Relevant bibliographies by topics / Anti-cancer drugs

Academic literature on the topic 'Anti-cancer drugs'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Anti-cancer drugs"

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Tahara, Makoto. "Anti-cancer drugs for thyroid cancer." Annals of Oncology 28 (October 2017): ix63. http://dx.doi.org/10.1093/annonc/mdx612.

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Kabir, Md Lutful, Feng Wang, and Andrew H. A. Clayton. "Intrinsically Fluorescent Anti-Cancer Drugs." Biology 11, no. 8 (July 28, 2022): 1135. http://dx.doi.org/10.3390/biology11081135.

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At present, about one-third of the total protein targets in the pharmaceutical research sector are kinase-based. While kinases have been attractive targets to combat many diseases, including cancer, selective kinase inhibition has been challenging, because of the high degree of structural homology in the active site where many kinase inhibitors bind. Despite efficacy as cancer drugs, kinase inhibitors can exhibit limited target specificity and rationalizing their target profiles in the context of precise molecular mechanisms or rearrangements is a major challenge for the field. Spectroscopic approaches such as infrared, Raman, NMR and fluorescence have the potential to provide significant insights into drug-target and drug-non-target interactions because of sensitivity to molecular environment. This review places a spotlight on the significance of fluorescence for extracting information related to structural properties, discovery of hidden conformers in solution and in target-bound state, binding properties (e.g., location of binding sites, hydrogen-bonding, hydrophobicity), kinetics as well as dynamics of kinase inhibitors. It is concluded that the information gleaned from an understanding of the intrinsic fluorescence from these classes of drugs may aid in the development of future drugs with improved side-effects and less disease resistance.
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Kondo, Shunsuke, and Nagahiro Saijo. "Target-based anti-cancer drugs." Drug Delivery System 19, no. 2 (2004): 103–9. http://dx.doi.org/10.2745/dds.19.103.

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Lim, Young-Chai. "Pharmacogenomics of Anti-Cancer Drugs." Journal of Korean Society for Clinical Pharmacology and Therapeutics 12, no. 2 (2004): 93. http://dx.doi.org/10.12793/jkscpt.2004.12.2.93.

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Hofheinz, Ralf-Dieter, Senta Ulrike Gnad-Vogt, Ulrich Beyer, and Andreas Hochhaus. "Liposomal encapsulated anti-cancer drugs." Anti-Cancer Drugs 16, no. 7 (August 2005): 691–707. http://dx.doi.org/10.1097/01.cad.0000167902.53039.5a.

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Jaouen, Gérard, Anne Vessières, and Siden Top. "Ferrocifen type anti cancer drugs." Chemical Society Reviews 44, no. 24 (2015): 8802–17. http://dx.doi.org/10.1039/c5cs00486a.

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Olejniczak, K. "Application to anti-cancer drugs." Toxicology Letters 205 (August 2011): S2. http://dx.doi.org/10.1016/j.toxlet.2011.05.010.

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Wu, Nan, Yizhen Xie, and Burton B. Yang. "Anti-cancer drugs for cardioprotection." Cell Cycle 16, no. 2 (November 10, 2016): 155–56. http://dx.doi.org/10.1080/15384101.2016.1242536.

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Fallowfield, Lesley, Valerie Jenkins, Carolyn Langridge, Ivonne Solis-Trapala, Alison Jones, and Jane Barrett. "Discussing expensive anti-cancer drugs." British Journal of Healthcare Management 17, no. 5 (May 2011): 206–12. http://dx.doi.org/10.12968/bjhc.2011.17.5.206.

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Tembhe, Harshada, and Rupali Tasgaonkar. "Vinca Alkaloids – Anti cancer drugs." International Journal for Research in Applied Science and Engineering Technology 11, no. 1 (January 31, 2023): 408–16. http://dx.doi.org/10.22214/ijraset.2023.48559.

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Abstract: Cancer, one of the most common disease, is responsible for nearly 10 million deaths annually. The treatment of cancer typically includes surgery, chemotherapy, radiation therapy, and drug therapy which have a significant financial impact on patients. Also, over the time, patients may develop drug resistance. By applying evidence-based preventative techniques, a significant number of cancer cases can be avoided or treated. Plant-based medications have emerged as hopeful alternatives to chemotherapy in both developed and developing countries. Alkaloids are the secondary plant metabolites that have shown to be effective and acceptable for treating cancer. The secondmost popular family of cancer medications is vinca alkaloids, and they will continue to be utilised for cancer treatment. These medications, which include vinblastine, vincristine, vindesine, and vinorelbineare frequently used either alone or in combination with other medications. These cell cycle-dependent drugs work by preventing tubulin from polymerizing into microtubules, which causes cell death. There have been several studies looking at the pharmacological behaviour of this family of antitumor drugs in both humans and animals utilising diverse in vivo and in vitro models. Despite tremendous improvements in the prevention and control of cancer progression, there are still many flaws and space for growth. Several undesirable side effects might occasionally happen when receiving chemotherapy. Natural treatments, and hence the use of cancer therapy agents produced from plants, may reduce negative side effects.
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Dissertations / Theses on the topic "Anti-cancer drugs"

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Yeh, Teng-Kuang. "Pharmacokinetics of anti-aids and anti-cancer drugs : implications on drug delivery and drug interaction /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu148654688938101.

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Soldevila, Barreda Joan Josep. "Design of catalytic organometallic anti-cancer drugs." Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/63808/.

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This thesis is concerned with the design of organometallic half sandwich complexes which can catalyse the conversion of oxidised coenzyme nicotinamide adenine dinucleotide to its reduced form. The coenzyme pair NAD+/NADH is involved in many biological processes, such as regulation of the redox balance, and DNA repair. Disturbance of the NAD+/NADH ratio can lead to cell death. In particular, cancer cells are under constant oxidative stress and therefore might be more susceptible to changes in the NAD+/NADH levels. A series of neutral Ru(II) complexes of the type [(η6-arene)Ru(N,N’)(L)] (arene = p-cymene (p-cym), hexamethylbenzene (hmb), biphenyl (bip), benzene (bn); N,N’ = N-(2-aminoethyl)-4-(trifluoromethyl)benzenesulfonamide (TfEn), N-(2-aminoethyl)-toluensulfonamide (TsEn), or N-(2-aminoethyl)-4-methylensulfonamide (MsEn)) were synthesized and fully characterized. The complexes were shown by 1H-NMR to catalyse region-selectively the transfer hydrogenation of NAD+ to 1,4-NADH. Comparison of the turnover frequencies (TOF) for the complexes show a trend in which a decrease in catalytic activity with the arene ligand follows the order bn > bip > p-cym > hmb and TfEn > TsEn > MsEn. Complex [(η6-bn)Ru(TfEn)Cl] (12) was found to be the most active with a TOF of 10.4 h-1. The catalytic cycle for the transfer hydrogenation reaction was studied for complex [(p-cym)Ru(TsEn)Cl] (2). The monotosylate ethylenediamine Ru(II) complexes were used to carry out, for the first time, transfer hydrogenation reactions in cellulo (A2780 ovarian cancer cells) using formate as a hydride source. The antiproliferative activity of six complexes on co-administration with non-toxic doses of sodium formate were studied. A significant potentiation of the antiproliferative activity by formate was observed. The concentrations of NAD+ and NADH in cells showed an important reduction in the NAD+/NADH ratio. This study demonstrates that it may be possible to use catalytic transfer hydrogenation as a strategy for multi-targeted redox mechanisms of action for anticancer drugs. In order to compare the anticancer mechanism of the monotosylate ethylenediamine Ru(II) complexes with the corresponding ethylenediamine (en) complexes, DNA binding studies were carried out. The complexes were shown to bind to nucleobases only moderately strongly and no direct coordination to calf thymus DNA was observed. The complexes can destabilize DNA, but they display low affinity towards DNA, which suggests that DNA is probably not involved in the mechanism of these family of compounds. Interaction of complex [(p-cym)Ru(TsEn)] (2) with glutathione (GSH) was also studied. The complex undergoes ligand substitution. Two Ru(II) dimers were formed as the main products of the reaction: ([((p-cym)Ru)2(μ-GS)3] and [((p-cym)Ru)2(μ-GS)2]). These dimers share structural similitudes with other reported Ru(II) arene anticancer drugs, which suggests that they could be responsible for the moderate antiproliferactive activity of complex 2. A series of CpxRh(III) (CpX = CpXPhPh, CpXPh or Cp*) complexes containing en or TfEn were synthesised and fully characterised. The complexes were shown to catalyse regioselectively the transfer hydrogenation of NAD+ to 1,4-NADH with higher TOF than their Ru(II) analogues. Rh(III)-en compounds were shown to be more active than the Rh(III)-TfEn analogues. The nature of the Cpx ring was shown to influence significantly the catalytic activity of the complexes following the trend: CpXPhPh > CpXPh > Cp*. Complex [(CpXPhPh)Rh(en)Cl]+ (19) was the most active, with a TOF of 24.2 h-1. The catalytic cycle for the transfer hydrogenation reaction was studied using complex [(Cp*)Rh(en)Cl]+ (17) and compared to that of the Ru(II) analogues, and was found to be similar. Antiproliferative activity of the complexes in combination with formate, in A2780 cells, was investigated, but the potentiation due to the transfer hydrogenation was much lower than that obtained with Ru(II) compounds.
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Butler, Gregory James. "Non-steroidal anti-inflammatory drugs and skin cancer /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19122.pdf.

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Moorad, Razia. "Computer-aided drug design and the biological evaluation of anti-cancer drugs." Doctoral thesis, University of Cape Town, 2016. http://hdl.handle.net/11427/20715.

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Computer-aided drug design has become a promising alternative to high-throughput screening by identifying potential hits in silico for in vitro evaluation. In this study a combination of ligand-based and structure-based virtual screening was performed to identify in silico hits. This was based on finding similar inhibitors to 6-amino-4-(4-phenoxyphenylethylamino) quinazoline, a potent inhibitor of the Nuclear Factor kappa B (NF-κB), a transcription factor that has a pivotal role in cancer survival and Pentamidine, an anti-parasitic drug that has recently been demonstrated to possess tumour-killing activity. A hierarchical methodology consisting of a similarity search followed by structure-based virtual screening of the ZINC database was performed. In order to perform the docking studies, binding sites for 6-amino-4-(4-phenoxyphenylethylamino) quinazoline on the NF-κB/IκBα complex were identified through blind docking. In addition, the National Cancer Institute (NCI) database was screened, utilising existing structure-activity relationship data from literature. A pharmacophore search was designed to test the hypothesis of the structural features necessary for activity as seen with quinazoline inhibitors of NF-κB. No virtual hits from the ZINC database were confirmed with in vitro activity. On the other hand, three compounds identified from the pharmacophore search were confirmed to inhibit cancer cell proliferation in vitro, with compound NSC727152 demonstrating the most potent activity. In order to determine if NSC727152 acted similarly to 6-amino-4-(4-phenoxyphenylethylamino) quinazoline by inhibiting NF-κB, the effects of NSC727152 on the expression of NF-κB targeted genes, including the Growth Arrest and DNA Damage 45 (GADD45) α and γ and the Interleukin 6 (IL-6) genes were evaluated. GADD45 α and γ have been shown to be regulated by NF-κB during cancer progression and aberrant IL-6 gene expression has been implicated in cancer progression and mortality and its expression is at least partially mediated via constitutive activation of NF-κB. In this study, it has been demonstrated that GADD45 α and γ are upregulated after treatment with NSC727152. A down-regulation of the IL-6 promoter activity and mRNA expression in cancer cells treated with NSC727152 has also been demonstrated in this study. However, no hits similar to Pentamidine were confirmed with in vitro activity. In conclusion, the compound NSC727152 has been shown to inhibit NF-κB and further analysis is necessary to determine its full potential as an NF-κB inhibitor.
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Gascoigne, Karen Elizabeth. "The response of cancer cells to anti-mitotic drugs." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493935.

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In 2007 over 12 million people were diagnosed with cancer. At least one third of these individuals are not expected to survive the disease, making cancer the second most prevalent cause of death worldwide. Systemic chemotherapy forms the mainstay of cancer treatment. In particular, this thesis focuses on antimitotic drugs, which are now common chemotherapeutic agents used to treat a wide variety of cancers. These compounds have seen success in the clinic, however, patient response remains highly unpredictable and resistance to treatment is commonplace. Anti-mitotic drugs such as taxol and the vinca alkaloids are thought to inhibit tumour proliferation by disrupting formation of the mitotic spindle, preventing normal Prolonged mitotic arrest due to chronic activation of the spindle assembly checkpoint (5AC). It is presumed that this prolonged arrest leads to cell death, however, the molecular links between mitotic arrest and cell death are ill-defined.
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Wahed, I. A. "Testicular toxicity of standard and investigational anti-cancer drugs." Thesis, University of Bradford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380578.

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Abumansour, Hamza M. A. "Quantitative pharmacoproteomics investigation of anti-cancer drugs in mouse : development and optimisation of proteomics workflows for evaluating the effect of anti-cancer drugs on mouse liver." Thesis, University of Bradford, 2016. http://hdl.handle.net/10454/15724.

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Minimizing anti-cancer drug toxicity is a major challenge for the pharmaceutical industry. Toxicity is most frequently due to either the direct interaction of the drug on previously unidentified targets or its conversion to metabolites by drug metabolizing enzymes (e.g. CYP450 enzymes) that cause cellular, tissue or organ damage. Pharmacoproteomics is beginning to take a central role in studying changes in protein expression corresponding to drug administration, the results of which, inform about the mode of action, toxicity, and resistance in pre-clinical and clinical stages of drug development. The main aim of this research is to apply comparative proteomics studies on livers from male and female mice xenograft models treated with major anti-cancer drugs (5-flourouracil, paclitaxel, cisplatin, and doxorubicin) and CYP inducer, TCPOBOP, to investigate their effect on protein expression profiles (proteome). Within this thesis, an attention is paid to optimise a highly validated proteomics workflow for biomarker identification. Proteins were extracted from liver microsomes of mice treated in two separate sets; Set A – male (5-fluoruracil, doxorubicin, cisplatin and untreated) or Set B – female (5-fluoruracil, paclitaxel, TCPOBOP and untreated) using cryo-pulverization and sonication method. The extracts were digested with trypsin ii and the resulting peptides labelled with 4-plex iTRAQ reagents. The labelled peptides were subjected for separation in two-dimensions by iso-electric focusing (IEF) and RP-HPLC techniques before analysis by mass spectrometry and database searching for protein identification. Set A and Set B resulted in identification and quantification of 1146 and 1743 proteins, respectively. Moreover, Set A and Set B recovered 26 and 34 cytochrome P450 isoforms, respectively. The microsomal changes after drug treatments were quite similar. However, more changes were observed in the male set. Up-regulation of MUPs showed the greatest distinction in the protein expression patterns in the treated samples comparing to the untreated controls. In Set A, 5-fluoruracil and cisplatin increased the expression of three isoforms (MUP1, 2, and 6), whereas doxorubicin has increased the expression of four isoforms (MUP1, 2, 3, and 6). On the other side, only TCPOBOP in Set B has increased the expression of two isoforms (MUP1 and 6). Our findings showed that the expression of MUP, normally involved in binding and excretion of pheromones, have drug- and sex-specific differences. The mechanism and significance of MUP up-regulation are ambiguous. Therefore, the impact of each therapeutic agent on MUP and xenobiotic enzymes will be discussed.
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O'Riley, Hannah Adele. "Mechanisms of the Anti-Metastatic and Cytotoxic Properties of Ruthenium Anti-Cancer Drugs." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13881.

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Despite significant advances in the treatment of primary tumours through radiotherapy, surgery and chemotherapy; treatment and prevention of metastasis remains problematic. The benefits that traditional Pt chemotherapies have had on patient outcomes have been hampered by drug resistance and severe patient side-effects. These disadvantages have spurred fresh research into other metal-based pharmaceuticals and Ru complexes have been identified as promising drugs for cancer therapy. In this work, the mechanism of action of NAMI-A, KP1019 and other Ru complexes were investigated. A series of RuII complexes containing neutral face-capping sulfur macrocycle ligands, 1,4,7-trithiacyclononane ([9]aneS3), and 1,4,7,10-tetrathiacyclododecane ([12]aneS4) were synthesized, characterized and investigated to determine the significance of the kinetically driven activity of Ru drugs. As these Ru complexes ([RuCl2([9]aneS3)(S-dmso)], [RuBr2([9]aneS3)(S-dmso)], and [RuCl([12]aneS4)(S-dmso)]Cl) have structural similarities, relationships between the kinetic rates of halido ligand substitution (determined by UV-vis spectroscopy) and in vitro activity were established. The ligand 1,4,7-trimethyltriazacyclononane (Me3tacn), is a neutral face capped ligand investigated in this work. The reactivity and biological activity of the RuII/III trimer complex [Ru3Br6(Me3tacn)2]Br was studied. Previous studies have shown that Ru complexes such as NAMI-A and KP1019 behave as pro-drugs, and that their interaction with blood serum proteins is essential to their activity. Structural properties of the adducts of Ru with various serum proteins were revealed with the use X-ray absorption spectroscopy. The nature of Ru interaction with serum proteins was investigated with gel electrophoresis X-ray fluorescence mapping. This work provided insight into the nature of the reactions that occur when Ru pro-drugs are administered intravenously, and the results of these interactions on anti-cancer activity.
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Zhao, Yunjie Physical Environmental &amp Mathematical Sciences Australian Defence Force Academy UNSW. "Cucurbit[n]uril - a delivery host for anti-cancer drugs." Publisher:University of New South Wales - Australian Defence Force Academy. Physical, Environmental & Mathematical Sciences, 2009. http://handle.unsw.edu.au/1959.4/44380.

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Puri, Sanyogitta. "Novel functionalized polymers for nanoparticle formulations with anti cancer drugs." Thesis, University of Nottingham, 2007. http://eprints.nottingham.ac.uk/10316/.

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The chemistry and structure of Poly (glycerol adipate) facilitate its substitution with various pendant functional groups leading to modifications of the physicochemical properties of the polymer. Modified backbones then can be selected based upon the properties of the compound to be incorporated. Thus, this could be explored as a drug delivery system without many of the limitations of commercially available polymers. The aim of this study was investigate whether various polymers and drugs interact in a specific manner and whether the nature of these interactions influence the physicochemical characteristics of the particles and their drug loading and release profile. By investigating drugs belonging to various classes and with different properties it has been possible to correlate properties associated with drugs and pendant functional groups of the polymer which are ultimately responsible for the drug loading and release characteristics. For some drug polymer formulations, good loading and controlled release rates have been achieved. Compared to various conventional polymer systems reported for nanoparticle formulations, poly (glycerol adipate) polymers have also demonstrated the ability to control rate of release of highly water soluble drugs, even from the most hydrophilic polymer backbone in its unsubstituted form. From the various drug loading and release profiles it has been demonstrated that, unlike reported literature, particle size is not the primary factor influencing drug release over the relatively small range of particle sizes seen in this study. Neither is the water solubility of either the drug or the polymer alone responsible for the rapid and uncontrolled release profile from nanoparticles. Thus, Drug polymer interactions are more likely to influence drug loading and release and unlike common reports in the literature, hydrophilicity, molecular weight or concentration of polymer / drug are less likely to affect these parameters in isolation.
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Books on the topic "Anti-cancer drugs"

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Garth, Powis, and Prough Russell A, eds. Metabolism and action of anti-cancer drugs. London: Taylor & Francis, 1987.

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Hiscox, Stephen, Julia Gee, and Robert I. Nicholson, eds. Therapeutic Resistance to Anti-Hormonal Drugs in Breast Cancer. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-8526-0.

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Julia, Gee, Nicholson Robert I, and SpringerLink (Online service), eds. Therapeutic Resistance to Anti-Hormonal Drugs in Breast Cancer: New Molecular Aspects and their Potential as Targets. Dordrecht: Springer Netherlands, 2009.

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Bourgeade, Pierre. Synthesis of the anti-cancer drug (R)-aminoglutethimide. Manchester: UMIST, 1998.

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Ken, Stanley &. Toxicity Of Anti-Cancer Drugs. Pan Macmillan, 1997.

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Bankovic, Jasna, ed. Anti-cancer Drugs - Nature, Synthesis and Cell. InTech, 2016. http://dx.doi.org/10.5772/62959.

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Morbidelli, Lucia. Anti-Angiogenic Drugs As Chemosensitizers in Cancer Therapy. Elsevier Science & Technology, 2022.

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Morbidelli, Lucia. Anti-Angiogenic Drugs As Chemosensitizers in Cancer Therapy. Elsevier Science & Technology Books, 2022.

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(Editor), M. J. Waring, and B. A. Ponder (Editor), eds. The Search for New Anti-Cancer Drugs (Cancer Biology and Medicine). Springer, 1992.

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Powis, Garth, and G. Powis. Metabolism & Reaction of Anti Cancer Drugs, 2-Volume Set. Elsevier Science Publishing Company, 1994.

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Book chapters on the topic "Anti-cancer drugs"

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Dunlap, Norma, and Donna M. Huryn. "Anti-cancer drugs." In Medicinal Chemistry, 287–318. New York, NY : Garland Science, Taylor & Francis Group, LLC, [2018]: Garland Science, 2018. http://dx.doi.org/10.1201/9781315100470-10.

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Lovejoy, David B., Yu Yu, and Des R. Richardson. "Chelators as Anti-Cancer Drugs." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1053-3.

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Lovejoy, David B., Yu Yu, and Des R. Richardson. "Chelators as Anti-Cancer Drugs." In Encyclopedia of Cancer, 911–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_1053.

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Dancey, J., and S. Arbuck. "Cancer Drugs and Cancer Drug Development for the New Millennium." In Progress in Anti-Cancer Chemotherapy, 91–109. Paris: Springer Paris, 2000. http://dx.doi.org/10.1007/978-2-8178-0920-5_6.

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Boukalova, Stepana, Katerina Rohlenova, Jakub Rohlena, and Jiri Neuzil. "Mitocans: Mitochondrially Targeted Anti-cancer Drugs." In Mitochondrial Biology and Experimental Therapeutics, 613–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73344-9_27.

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Veni, T., T. Pushpanathan, and G. Vimala. "Plant Constituent as Anti-Cancer Drugs." In Drug Development for Cancer and Diabetes, 43–57. Includes bibliographical references and index.: Apple Academic Press, 2020. http://dx.doi.org/10.1201/9780429330490-5.

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Sukjoi, Witchuda, Jarunya Ngamkham, Paul V. Attwood, and Sarawut Jitrapakdee. "Targeting Cancer Metabolism and Current Anti-Cancer Drugs." In Advances in Experimental Medicine and Biology, 15–48. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-55035-6_2.

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Satake, Kazuhiro, Yu Toyoda, and Hiroshi Nakagawa. "Drugs Affecting Epigenetic Modifications of ABC Transporters for Drug Resistance." In Resistance to Targeted Anti-Cancer Therapeutics, 273–97. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09801-2_11.

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Bennett, A., and J. D. Gaffen. "Interactions between Anti-Inflammatory Drugs and Cancer Chemotherapy." In Prostanoids and Drugs, 243–48. New York, NY: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-7938-6_25.

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Moraes, Denise Fernandes Coutinho, Ludmilla Santos Silva de Mesquita, Flavia Maria Mendonça do Amaral, Maria Nilce de Sousa Ribeiro, and Sonia Malik. "Anticancer Drugs from Plants." In Biotechnology and Production of Anti-Cancer Compounds, 121–42. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53880-8_5.

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Conference papers on the topic "Anti-cancer drugs"

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Lally, Beth, Robert Gettens, and Shabnam Sani. "Delivery of Anti-Cancer Drugs Using Nanocarriers." In 2013 39th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2013. http://dx.doi.org/10.1109/nebec.2013.74.

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Yalcin, Huseyin, Hissa Al-Thani, and Samar Shurbaji. "Development and In Vivo Testing of Smart Nanoparticles for Enhanced Anti-Cancer Activity and Reduced Cardiotoxicity Associated with Tyrosine Kinase Inhibitors." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0088.

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Tyrosine kinase inhibitors (TKIs) are new generation of anti-cancer drugs with very high efficiency against cancer cells. However, TKIs are associated with severe cardiotoxicity limiting their clinical benefits. One TKI that has been developed recently but not explored much is Ponatinib. The use of nanoparticles as a better therapeutic agent to deliver anti-cancer drugs and reduce their cardiotoxicity has been recently considered. In this study, PLGA-PEG-PLGA nanoparticles were synthesized to deliver Ponatinib while reducing its cardiotoxicity for treatment of chronic myeloid leukemia. Shape, size, surface charge and drug uptake ability of these nanoparticles were assessed using transmission electron microscopy (TEM), ZetaSIZER NANO and high-performance liquid chromatography (HPLC). Cardiotoxicity of Ponatinib, unloaded and loaded PLGA-PEG-PLGA nanoparticles were studied on zebrafish model through measuring the survival rate and cardiac function parameters, to optimize efficient drug concentrations in an in vivo setting. These particles were tested on zebrafish cancer xenograft model in which, K562 cell line, was transplanted into zebrafish embryos. We showed that, at an optimal concentration (0.0025mg/ml), Ponatinib loaded PLGA-PEG-PLGA particles are non-toxic/non-cardio-toxic and are very efficient against cancer growth and metastasis. Zebrafish is a good animal model for investigating the cardiotoxicity associated with the anti-cancer drugs such as TKIs, to determine the optimum concentration of smart nanoparticles with the least side effects and to generate xenograft model of several cancer types. Also, PLGA-PEG-PLGA NPs could be good candidate for CML treatment, but their cellular internalization should be enhanced. This could be achieved by coating and labeling the surface of PLGA-PEG-PLGA NPs with specific ligands that are unique to CML cells.
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Anders, Lars, Matthew G. Guenther, Jun Qi, Zi Peng Fan, Jason J. Marineau, Peter B. Rahl, Jakob Lovén, et al. "Abstract 3230: Genome-wide localization of anti-cancer drugs." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3230.

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Cain, Charles, Russell Jeffers, Ruo Qin Feng, Brian Fowlkes, and David Kessel. "Activation of anti-cancer drugs with ultrasound: Sonodynamic therapy." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761002.

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Cain, Jeffers, Ruo Qin Feng, Fowlkes, and Kessel. "Activation Of Anti-cancer Drugs With Ultrasound: Sonodynamic Therapy." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.589778.

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Settleman, Jeff. "Abstract IA09: Non-mutational resistance to anti-cancer drugs." In Abstracts: AACR Precision Medicine Series: Targeting the Vulnerabilities of Cancer; May 16-19, 2016; Miami, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.pmccavuln16-ia09.

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Dereli-Korkut, Zeynep, and Sihong Wang. "Microfluidic Cell Arrays to Mimic 3D Tissue Microenvironment." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80411.

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We developed a functional high throughput 3D microfluidic living cell array (MLC) for anti-cancer drug screening and mechanism discovery. Contemporary drug screening methods suffer from low sample throughput and lack of abilities of mimicking the 3D microenvironment of mammalian tissues. The poor performance of anti-cancer drugs limits the efficacy at controlling the complex disease system like cancer. Systematic studies of apoptotic signaling pathways can be prominent approaches for searching active and effective treatments with less drug resistance. Hence, innovative bio-devices are needed to represent tumor microenvironment to understand the molecular signatures of apoptosis for testing new anticancer therapies targeting apoptosis. Our novel 3D MLC design is the prototype of a high-throughput drug screening platform targeting apoptotic signaling pathways.
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Zhukovets, T. A., M. А. Khancheuski, I. V. Koktysh, E. I. Kvasyuk, and A. G. Sysa. "ANTIOXIDANT EFFECTS OF EMOXYPINE AS ADJUVANT OF ANTI-CANCER DRUGS." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-52-55.

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Antioxidants are known to minimize oxidative stress by interacting with free radicals produced as a result of cell aerobic reactions. Oxidative stress has long been linked to many diseases, especially tumours. Therefore, antioxidants play a crucial role in the prevention or management of free radical-related diseases. However, most of these antioxidants have anticancer effects only if taken in large doses. Therefore, the combined use of antioxidants with chemotherapeutic agents is an attractive strategy to combat various tumours. This article focuses on the antioxidant effect of emoxypine. The contribution of this molecule in enhancing the anticancer potentials of nelarabine will be demonstrated.
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Chang, Christina L., Chien-Yuan Chiu, Jhih-Ying Chi, Chang-Lin Wu Chang-Lin Wu, I.-Chen Li, and Siao-Ru Jian. "Abstract 3899: Anti-cancer drugs increases microsatellite instability in human colorectal cancer cells." 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.am2011-3899.

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Lichtenfels, Martina, Camila Alves Silva, Caroline Brunetto Farias, Alessandra Borba Anton Souza, and Antônio Luiz Frasson. "TIN VITRO BREAST CANCER CHEMORESISTANCE TEST." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1058.

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Introduction: Tumor resistance is the main cause of treatment failure leading to cancer progression and is classified into intrinsic and acquired resistance. Intrinsic resistance is related to a preexisting condition and acquired resistance is induced by a drug. Some methods are already available worldwide to assess drug resistance, however, in Brazil no in vitro chemoresistance test for cancer is validated for clinic use. Objectives: The aim of our study was to validate the in vitro chemoresistance test Chemobiogram for the drugs used in breast cancer (BC) treatment. An incomplete response to neoadjuvant treatment was used to validate the results at a short-term follow-up and treatment after primary BC will be used to validate the test in a long-term follow-up. Methods: Patients with invasive breast cancer were included in this initial report. Fresh tumor samples were collected during surgery and subsequently dissociated to obtain tumor cells. The tumor cells were cultured in a 96 well plate with the several drugs used for BC treatment, including cytotoxic, hormonal, antiHER2, and target therapies, and after 72 hours, cell viability was evaluated. The test result is defined based on cell viability as low (60%) resistance. The test result is compared to the patient`s response to the treatment. Results: To validate the dissociation and BC primary culture techniques we collected samples from six patients with in situ and invasive tumors. These samples were not tested in Chemobiogram. Samples from five BC patients undergoing neoadjuvant treatment and from three patients with primary BC were tested in the Chemobiogram. Of the five patients who underwent neoadjuvant treatment, two performed hormone therapy and three underwent chemotherapy. Four patients presented incomplete response to the treatment and one patient who underwent neoadjuvant chemotherapy presented disease progression during treatment. The chemoresistance test was able to demonstrate medium to high resistance for the drugs used in the neoadjuvant treatments (acquired resistance). The three patients with primary BC were diagnosed with Luminal tumors-HER2 negative. In the chemoresistance test all samples presented medium to high resistance to anti-HER2 drugs (intrinsic resistance) and low to medium resistance to cytotoxic drugs. These patients will be followed in the long term to compare patient outcomes with the test results. Conclusions: The primary culture of breast tumors was efficiently established and the preliminary result of the chemoresistance test was in accordance with the outcomes from five patients who underwent neoadjuvant treatment. This preliminary finding showed the capacity of the Chemobriogram to demonstrate drug resistance in accordance with the clinic and highlighted the importance of the in vitro chemoresistance test to avoid the use of inefficient drugs, improving and personalizing breast cancer treatment.
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Reports on the topic "Anti-cancer drugs"

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Collins, Tammy R., and Tao-shih Hsieh. Mechanistic Basis of Sensitivity/Resistance Towards Anti-Cancer Drugs Targeting Topoisomerase II. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada437191.

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Collins, Tammy R., and Tao-shih Hsieh. Mechanistic Basis of Sensitivity/Resistance Towards Anti-cancer Drugs Targeting Topoisomerase II. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada455978.

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Zou, Yihua, Fangqin Tong, Meng Guan, Chun Bi, and Xia Wang. Efficacy and safety of Anti-angiogenesis combined with chemoradiotherapy in the treatment of locally advanced cervical cancer: A Meta-Analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0077.

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Review question / Objective: To Systematicly evaluate of the clinical efficacy and safety of the combination of anti-angiogenesis and simultaneous radiotherapy in the treatment of cervical cancer. Condition being studied: Locally advanced cervical cancer. We searched databases including PubMed, Cochrane Library, Embase, Web of Science CNKI, Wanfang, VIP and CBM, and the International Clinical Trial Registry Platform (ICTRP) and the Chinese Clinical Registry(ChiCTR) to collect the clinical studies about the randomized controlled trial (RCTS) of anti-angiogenic drugs (mainly Endu, apatinib and bevacizumab) combined with chemoradiotherapy in the treatment of cervical cancer. The time limit is from the establishment of the database to April 2022. RevMan 5.4 software was used to analyze the short-term efficacy and the incidence of adverse reactions.
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I. A. Parshikov, Igor A. OXIDATION OF GERANYL-N-PHENYLCARBAMATE BY FUNGUS BEAUVERIA BASSIANA WITH AIM TO OBTANING OF NEW ANTI-CANCER DRUGS. Intellectual Archive, October 2020. http://dx.doi.org/10.32370/iaj.2427.

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The microbial oxidation of geranyl-N-phenylcarbamate by fungus Beauveria bassiana was investigated. Oxidation of the C3 – C4 double bond of the parent molecule leads to regioselective formation of O-3,4-epoxyheranyl-N-phenylcarbamate in 30 % yield
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Yen, Timothy J. Validate Mitotic Checkpoint and Kinetochore Motor Proteins in Breast Cancer Cells as Targets for the Development of Novel Anti-Mitotic Drugs. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada439249.

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Yen, Timothy J. Validate Mitotic Checkpoint and Kinetochore Motor Proteins in Breast Cancer Cells as Targets for the Development of Novel Anti-Mitotic Drugs. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407481.

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Yen, Timothy J. Validate Mitotic Checkpoint and Kinetochore Motor Proteins in Breast Cancer Cells as Targets for the Development of Novel Anti-Mitotic Drugs. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada428246.

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Jin, Dachuan, Gao Peng, Shunqin Jin, Tao Zhou, Baoqiang Guo, and Guangming Li. Comparison of therapeutic effects of anti-diabetic drugs on non-alcoholic fatty liver disease patients without diabetes: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0014.

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Review question / Objective: To evaluate the efficacy of different anti-diabetic drugs in the treatment of non-diabetic non-alcoholic disease by network meta-analysis, and find the best intervention. Condition being studied: Non-alcoholic fatty liver disease (NAFLD) refers to the disease in which the liver fat content exceeds 5%, and excludes the secondary causes of alcohol, infection, drugs or other specific metabolic diseases. As a spectrum of disorders, it includes hepatocyte steatosis and steatohepatitis at the initial stage, liver fibrosis at the later stage, cirrhosis at the final stage, and even liver cancer. Nowadays Non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world with an incidence rate as high as 25% which has been rising steadily worldwide in the past 30 years. Currently there are still no approved specific therapeutic agents and global treatment guidelines for NAFLD. For non-diabetic NAFLD, there is far from a consensus, too.
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Bellows, David S. Anti-Cancer Drug Discovery Using Synthetic Lethal Chemogenetic (SLC) Analysis. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada434327.

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Bellows, David S. Anti-Cancer Drug Discovery Using Synthetic Lethal Chemogenetic (SLC) Analysis. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada460468.

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