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Bibliografias temáticas / Drug Resistance

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Literatura científica selecionada sobre o tema "Drug Resistance"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 2 de novembro de 2024

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Artigos de revistas sobre o assunto "Drug Resistance"

1

K, Tiwari. "Drug Resistance: Challenges and Updates". Journal of Natural & Ayurvedic Medicine 3, n.º 3 (15 de julho de 2019): 1–2. http://dx.doi.org/10.23880/jonam-16000196.

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Use of antibiotics increased dramatically in last two decades. To cure most of the diseases broad spectrum antibiotics given. Human society and healthcare is going in wrong direction. One way the pharmaceutical companies are making huge money from it. The other way around is the overuse of these antibiotics, by patients knowing or unknowingly, not only making pathogens adapted but also the normal flora organisms becoming pathogens in coming future? Present article highlight the issues and possible solution of the present scenario.

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Singh, Amresh Kumar. "Resistance patterns and trends of extensively drug-resistant tuberculosis: 5-year experience". Journal of Microbiology and Infectious Diseases 03, n.º 04 (1 de dezembro de 2013): 169–75. http://dx.doi.org/10.5799/ahinjs.02.2013.04.0103.

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Dyary, Hiewa Othman. "Veterinary Anthelmintics and Anthelmintic Drug Resistance". Journal of Zankoy Sulaimani - Part A 18, n.º 1 (12 de novembro de 2015): 191–206. http://dx.doi.org/10.17656/jzs.10463.

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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, n.º 1 (1 de março de 2014): 7–12. http://dx.doi.org/10.5799/ahinjs.02.2014.01.0116.

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5

Giaccone, Giuseppe, e Herbert M. Pinedo. "Drug Resistance". Oncologist 1, n.º 1-2 (fevereiro de 1996): 82–87. http://dx.doi.org/10.1634/theoncologist.1-1-82.

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Hochhauser, D., e A. L. Harris. "Drug resistance". British Medical Bulletin 47, n.º 1 (1991): 178–96. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072454.

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Prichard, R. K. "Drug resistance". International Journal for Parasitology 29, n.º 1 (janeiro de 1999): 137–38. http://dx.doi.org/10.1016/s0020-7519(98)00191-x.

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Texidó, Gemma, e Jürgen Moll. "Drug resistance". Drug Discovery Today: Technologies 11 (março de 2014): 1–3. http://dx.doi.org/10.1016/j.ddtec.2014.03.013.

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9

Köser, Claudio U., Babak Javid, Kathleen Liddell, Matthew J. Ellington, Silke Feuerriegel, Stefan Niemann, Nicholas M. Brown et al. "Drug-resistance mechanisms and tuberculosis drugs". Lancet 385, n.º 9965 (janeiro de 2015): 305–7. http://dx.doi.org/10.1016/s0140-6736(14)62450-8.

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Coen, Donald M., e Richard J. Whitley. "Antiviral drugs and antiviral drug resistance". Current Opinion in Virology 1, n.º 6 (dezembro de 2011): 545–47. http://dx.doi.org/10.1016/j.coviro.2011.10.024.

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Teses / dissertações sobre o assunto "Drug Resistance"

1

Abate, Getahun. "Drug resistance in mycobacterium tuberculosis /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3833-4/.

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Marijani, Theresia. "Modelling drug resistance in malaria". Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/4063.

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Johnson, Rabia. "Understanding the mechanisms of drug resistance in enhancing rapid molecular detection of drug resistance in Mycobacterium tuberculosis". Thesis, Link to the online version, 2007. http://hdl.handle.net/10019.1/1265.

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4

Tam, Stanton Sui Yin. "Anticancer Drug Combinations to Overcome Drug Resistance in Breast Cancer". Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/27733.

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For triple negative breast cancer (TNBC) patients, taxanes are the mainstays of chemotherapy but remain susceptible to resistance. Combination therapy of paclitaxel/docetaxel and tyrosine kinase inhibitors (TKIs) improves overall response rates in TNBC patients. Ixabepilone, mechanistically similar to taxanes, shows efficacy in TNBCs refractory to paclitaxel/docetaxel. Yet, there is a lack of studies on ixabepilone-TKI combinations. The first aim was to investigate the efficacy of these combinations in docetaxel-resistant MDA-MB-231 (TXT) cells and parental non-resistant MDA-MB-231 (231C) cells. In preliminary studies, ixabepilone, vandetanib and gefitinib monotherapy inhibited proliferative activity in both cell lines. Vandetanib and ixabepilone showed drug synergism and increased inhibition of cell proliferation. Gefitinib and ixabepilone demonstrated drug antagonism and reduced cell proliferation. Annexin V-FITC/7AAD staining demonstrated increased cell killing after vandetanib-ixabepilone treatment and ascertained apoptosis as the mechanism of cell death in both cell lines. It revealed that vandetanib increases apoptosis when in combination compared to ixabepilone alone. This was supported by Western blotting which yielded altered protein expression of apoptotic players, cleaved-caspase-3 and Bcl-2. The second aim was to determine how the vandetanib-ixabepilone combination induces apoptosis and overcomes resistance in both cell lines. Using Western blotting, it was determined that vandetanib does not contribute to increased cell death via microtubule stabilisation – the principal apoptotic mechanism of ixabepilone. Instead, in 231C and TXT cells, vandetanib increased proapoptotic NOXA and PUMA respectively. This thesis reveals a novel combination with antiproliferative/apoptotic activity in docetaxel-resistant and non-resistant TNBC cell lines and lays the foundation for more combinations to overcome resistance and provide novel therapies for TNBC patients.

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Abrahem, Abrahem F. "Mechanisms of drug resistance in malaria". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0033/MQ50704.pdf.

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6

Scott, F. M. "Drug resistance mechanisms in multiple myeloma". Thesis, University of Edinburgh, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.661665.

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The aim of this thesis was to investigate expression of putative drug resistance markers in myeloma both by examining clinical material and through the development of a xenograft model. Pgp expression was examined in 57 samples from 37 patients with myeloma. Of 23 samples at presentation and 37 at relapse, 7 and 26 respectively were Pgp positive. A myeloma xenograft model was established to examine the acute effects of cytotoxic drugs on the expression of "classical" drug resistance markers and genes involved in regulation of apoptosis. The untreated xenografts were Pgp negative, expressed low levels of glutathione S-transferase-P (GSTP) and had readily detectable topo I and II. Little p62 myc or p53 were detected, whereas bcl-2 was strongly expressed. Treated xenografts contained only scattered apoptotic cells, but the majority demonstrated cell cycle arrest at the G2/M transition, and GSTP and topo IIα expression were increased. Pgp expression was also increased in animals treated on 3 consecutive days. C-myc was detected in dead or dying cells, but there was no mutational inactivation of p53, and bcl-2 expression was unaltered. The increased Pgp and GSTP expression following therapy, rather than inducing a resistant phenotype, may reflect activation of expression by drug administration. Cellular resistance occurred despite evidence of DNA damage suggesting that resistance arose from failure to engage apoptosis, possibly due to the strong bcl-2 expression. Bcl-2 expression was therefore evaluated in 40 samples from 31 individuals, with strong expression observed in over 80% of cases. This was not associated with rearrangement of the bcl-2 locus. The presence of abundant bcl-2 protein in the majority of cases has potentially important implications for drug resistance in this disease and suggests that future assessment of drug resistance in myeloma may be better directed downstream of immediate drug-target interactions to regulation of engagement of apoptosis.

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Pongtavornpinyo, Wirichada. "Mathematical modelling of antimalarial drug resistance". Thesis, University of Liverpool, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428249.

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Wildridge, David. "Metabolism and drug resistance in Trypanosomatids". Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3622/.

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The principle aim of this project is the investigation of metabolism and mechanisms of pentamidine resistance in trypanosomatids. An understanding of these mechanisms may allow the development of novel drugs to treat Leishmaniasis and human African trypanosomiasis (HAT), caused by the protozoan parasites Leishmania spp and Trypanosoma brucei. In this study a pentamidine resistance L. mexicana promastigote cell line was generated in vitro. This cell line was 20-fold resistant to pentamidine when compared to the parental wild type cells. Furthermore, these lines were cross resistant to other diamidine compounds. A proteomic analysis of these cell lines revealed numerous changes to the proteome, with the down regulation of several flagellar proteins. A hypothesis to investigate a role of the voltage dependent anion channel (VDAC) in pentamidine resistance was also explored. The metabolomic approach involved the investigation of transketolase and the pentose phosphate pawthway. A previous study involving a transketolase knockout T. brucei cell line indicated that an increased sensitivity to pentamidine and methylene blue. A transketolase deficient L. mexicana cell line was generated to test this hypothesis in Leishmania, however the differences were minimal. A metabolomic analysis of the L. mexicana tkt null cell line (lmtkt-/-) revealed an increase in ribose 5-phosphate, a key substrate of transketolase. Erythrose 4-phosphate also increased in the lmtkt-/- cells, indicating a source of this metabolite independent of TKT. It appears that the deletion of TKT prevents any flux through the oxidative branch of the PPP returning to the glycolytic pathway. Interestingly, the lmtkt-/- cells do not acidify the medium to the same extent as the wild type cells; however a glucose assay indicated that both cell lines used similar quantities of glucose. This would suggest that there is a change in the metabolites excreted by the lmtkt-/- cell line. Finally, a global metabolomics approach was investigated using high resolution mass spectrometry. Metabolomics is a rapidly developing field in systems biology, and whilst significant improvements have been made in mass spectrometry; the ability to analyse and interpret raw metabolomic datasets on a global scale has been largely neglected. Consequently, a database program to query these complex datasets was constructed.

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Doherty, Catherine Jean. "Drug resistance mechanisms in multiple myeloma". Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/22154.

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ROMANO, GABRIELE. "Molecular mechanisms of cancer drug resistance". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/93577.

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Colorectal cancer (CRC) is one of the most prevalent and incident cancers worldwide and it has become soon an important public health issue. Although surgery represents the principal curative treatment, chemotherapy is one of the most important tools currently available for the treatment of CRC. 5-fluorouracil (5FU) is the chemotherapeutic agent of election for CRC treatment. Two main problems affect the outcome of cancer chemotherapy: the use of poorly specific drugs and, in a high percentage of patients, the lack of response due to drug resistance, seen as a major obstacle to improve the overall response and survival of cancer patients, limiting the effectiveness of chemotherapy. GSK-3β and TGF-β are known to be master regulators of a plethora of signalling pathways in various mechanisms involved in cancer development, resistance and dissemination. In this thesis is shown that inhibition of GSK-3β (mediated by shRNA or Lithium) is able to revert chemoresistance to 5-FU in HCT116 P53-/- cells (a colon cancer cell line resistant to chemotherapy because of P53 deletion), both in vitro and in vivo through a heterotopic xenograft model. We started from this model of restoration of chemosensitivity to analyze some major features of the TGF-β pathway. Microvasculature analysis on xenografted tumor sections, revealed a dramatic increase of tumor vascularization in consequence of 5FU administration whereas Lithium and 5FU combination was able to significantly decrease the vasculature density, restoring the basal value. Moreover, 5FU is able to stimulate nuclear translocation of SMAD3 and the transcription of specific genes such as ACVRL1,FN1 and TGFB1. Contrarily, the specific inhibition of TGF-βRI, not only is able to inhibit the 5FU-induced genes transcription, but also restores the sensitivity of chemoresistant cells to the action of chemotherapeutic, causing the repression of BCL2L1 and ID1 genes. Chemoresistant cells behavior was consistent to a sort of autocrine protective loop acted by TGFB1 in consequence of 5FU administration. Moreover, in this work is presented a bioinformatics study on colorectal cancer patients. Patients enrolled in the study underwent preoperative chemoradiotherapy, followed by surgical excision. By determining gene expression profiles, responders and non-responders showed significantly different expression levels for 19 genes (P < 0.001). We fitted a logistic model selected with a stepwise procedure optimizing the Akaike Information Criterion (AIC) and then validated by means of leave one out cross validation (LOOCV, accuracy D 95%). Four genes were retained in the achieved model: ZNF160, XRCC3, HFM1 and ASXL2. Real time PCR confirmed that XRCC3 is overexpressed in responders group. In vitro test on colon cancer resistant/susceptible to chemoradioterapy cells, finally prove that XRCC3 deregulation is extensively involved in the chemoresistance mechanisms. Protein-protein interactions (PPI) analysis involving the predictive classifier revealed a network of 45 interacting nodes (proteins) with TRAF6 gene playing a keystone role in the network. In this thesis is also presented a work on Glioblastoma multiforme (GBM) drug resistance. GBM is one of the most fatal and least successfully treated solid tumors: current therapies provide a median survival of 12-15 months after diagnosis, due to the high recurrence rate. Glioma Stem Cells (GSCs) are believed to be the real driving force of tumor initiation, progression and relapse. Therefore, better therapeutic strategies GSC-targeted are needed. Resveratrol (RSV) is a polyphenolic phytoalexin found in fruits and vegetables displaying pleiotropic health benefits. Results showed that response to RSV exposure was highly heterogeneous among GSC lines, but generally it was able to inhibit cell proliferation, increasing cell mortality, and strongly decrease cell motility, modulating the Wnt signaling pathway.

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Livros sobre o assunto "Drug Resistance"

1

Hait, William N., ed. Drug Resistance. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3.

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2

Imperial Cancer Research Fund (Great Britain). Drug resistance. Editado por Stark, George R. (George Robert), 1933- e Calvert H. Oxford, U.K: Published for the Imperial Cancer Research Fund by Oxford University Press, 1986.

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3

N, Hait William, ed. Drug resistance. Boston: Kluwer Academic Publishers, 1996.

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4

Baiocchi, Marta, ed. Cancer Drug Resistance. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2513-2.

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5

Mayers, Douglas L., Jack D. Sobel, Marc Ouellette, Keith S. Kaye e Dror Marchaim, eds. Antimicrobial Drug Resistance. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-46718-4.

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6

Teicher, Beverly A., ed. Cancer Drug Resistance. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-035-5.

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Goldstein, Lori J., e Robert F. Ozols, eds. Anticancer Drug Resistance. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2632-2.

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Mayers, Douglas L., Jack D. Sobel, Marc Ouellette, Keith S. Kaye e Dror Marchaim, eds. Antimicrobial Drug Resistance. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47266-9.

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Mayers, Douglas L., ed. Antimicrobial Drug Resistance. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-595-8.

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Mayers, Douglas L., ed. Antimicrobial Drug Resistance. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-180-2.

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Capítulos de livros sobre o assunto "Drug Resistance"

1

Saez, S. "Drug Resistance". In Endocrine Therapy of Breast Cancer III, 17–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74504-1_3.

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2

Wang, Bo. "Drug Resistance". In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1739-7.

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3

Tomasetti, Cristian. "Drug Resistance". In A Systems Biology Approach to Blood, 303–16. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2095-2_15.

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4

Tew, Kenneth D. "Drug Resistance". In Basic Science of Cancer, 187–215. London: Current Medicine Group, 2000. http://dx.doi.org/10.1007/978-1-4684-8437-3_10.

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Tu, Shi-Ming. "Drug Resistance". In Cancer Treatment and Research, 161–75. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-5968-3_15.

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Wang, Bo. "Drug Resistance". In Encyclopedia of Cancer, 1431–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_1739.

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7

Weber, Georg F. "Drug Resistance". In Molecular Therapies of Cancer, 407–21. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13278-5_16.

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Mounsey, Kate E., Robert J. Harvey e Bart J. Currie. "Drug Resistance". In Scabies, 397–418. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-26070-4_27.

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Ashraf, Saima, Nabila Bashir, Nadia Rashid, Adeel Hussain Chughtai, Khalid Mahmood Zia, Saadat Majeed, Muhammad Naeem Ashiq, Ghulam Murtaza e Muhammad Najam-ul-Haq. "Introduction to Drugs, Drug Targets and Drug Resistance". In Biochemistry of Drug Resistance, 1–31. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-76320-6_1.

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Ford, James M., Jin-Ming Yang e William N. Hait. "P-Glycoprotein-Mediated Multidrug Resistance: Experimental and Clinical Strategies for its Reversal". In Drug Resistance, 3–38. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3_1.

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Trabalhos de conferências sobre o assunto "Drug Resistance"

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Asnaashari, Tina Ghodsi, e Young Hwan Chang. "Optimal drug treatment for reducing long-term drug resistance". In 2022 IEEE 61st Conference on Decision and Control (CDC). IEEE, 2022. http://dx.doi.org/10.1109/cdc51059.2022.9992804.

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Khamenehfar, Avid, Ji Liu, Jia Cai, Michael Wong, Paul C. H. Li, Patrick Ling e Pamela Russell. "Drug Accumulation Into Single Drug-Sensitive and Drug-Resistant Prostate Cancer Cells Conducted on the Single Cell Bioanalyzer". In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-36166.

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Multidrug resistance (MDR) occurs in prostate cancer, and this happens when the cancer cells resist chemotherapeutic drugs by pumping them out of the cells. MDR inhibitors such as cyclosporin A (CsA) can stop the pumping and enhance the drugs accumulated in the cells. The cellular drug accumulation is monitored using a microfluidic chip mounted on a single cell bioanalyzer. This equipment has been developed to measure accumulation of drugs such as doxorubicin (DOX) and fluorescently labeled paclitaxel (PTX) in single prostate cancer cells. The inhibition of drug efflux on the same prostate cell was examined in drug-sensitive and drug-resistant cells. Accumulation of these drug molecules was not found in the MDR cells, PC-3 RX-DT2R cells. Enhanced drug accumulation was observed only after treating the MDR cell in the presence of 5 μM of CsA as the MDR inhibitor. We envision this monitoring of the accumulation of fluorescent molecules (drug or fluorescent molecules), if conducted on single patient cancer cells, can provide information for clinical monitoring of patients undergoing chemotherapy in the future.

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Ayati, Marzieh, Golnaz Taheri, Shahriar Arab, Limsoon Wong e Changiz Eslahchi. "Overcoming drug resistance by co-targeting". In 2010 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2010. http://dx.doi.org/10.1109/bibm.2010.5706562.

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Bumin, Aysegul, Megan Shah, Kejun Huang e Tamer Kahveci. "Vulture: VULnerabilities in impuTing drUg REsistance". In BCB '23: 14th ACM International Conference on Bioinformatics, Computational Biology, and Health Informatics. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3584371.3612993.

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Sallum, Ulysses W., Xiang Zheng, Sarika Verma e Tayyaba Hasan. "Exploiting bacterial drug resistance: a single construct for the diagnosis and treatment of drug resistant infections". In 12th World Congress of the International Photodynamic Association, editado por David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.828202.

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Shurbeska, Boneva, Jasmina Nikolovska, Vladimir Mitrevski, Sead Zejnel, Nikola Chamurovski, Ersin Merdžanovski, Ivanovska Savin et al. "Following the resistance pattern of mycobacterium tuberculosis". In Proceedings of the International Congress Public Health - Achievements and Challenges, 74. Institute of Public Health of Serbia "Dr Milan Jovanović Batut", 2024. http://dx.doi.org/10.5937/batutphco24029s.

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Background: Tuberculosis (TB) accounts for over 40% of all mortality cases from communicable diseases in Europe.Multidrug-resistant TB (MDR-TB) is TB that does not respond to at least isoniazid and rifampicin, the 2 most powerful anti-TB drugs. 30 countries worldwide are classified as high multi drug resistant (MDR) TB burden countries, nine are in the European Region. The emergence of combined resistance to rifampicin and isoniazid (MDR-TB) is a matter of global concern. Methods and Objectives: Over a period of 10 years we examined patient specimens for TB. Culture-positive samples were subjected to identification, and those cultures identified as M. tuberculosis (MTB) complex were subjected to drug susceptibility testing (DST). DST for first-line drugs was performed using proportional method on Lowenstein Jensen, and in recent years, rapid molecular techniques recommended by WHO (GeneXpert). DST for second line drugs was assessed using Geno Type MTBDRsl. Results: In the period 2012-2022 we tested 1554 TB strains, 1449 (93,24%) were found to be sensitive and 99 (6,37%) resistant to first-line drugs. 75 strains (4,83%) were monoresistant, 15 (0,96%) of which were resistant only to Rifampicin. Of the total 1423 strains, 22 (1,41%) were found to be MDR. Conclusions: Currently a low 1,41% of our isolates are MDR. It is necessary to strengthen our TB laboratory capacity for early detection of drug-resistant TB. This is best done by using rapid molecular diagnosis as an initial method for all cases with clinical suspicion of TB.

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Casagrande, Anne-Sophie, Florence Mahe, Vin Kotraiah, Matt Pando e Laurent Desire. "Abstract 4860: Identification of novel epitopes, drug resistance markers and drug resistance mechanism using alternative splicing studies". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4860.

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Taitt, Chris Rowe, Tomasz Leski, David Stenger, Gary J. Vora, Brent House, Matilda Nicklasson, Guillermo Pimentel et al. "Antimicrobial resistance determinant microarray for analysis of multi-drug resistant isolates". In SPIE Defense, Security, and Sensing. SPIE, 2012. http://dx.doi.org/10.1117/12.924569.

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9

Xiaxia Yu, Robert W. Harrison e Irene T. Weber. "HIV drug resistance prediction using multiple regression". In 2013 IEEE 3rd International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2013. http://dx.doi.org/10.1109/iccabs.2013.6629203.

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10

Sawyers, Charles L. "Abstract PL04-01: Overcoming cancer drug resistance". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-pl04-01.

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Relatórios de organizações sobre o assunto "Drug Resistance"

1

DeClerck, Yves A. Environment-Mediated Drug Resistance in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, outubro de 2013. http://dx.doi.org/10.21236/ada591172.

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2

DeClerck, Yves A. Environment-Mediated Drug Resistance in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, outubro de 2014. http://dx.doi.org/10.21236/ada616252.

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3

Perelson, A. S., B. Goldstein e B. T. Korber. Emerging pathogens: Dynamics, mutation and drug resistance. Office of Scientific and Technical Information (OSTI), outubro de 1997. http://dx.doi.org/10.2172/534529.

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4

Hiscott, John. Oncolytic Virotherapy Targeting Lung Cancer Drug Resistance. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2013. http://dx.doi.org/10.21236/ada589848.

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5

Shen, Youqing, Maciej Radosz e William J. Murdoch. Breast Cancer-Targeted Nuclear Drug Delivery Overcoming Drug Resistance for Breast Cancer Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, setembro de 2011. http://dx.doi.org/10.21236/ada559246.

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6

Kennedy, Katherine A. Physiological Stree-Induced Drug Resistance and Its Reversal. Fort Belvoir, VA: Defense Technical Information Center, julho de 2001. http://dx.doi.org/10.21236/ada398214.

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7

Kennedy, Katherine A. Physiological Stress-Induced Drug Resistance and Its Reversal. Fort Belvoir, VA: Defense Technical Information Center, julho de 2002. http://dx.doi.org/10.21236/ada408700.

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8

Kennedy, Katherine. Physiological Stress-Induced Drug Resistance and Its Reversal. Fort Belvoir, VA: Defense Technical Information Center, julho de 2000. http://dx.doi.org/10.21236/ada383040.

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9

Kennedy, Katherine. Physiological Stress-Induced Drug Resistance and its Reversal. Fort Belvoir, VA: Defense Technical Information Center, julho de 2004. http://dx.doi.org/10.21236/ada474449.

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10

Shannon, Kevin. Drug Response and Resistance in Advanced NF1-Associated Cancers. Fort Belvoir, VA: Defense Technical Information Center, abril de 2013. http://dx.doi.org/10.21236/ada581891.

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