to correlate with P-glycoprotein activity in a number of organisms. Results from this assay suggest that an energy-dependent efflux mechanism for Rh123 is present in azole-resistant strain 3302 but not in azole-sensitive strain 3153. The P-glycoprotein inhibitor, reserpine, inhibited Rh123 efflux. However, azoles did not appear to compete with Rh123 for efflux in the azole-resistant strain 3302, suggesting that azole-resistance in this strain is not mediated by a P-glycoprotein like mechanism. Southern analysis showed that sequences homologous to MDR genes existed in C.albicans. A PCR strategy was used to clone gene fragments containing the Walker motif which is found in MDR genes.
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Norris-Cervetto, Edward. "Glycolipids and multidrug resistance in cancer." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419326.

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Bellamy, William Tracey. "Mechanisms of doxorubicin resistance in multidrug resistant human myeloma cells." Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184448.

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Multidrug resistance is a phenomenon associated with the emergence of simultaneous cross-resistance to the cytotoxic actions of a wide variety of structurally and functionally unrelated antineoplastic agents. One of the agents to which cross-resistance is commonly observed is doxorubicin, a commonly used antineoplastic. Studies were undertaken to determine the mechanism of doxorubicin resistance in multidrug resistant 8226 human myeloma cells. When sensitive and resistant cells were exposed to the same extracellular concentration of doxorubicin there was a decrease in the quantity of DNA lesions in the resistant subline which corresponded to a decrease in doxorubicin accumulation. When the extracellular concentration of drug was adjusted to yield equivalent intracellular levels these differences were removed. Studies utilizing an isolated nuclei system revealed no differences in the formation of DNA lesions between the sensitive and resistant cells when exposed to the same concentration of drug. Studies were undertaken to determine if the resistant subline had an increased capacity to detoxify doxorubicin via glutathione-based enzyme systems. The activities of glutathione-s-transferase and glutathione peroxidase were not found to be elevated in the resistant subline. There was a significant elevation in the nonprotein sulfhydryl content of the resistant cells as compared to the drug-sensitive line. This elevation was unstable in the absence of doxorubicin, displaying a steady decline until reaching baseline levels found in the sensitive cells. The decrease in NPSH content in the resistant line was not accompanied by an alteration in doxorubicin resistance. Thus, it appears that glutathione-based enzymatic detoxification is not causally related to doxorubicin resistance in 8226 human myeloma cells. Verapamil, an agent shown by previous studies to modulate doxorubicin resistance, led to an increase in the formation of doxorubicin-induced DNA lesions in the resistant cells secondary to an increase in intracellular drug accumulation. It had no effect on doxorubicin-induced DNA lesions or drug accumulation in the sensitive cells. Verapamil thus appears to be reversing doxorubicin resistance by increasing drug accumulation and thereby enhancing DNA damage. Under these circumstances there was a good correlation between doxorubicin accumulation, DNA damage, and cytotoxicity in the 8226 cells. The conclusion is drawn that drug accumulation accounts for the majority of doxorubicin resistance in the 8226 human myeloma cell line.
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Egger, Michael. "Inhibition of ABC transporters with multidrug resistance." kostenfrei, 2009. http://epub.uni-regensburg.de/13404/.

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Atalay, Mustafa Can. "Multidrug Resistance In Locally Advanced Breast Cancer." Phd thesis, METU, 2004. http://etd.lib.metu.edu.tr/upload/12604991/index.pdf.

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ABSTRACT MULTIDRUG RESISTANCE IN LOCALLY ADVANCED BREAST CANCER ATALAY, Mustafa Can Ph. D., Department of Biotechnology Supervisor: Prof. Dr. Ufuk GÜ
NDÜ
Z June 2004, 70 pages Breast cancer is the most frequently detected cancer among women. Early diagnosis leads to long term survival when the patients are treated with surgery, radiotherapy, chemotherapy, and hormone therapy. Unfortunately, advanced disease could still be encountered in some patients resulting in a poorer prognosis. The primary treatment modality is chemotherapy for this group of patients. Drug resistance is a serious problem resulting in the use of different drugs during chemotherapy and knowing the possibility of resistance before initiating first line chemotherapy may save time and money, and most importantly, may increase patient&rsquo
s survival. Therefore in this study, multidrug resistance is studied in locally advanced breast cancer patients. The breast tissues obtained from 25 patients both before and after chemotherapy were examined for drug resistance. Reverse transcriptase polymerase chain reaction was used for the detection of mdr1 and mrp1 gene expression. In addition, immunohistochemistry technique was used for P-glycoprotein and MRP1 detection. JSB-1 and QCRL-1 monoclonal antibodies were utilized to detect P-glycoprotein and MRP1, respectively. Five patients were unresponsive to chemotherapy. In four of these patients mdr1 gene expression was induced by chemotherapy where as the fifth patient initially had mdr1 gene expression. In addition, Pgp positivity was detected in 9 patients after chemotherapy. Both the induction of mdr1 gene expression (p<
0.001) and Pgp positivity (p<
0.001) during chemotherapy were significantly related with clinical response. On the other hand, mrp1 gene expression and MRP1 positivity were detected in 68% of the patients before the therapy. After chemotherapy, mrp1 expression increased to 84%. Although 80% of the clinically unresponsive patients had mrp1 gene expression, the relation between mrp1 expression and clinical drug response was not strong. Thus, it can be concluded that in locally advanced breast cancer mdr1 gene expression during chemotherapy contributed to clinical unresponsiveness. However, mrp1 gene expression did not correlate strongly with the clinical response. When RT-PCR and immunohistochemistry methods are compared in terms of detection of drug resistance, it seems that both methods gave similar and reliable results.
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Rawson, Emma. "Int6-induced multidrug resistance in S. pombe." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436992.

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Findlay, Jacqueline. "Klebsiella pneumoniae : a progression to multidrug resistance." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6473.

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Klebsiella pneumoniae is a common cause of nosocomial and community-acquired infections, and the increasing incidence and prevalence of antibiotic resistant strains is proving to be particularly problematic to clinicians. K. pneumoniae is capable of employing a multitude of mechanisms by which to confer resistance to most available antibiotics. The carbapenem antibiotics are usually reserved for the treatment of complicated or multidrug resistant (MDR) K. pneumoniae infections. The recent emergence of not only MDR but also pan-drug resistant (PDR) K. pneumoniae strains has signified that it is now more important than ever to understand the mechanisms by which these strains confer resistance so that we may find ways to combat or hinder this progression. This project aimed to investigate the regulation of the transcriptional activator RamA, its ability to confer a MDR phenotype, and the mechanisms employed by K. pneumoniae to confer levels of carbapenem resistance sufficient to result in therapy failure. The analysis of a panel of K. pneumoniae strains, containing both RamA expressers and non-expressers, demonstrated that the overexpression of RamA was sufficient to confer an MDR phenotype. Two compounds, chlorpromazine (CPZ) and tigecycline, were shown to act as inducers of ramA, romA and acrA transcription. CPZ exhibited synergy with the antibiotics chloramphenicol, norfloxacin and tetracycline, all of which are known substrates of the AcrAB efflux pump. The current lack of novel classes of antimicrobials in development indicate a potential for a compound, such as CPZ, to be developed and exploited for clinical use. The ability of both CPZ and tigecycline to cause mutations within ramR however, indicate that both compounds may have the ability to select for efflux mutants as a result of their ability to upregulate ramA, which in turn causes the upregulation of the AcrAB efflux pump. The regulation of RamA by the upstream gene ramR, which encodes a TetR family protein was investigated in K. pneumoniae isolates. Sequencing of the ramR genes revealed that strains exhibiting an MDR phenotype commonly contained mutations within their gene sequences. The complementation of a wildtype ramR into a strain containing a 32 amino acid deletion within its ramR, was shown to increase susceptibility to various antibiotics of different classes, and additionally downregulate the expression of ramA, romA and acrA. CPZ, ciprofloxacin and tigecycline K. pneumoniae mutants were shown to exhibit increased MICs to a broad spectrum of antibiotics with respect to their parent strains, and possess mutations within their ramR genes. Complementation of the wildtype ramR resulted in partial reversion to the parental phenotypes, indicating another mechanism must also be involved in conferring the MDR phenotypes. These studies indicated that RamR plays an important role as a negative regulator of RamA, but also that it is not the sole regulator. The development of reduced susceptibility to the carbapenems was investigated in two clinical strains of K. pneumoniae, K1 and K2, isolated from the urine of a single patient at different stages of antibiotic therapy. The strains were shown to exhibit similar resistance phenotypes with the exception of their susceptibilities to the carbapenems. PCR and phenotypic analyses revealed that neither strain contained any carbapenemases or AmpC enzymes, but both contained OXA-1, SHV-1 TEM-1 and CTX-M-15. Analysis of their OMP profiles indicated that both strains lacked OmpK35, and K2 additionally lacked OmpK36. Mutation studies showed that the phenotype and OMP profile exhibited by K2 could be achieved in K1 via single step mutations using ertapenem, imipenem or meropenem. Susceptibility testing of CTXM- 15 clinical strains showed that strains containing CTX-M-15 showed reduced activity against ertapenem in the presence of clavulanic acid. These studies indicated a potential role for CTX-M-15 in conferring reduced susceptibility to the carbapenems when found in conjunction with altered permeability and active efflux. The mechanisms of antibiotic resistance employed by K. pneumoniae are numerous and complex. This work highlights several of these mechanisms and, more importantly, how they can work in synergy with one another to devastating consequences.
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Davies, Claire Louise. "Multidrug resistance in bladder and breast cancer." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299289.

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Books on the topic "Multidrug resistance"

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T, Paulsen Ian, and Lewis Kim, eds. Microbial multidrug efflux. Wymondham: Horizon Scientific, 2002.

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Boumendjel, Ahcne, Jean Boutonnat, and Jacques Robert, eds. ABC Transporters and Multidrug Resistance. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2009. http://dx.doi.org/10.1002/9780470495131.

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Ahcène, Boumendjel, Boutonnat Jean, and Robert Jacques M. D, eds. ABC transporters and multidrug resistance. Hoboken, N.J: John Wiley & Sons, 2009.

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A, Kellen John, ed. Reversal of multidrug resistance in cancer. Boca Raton, Fla: CRC Press, 1994.

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Kellen, John A., ed. Alternative Mechanisms of Multidrug Resistance in Cancer. Boston, MA: Birkhäuser Boston, 1995. http://dx.doi.org/10.1007/978-1-4615-9852-7.

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A, Kellen John, ed. Alternative mechanisms of multidrug resistance in cancer. Boston: Birkhäuser, 1995.

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Parliamentary Office of Science and Technology. Diseases fighting back. London: Parliamentary Office of Science and Technology, 1994.

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Lee, Peter Daniel. Analysis of multidrug resistance gene expression in osteosarcoma. Ottawa: National Library of Canada, 1994.

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Ulincy, Loretta D. Multidrug resistance: January 1988 through September 1992 : 2250 citations. Bethesda, Md. (8600 Rockville Pike, Bethesda 20894): U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Library of Medicine, Reference Section, 1992.

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Border, Peter. Diseases fighting back: The growing resistance of TB and other bacterial diseases to treatment. London: Parliamentary Office of Science and Technology, 1994.

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Book chapters on the topic "Multidrug resistance"

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Yagüe, Ernesto, and Selina Raguz. "Multidrug Resistance." In Methods of Cancer Diagnosis, Therapy, and Prognosis, 121–33. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3186-0_9.

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Dorn-Beineke, Alexandra, and Cornelia Keup. "Multidrug Resistance." In Cellular Diagnostics, 426–58. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000209174.

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Nahler, Gerhard. "multidrug resistance (MDR)." In Dictionary of Pharmaceutical Medicine, 116. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-89836-9_883.

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Gottesman, Michael M., Suresh V. Ambudkar, Marilyn M. Cornwell, Ira Pastan, and Ursula A. Germann. "Multidrug Resistance Transporter." In Molecular Biology of Membrane Transport Disorders, 243–57. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1143-0_13.

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Clay, Adam T., and Frances J. Sharom. "Multidrug Resistance Protein." In Drug Transporters, 141–60. Hoboken, NJ: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118705308.ch9.

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Hahn, Matthias, and Michaela Leroch. "Multidrug Efflux Transporters." In Fungicide Resistance in Plant Pathogens, 233–48. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55642-8_15.

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Luker, G. D., K. E. Luker, V. Sharma, V. V. Rao, and D. Piwnica-Worms. "Assessment of Multidrug Resistance." In Nuclear Oncology, 371–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58643-9_20.

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Beck, W. T., M. K. Danks, and T. Funabiki. "Issues in multidrug resistance." In Proceedings of the 3rd International Congress on Neo-Adjuvant Chemotherapy, 385–88. Paris: Springer Paris, 1991. http://dx.doi.org/10.1007/978-2-8178-0782-9_93.

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Han, Min, and Jian-Qing Gao. "Nanotherapeutics in Multidrug Resistance." In Cancer Targeted Drug Delivery, 389–412. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7876-8_15.

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Baguley, Bruce C. "Multidrug Resistance in Cancer." In Methods in Molecular Biology, 1–14. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-416-6_1.

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Conference papers on the topic "Multidrug resistance"

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Ćurcic, Radmila, Dragana Vukovic, Irena Zivanovic, Ivana Dakic, and Branislava Savic. "Resistance genotypes of multidrug-resistant Mycobacterium tuberculosis isolates in Serbia." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4632.

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Diddens, Heyke C. "Role of multidrug resistance in photodynamic therapy." In OE/LASE '92, edited by Thomas J. Dougherty. SPIE, 1992. http://dx.doi.org/10.1117/12.60934.

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Pillai, Nisha, Bindu Nanduri, Michael J. Rothrock, Zhiqian Chen, and Mahalingam Ramkumar. "Towards Optimal Microbiome to Inhibit Multidrug Resistance." In 2023 IEEE Conference on Computational Intelligence in Bioinformatics and Computational Biology (CIBCB). IEEE, 2023. http://dx.doi.org/10.1109/cibcb56990.2023.10264914.

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Hasegawa, Hirotsugu, Naoki Inui, Takafumi Suda, Dai Hashimoto, Tomoyuki Fujisawa, Noriyuki Enomoto, Yutaro Nakamura, and Kingo Chida. "Multidrug Resistance Protein 1 And Multidrug Resistance-Associated Protein 1 Expression In Young And Aged Murine Lung Dendritic Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2842.

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Rocchi, Emmanuelle, Jean-Marie Salmon, Jean Vigo, and Pierre M. Viallet. "Multiwavelength videomicrofluorometry for multiparametric investigations of multidrug resistance." In Photonics West '96, edited by Daniel L. Farkas, Robert C. Leif, Alexander V. Priezzhev, Toshimitsu Asakura, and Bruce J. Tromberg. SPIE, 1996. http://dx.doi.org/10.1117/12.239505.

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Giraldo Montoya, Angela María, Giovanni Garcia Castro, Luisa Fernanda Sierra Garzon, and Laura Sofia Garcia Giraldo. "Relationship between PTLD and multidrug resistance to Tuberculosis." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa4538.

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Adams, Mark D. "The Evolution of Multidrug Resistance in a Hospital Pathogen." In 2009 Ohio Collaborative Conference on Bioinformatics (OCCBIO). IEEE, 2009. http://dx.doi.org/10.1109/occbio.2009.10.

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Alageedi, Neyaf Majid, and Kareem Ibrahim Mubarak. "Detection of multidrug resistance (MDR) and pattern of resistance among clinical Pseudomonas aeruginosa isolates." In 2ND INTERNATIONAL CONFERENCE ON MATHEMATICAL TECHNIQUES AND APPLICATIONS: ICMTA2021. AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0102844.

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Dias, Paulo J., Catarina P. Costa, Isabel Sa-Correia, Miguel C. Teixeira, Pedro T. Monteiro, Arlindo L. Oliveira, and Ana T. Freitas. "Using systems biology approaches to study a multidrug resistance network." In 2011 1st Portuguese Meeting in Bioengineering ¿ The Challenge of the XXI Century (ENBENG). IEEE, 2011. http://dx.doi.org/10.1109/enbeng.2011.6026073.

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Ding, Rui, Jia Shi, and Kathleen W. Scotto. "Abstract 1523: Caffeine antagonizes multidrug resistance by down-regulating ABCG2." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1523.

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Reports on the topic "Multidrug resistance"

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Chang, Geoffrey, M. G. Finn, and Ina Urbatsch. Discovery of Potent Inhibitors for Breast Cancer Multidrug Resistance. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada452780.

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Muggia, Franco. Multidrug Resistance in Breast Cancer: Occurrence and Therapeutic Implications. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada303254.

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Sanders, Michael M. Regulation of the Multidrug Resistance-Associated Protein Gene by Estrogen. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada410077.

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Frank, Markus H. Role of ABCB5 P-Glycoprotein in Breast Cancer Multidrug Resistance. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada448637.

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Packard, Alan B. Functional Imaging of Multidrug Resistance in Breast Cancer With PET. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada419633.

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Packard, Alan. Functional Imaging of Multidrug Resistance in Breast Cancer wit PET. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada391036.

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Sanders, Michel. Regulation of the Multidrug Resistance-Associated Protein Gene by Estrogen. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada381694.

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Vaghela, Devan, and Umang Agrawal. Drug treatment of GUTB: short course DOTS and multidrug resistance management. BJUI knowledge, February 2023. http://dx.doi.org/10.18591/bjuik.0564.v2.

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Levenson, Victor V. Lysosome-mediated Cell Death and Autophagy-Dependent Multidrug Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada495800.

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Liu, Yong-Yu. Antisense Oligonucleotides to Glucosylceramide Synthase Can Reverse Multidrug Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada407440.

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You might also be interested in the extended bibliographies on the topic 'Multidrug resistance' for particular source types:
Journal articles Dissertations / Theses Books
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