Bibliografías temáticas / Anticancer drugs

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Literatura académica sobre el tema "Anticancer drugs"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 6 de septiembre de 2023

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Artículos de revistas sobre el tema "Anticancer drugs"

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D, Subba Reddy, Prasanthi G, Amruth Raj S, Hari Krishna T, Sowjanya K y Shantha Kumari K. "EVALUATION OF ANTICANCER GENERIC DRUGS AND BRANDED DRUGS". Indian Research Journal of Pharmacy and Science 5, n.º 1 (marzo de 2018): 1378–91. http://dx.doi.org/10.21276/irjps.2018.5.1.16.

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Reese, David M. "Anticancer drugs". Nature 378, n.º 6557 (diciembre de 1995): 532. http://dx.doi.org/10.1038/378532c0.

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Kutty, Dr A. V. M. "Usefulness of Phytochemicals as Anticancer Drugs". JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 16, n.º 1 (19 de marzo de 2019): 1–2. http://dx.doi.org/10.58739/jcbs/v09i1.7.

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Cancer is a state of uncontrolled proliferation and dedifferentiation of cells in any tissues or organs of the body. The incidence of cancer is rising alarmingly and is one of the leading causes of morbidity and mortality globally. Normal cell division is precisely a planned biological process controlled by regulatory genes and specific metabolic pathways. Exposure of normally functioning cells to carcinogens leads to mutations in the genes causing loss of control of cell division and transform into cancerous. Over a period of time, these cancer cells acquire more mutations; invade to adjoining tissues, escape the process of apoptosis and the cells become eternal. Breakaway parts of the cancer tissues / cells travel through the lymphatic and blood vessels and get deposited in other tissues / organs leading to metastasis, the spread of cancer.
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Atkins, Joshua H. y Leland J. Gershell. "Selective anticancer drugs". Nature Reviews Drug Discovery 1, n.º 7 (julio de 2002): 491–92. http://dx.doi.org/10.1038/nrd842.

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Atkins, Joshua H. y Leland J. Gershell. "Selective anticancer drugs". Nature Reviews Cancer 2, n.º 9 (septiembre de 2002): 645–46. http://dx.doi.org/10.1038/nrc900.

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Bibby, M. C. "Combretastatin anticancer drugs". Drugs of the Future 27, n.º 5 (2002): 475. http://dx.doi.org/10.1358/dof.2002.027.05.668645.

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Meegan, Mary J. y Niamh M. O’Boyle. "Special Issue “Anticancer Drugs”". Pharmaceuticals 12, n.º 3 (16 de septiembre de 2019): 134. http://dx.doi.org/10.3390/ph12030134.

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The focus of this Special Issue of Pharmaceuticals is on the design, synthesis, and molecular mechanism of action of novel antitumor, drugs with a special emphasis on the relationship between the chemical structure and the biological activity of the molecules. This Special Issue also provides an understanding of the biologic and genotypic context in which targets are selected for oncology drug discovery, thus providing a rationalization for the biological activity of these drugs and guiding the design of more effective agents. In this Special Issue of Pharmaceuticals dedicated to anticancer drugs, we present a selection of preclinical research papers including both traditional chemotherapeutic agents and newer more targeted therapies and biological agents. We have included articles that report the design of small molecules with promising anticancer activity as tubulin inhibitors, vascular targeting agents, and topoisomerase targeting agents, alongside a comprehensive review of clinically successful antibody-drug conjugates used in cancer treatment.
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Ciarimboli, Giuliano. "Anticancer Platinum Drugs Update". Biomolecules 11, n.º 11 (4 de noviembre de 2021): 1637. http://dx.doi.org/10.3390/biom11111637.

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Zhang, Jason Y. "Apoptosis-based anticancer drugs". Nature Reviews Drug Discovery 1, n.º 2 (febrero de 2002): 101–2. http://dx.doi.org/10.1038/nrd742.

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Blagosklonny, Mikhail V. "Teratogens as Anticancer Drugs". Cell Cycle 4, n.º 11 (22 de agosto de 2005): 1518–21. http://dx.doi.org/10.4161/cc.4.11.2208.

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Tesis sobre el tema "Anticancer drugs"

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Apps, MIchael Garry. "Platinum anticancer drugs and drug delivery systems". Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14409.

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In this thesis two different ways to improve platinum-based chemotherapy were investigated. The first was through the use of a new slow release clay-based drug delivery vehicle and the second through the design and synthesis of novel dinuclear platinum complexes. For the clay-based drug delivery research, the platinum anticancer complex [(1,10-phenanthroline)(1S,2S-diaminocyclohexane)platinum(II)] chloride, PHENSS, was loaded into montmorillonite (MMT) clay. The PHENSS was found to be incompletely burst released from the MMT. The MMT also had a negative effect on the in vitro cytotoxicity of PHENSS in the human breast cancer cell lines MCF-7 and MDA-MB-231. Overall the results demonstrate that MMT is not a suitable slow release vehicle for PHENSS. For the dinuclear platinum complex synthesis research, new bispyridine-based bridging ligands were synthesised using an amide coupling reaction. The bridging ligands were then reacted with transplatin to yield the dinuclear platinum complexes. The platinum complexes have potential application as anticancer agents and the synthetic method can be modified to produce other multinuclear complexes.
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Kozlowska, Hanna. "Interaction of dexrazoxane with anticancer drugs". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0001/MQ32158.pdf.

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Tao, Zhimin. "Analysis of cytotoxicity of anticancer drugs". Related electronic resource:, 2007. http://proquest.umi.com/pqdweb?did=1407688361&sid=4&Fmt=2&clientId=3739&RQT=309&VName=PQD.

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Liu, Tong. "The synthesis of novel anticancer drugs". Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/4464/.

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Our studies on the synthesis and biological evaluation of novel anticancer drugs consist of three research areas; namely, synthesis of Mitogen Activated Protein (MAP) kinase inhibitors, Checkpoint (Chk1) inhibitors and nordihydroguaiaretic acid (NDGA) analogues. The first research area involved synthesis of MAP kinase inhibitors. MAP kinases are a family of serine I and threonine II kinases which can act together to generate a process of phosphorylation events within the cell signalling pathway leading eventually to cell division. The compounds made in this project were specifically designed to target the stress related kinases, a MAP kinase pathway which controls the expression of genes involved in cell proliferation. The stress related kinases are known to have serine or threonine joined to a proline III residue. In an attempt to prepare selective inhibitors of stress related kinases, compounds of types IV and V were deigned in which a conformationally restricted serine analogue is joined to L-proline via an amide link in one of two possible ways. Examples of these two sets of compounds were synthesised and those that were tested by Professor David Gillespie at the Beatson Institute for Cancer Research, Glasgow were shown not to be inhibitors of these kinases. (Fig. 1144A) The second research area concentrated on the checkpoint signalling pathway. Components in the DNA damage checkpoint signalling pathway such as ChK1 could be potential targets for chemical intervention. Caffeine VI and pentoxifylline VII have been shown to sensitise p53-deficient tumour cells to killing by DNA damage. We envisaged that the xanthine derivatives, caffeine VI and pentoxifylline VII might also disrupt the G2 checkpoint by preventing activation of Chk1. To test his hypothesis, a range of xanthine derivatives shown below were prepared by alkylation of theophylline VIII or theobromine IX. (Fig. 1144B) The biological evaluation of these xanthine derivatives by Professor Gillespie revealed that three of these compounds, X, XI and XII, suppressed G2/M arrest very effectively. All three active compounds possess a long aliphatic chain that provides a large degree of flexibility to the structures. The long aliphatic chains could bind to a hydrophobic pocket in the enzyme’s active site that might confer selectivity on the compounds. (Fig. 1144C) The third area, synthesis of NDGA analogues, was the major part of the synthetic work. NDGA XIII is known to be a selective inhibitor of lipoxygenase and blocks small cell lung cancer growth in vitro and in vivo. In addition to its lipoxygenase activity, NDGA was demonstrated to inhibit c-kit, a tyrosine kinase that has been observed preferentially in SCLC. The main drawbacks to the use of NDGA in cancer treatment are its poor solubility and moderate potency. Therefore chemical modifications are required to provide better compounds for clinical use. Preliminary work in our group was performed by McDonald and Macleod. They synthesised a range of analogues of NDGA which were tested for their activity in vitro by Professor Michael Seckl at the Medical Oncology Department of Hammersmith Hospital, London. Improved potency over NDGA for new analogues with 4-6 atoms between the two aromatic rings was observed. Furthermore introduction of an amide linkage between the two aromatic residues resulted in NDGA analogues which are more active than NDGA. Based on these preliminary results, the structural modifications proposed for this project focused on three areas. The main programme of research was drug solubilisation of new analogues which have higher potency than NDGA for in vivo work. The second area of study sought to introduce position variations of the amide linkage between the two aromatic residues. The third area of work involved modification of the substituents on the two aromatic rings. (Fig. 1144D) A range of NDGA analogues was successfully synthesised and evaluated for anticancer activity in vitro. Compounds XIV and XV were confirmed as lead compounds which are ten times more active than NDGA. Compound XIV was successfully transformed into a water soluble form XVI which is now available for in vivo work. In addition NDGA was converted into a water soluble form which was more potent than NDGA in vitro. Moreover a NDGA analogue XVII with no free hydroxy groups was found to be as active as NDGA, which was an unexpected discovery. (Fig. 1144E)
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Song, Di. "Bladder tissue pharmacokinetics of anticancer drugs /". The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487940308433249.

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Ratcliffe, Andrew J. "Synthesis of non-mutagenic anticancer drugs". Thesis, University of Bath, 1987. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378598.

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Pettersson, Hanna Ilse. "Quinolinequinones as anticancer agents". Thesis, University of Exeter, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249038.

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Wang, Shining. "DRUG DEVELOPMENT OF TARGETED ANTICANCER DRUGS BASED ON PK/PD INVESTIGATIONS". Diss., Temple University Libraries, 2008. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/2535.

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Pharmaceutics
Ph.D.
EGFR inhibitors, such as gefitinib, are examples of targeted anticancer drugs whose drug sensitivity is related to gene mutations that adds a pharmacogenetic [PG] dimension to any pharmacokinetic [PK] and pharmacodynamic [PD] analysis. The goal of this project was to characterize the PK/PD properties of gefitinib in tumors and then apply these results to design rational drug design regimens, and provide a foundation for future studies with EGFR inhibitors. Progressions of in vitro and in vivo studies were completed to understand the PK and PD behavior of gefitinib. In vitro cytotoxicity assays were first conducted to confirm the gefitinib sensitivity differences in a pair of human glioblastoma cell lines, LN229-wild-type EGFR and LN229-EGFRvIII mutant, an EGFR inhibitor-sensitizing mutation. Subsequent in vitro PD studies identified phosphorylated-ERK1/2 (pERK) as a common PD marker for both cell lines. To describe the most salient features of drug disposition and dynamics in the tumor, groups of mice bearing either subcutaneous LN229-wild-type EGFR or LN229-EGFRvIII mutant tumors were administered gefitinib at doses of 10 mg/kg intravenously (IV), 50 mg/kg intraarterially (IA) and 150 mg/kg orally (PO). In each group, gefitinib plasma and tumor concentrations were quantitated, as were tumoral pERK. Hybrid physiologically-based PK/PD models were developed for each tumor type, which consisted of a forcing function describing the plasma drug concentration-profile, a tumor compartment depicting drug disposition in the tumor, and a mechanistic target-response PD model characterizing pERK in the tumor. Gefitinib showed analogous PK properties in each tumor type, yet different PD characteristics consistent with the EGFR status of the tumors. Using the PK/PD model for each tumor type, simulations were done to define multiple-dose regimens for gefitinib that yielded equivalent PD profiles of pERK in each tumor type. Based on the designed PK/PD equivalent dosing regimens for each tumor type, gefitinib 150 mg/kg PO qd × 15 days and 65 mg/kg PO qd × 15 days multiple-dose studies were conducted in wild-type EGFR and EGFRvIII mutant tumor groups, respectively. In each tumor group, gefitinib plasma and tumor concentrations were measured on both day 1 and day 15, as were tumoral amounts of pERK. Different from single-dose model simulations, gefitinib showed nonlinear PK property in the wild-type tumor due to the down-regulation of membrane transporter ABCG2. Moreover, acquired resistance of tumoral pERK inhibition was observed in both tumor types. Nevertheless, gefitinib had an analogous growth suppression action in both tumor groups, supporting the equivalent PD dosing strategy. Overall, single-dose gefitinib PK/PD investigations in a pair of genetically distinct glioblastomas facilitated the development of hybrid physiologically-based PK/PD models for each tumor type, and further introduced a novel concept of PK/PD equivalent dosing regimens which could be applied in novel drug development paradigms. Preliminary multiple-dose gefitinib studies revealed more complex PK/PD characteristics that needed to be further explored.
Temple University--Theses
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Leczkowska, Anna. "Non-covalent DNA-binding ruthenium anticancer drugs". Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1695/.

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The research work described in this thesis concerns metal-based anticancer drugs with an emphasis on non-covalent DNA-binding supramolecular assemblies. The project involves the preparation of a series of mono- and bi-metallic ruthenium complexes with a primary focus on fluorescent dinuclear triple-stranded helicates with different structural topographies. Emphasis is then directed towards an investigation of the DNA binding characteristics of these molecules and an evaluation of their anticancer properties in human cancer cell lines. Attention is brought to the significance that the cylinder-building moieties and their structural characteristics have to these features. The studies also include an examination of the effects of chirality of the investigated supramolecular systems and the impact they have on molecular recognition. This is addressed via studies of the interaction of optical isomers of ruthenium triple-stranded helicates with DNA as a biomolecular target system and with Δ-TRISPHAT as a representative small chiral molecule.
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Yarema, Kevin J. (Kevin Jon). "Cellular responses to platinum-based anticancer drugs". Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/33495.

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Libros sobre el tema "Anticancer drugs"

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1938-, Pratt William B. y Pratt William B. 1938-, eds. The anticancer drugs. 2a ed. New York: Oxford University Press, 1994.

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Garth, Powis, ed. Anticancer drugs: Reactive metabolism and drug interactions. Oxford, England: Pergamon Press, 1994.

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Avendaño, Carmen. Medicinal chemistry of anticancer drugs. Amsterdam: Elsevier, 2008.

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Convention, United States Pharmacopeial. Fact sheets on anticancer drugs. [Washington, D.C.?]: National Cancer Institute [distributor], 1994.

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National Cancer Institute (U.S.), ed. Fact sheets on anticancer drugs. [Bethesda, Md.?: National Cancer Institute, 1994.

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Sotiris, Missailidis, ed. Anticancer therapeutics. Chichester: John Wiley & Sons, 2008.

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1964-, Spencer Peter y Holt Walter, eds. Anticancer drugs: Design, delivery and pharmacology. Hauppauge, NY: Nova Science Publishers, 2009.

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Saeidnia, Soodabeh. New Approaches to Natural Anticancer Drugs. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14027-8.

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Hacker, Miles P., John S. Lazo y Thomas R. Tritton, eds. Organ Directed Toxicities of Anticancer Drugs. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-2023-4.

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Hildebrand, Jerzy, ed. Neurological Adverse Reactions to Anticancer Drugs. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-76142-3.

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Capítulos de libros sobre el tema "Anticancer drugs"

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Schacter, Lee, Marcel Rozencweig, Claude Nicaise, Renzo Canetta, Susan Kelley y Laurie Smaldone. "Anticancer Drugs". En Early Phase Drug Evaluation in Man, 644–54. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-10705-6_49.

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Schwab, Matthias, Elke Schaeffeler y Hiltrud Brauch. "Anticancer Drugs". En Metabolism of Drugs and Other Xenobiotics, 365–78. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch13.

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Isnard-Bagnis, Corinne, Vincent Launay-Vacher, Svetlana Karie y Gilbert Deray. "Anticancer drugs". En Clinical Nephrotoxins, 511–35. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-84843-3_22.

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Zhao, Le, Zengyi Shao y Jacqueline V. Shanks. "Anticancer Drugs". En Industrial Biotechnology, 237–69. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2016. http://dx.doi.org/10.1002/9783527807833.ch8.

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Ganguly, A. K. y Sesha Sridevi Alluri. "Anticancer Drugs". En Medicinal Chemistry, 89–101. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003182573-4.

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Isnard-Bagnis, Corinne y Gilbert Deray. "Anticancer drugs". En Clinical Nephrotoxins, 353–72. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/1-4020-2586-6_18.

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Cateni, Francesca y Marina Zacchigna. "PEG–Anticancer Drugs". En Macromolecular Anticancer Therapeutics, 221–63. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0507-9_6.

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Kim, Kyu-Won, Jae Kyung Roh, Hee-Jun Wee y Chan Kim. "Immunotherapeutic Anticancer Drugs and Other Miscellaneous Anticancer Drugs". En Cancer Drug Discovery, 135–53. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-024-0844-7_7.

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Kim, Kyu-Won, Jae Kyung Roh, Hee-Jun Wee y Chan Kim. "Alkylating Anticancer Drugs". En Cancer Drug Discovery, 71–94. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-024-0844-7_4.

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Kim, Kyu-Won, Jae Kyung Roh, Hee-Jun Wee y Chan Kim. "Antimetabolic Anticancer Drugs". En Cancer Drug Discovery, 95–112. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-024-0844-7_5.

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Actas de conferencias sobre el tema "Anticancer drugs"

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Ma, Liang, Jeremy Barker, Changchun Zhou, Biaoyang Lin y Wei Li. "A Perfused Two-Chamber System for Anticancer Drug Screening". En ASME 2010 International Manufacturing Science and Engineering Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/msec2010-34326.

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A cell culture microfluidic device has been developed to test the cytotoxicity of anticancer drugs while reproducing multi-organ interactions in vitro. Cells were cultured in separate chambers representing the liver and tumor. The two chambers were connected through a channel to mimick the blood flow. Glioblastoma (GBM) cancer cells (M059K) and hepatoma cells (HepG2) were cultured in the tumor and the liver chambers, respectively. The cytotoxic effect of cancer treatment drug Temolozomide (TMZ) was tested using this two chamber system. The experimental results showed that with the liver cells, the cancer cells showed much higher viability than those without the liver cells. This indicates that the liver metabolism has strong effect on the toxicity of the anticancer drug. The results demonstrated that the perfused two chamber cell culture system has the potential to be used as a platform for drug screening in a more physiologically realistic environment.
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Schiestl, Robert H., Michael Davoren y Yelena Rivina. "Abstract 1793: Novel radiation mitigators and anticancer drugs". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1793.

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Settleman, Jeffrey E. "Abstract CN06-04: Reversible tolerance to anticancer drugs." En Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-cn06-04.

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Schiestl, Robert H., Yelena Rivina y Michael Davoren. "Abstract 3729: Novel radiation mitigators and anticancer drugs". En Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3729.

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Zhukovets, T. A., M. А. Khancheuski, I. V. Koktysh, E. I. Kvasyuk y A. G. Sysa. "ANTIOXIDANT EFFECTS OF EMOXYPINE AS ADJUVANT OF ANTI-CANCER DRUGS". En 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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Cao, Tingying, Xiangdong Gao y Yueqing Gu. "Biodegradable polylactide microspheres containing anticancer drugs used as injectable drug delivery system". En 2007 IEEE/ICME International Conference on Complex Medical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iccme.2007.4381726.

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Nikkhah, Mehdi, Jeannine S. Strobl y Masoud Agah. "Study the Effect of Anticancer Drugs on Human Breast Cancer Cells Using Three Dimensional Silicon Microstructures". En ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-66680.

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In this paper we report development of three dimensional silicon microenvironments in order to test the morphological changes and adhesion properties of human breast cancer cells after treatment with different anticancer drugs such as Trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA) and Scriptaid. Our results indicate that the cancer cells reorganize their cytoskeleton structure after treatment with TSA and Scriptaid. However, SAHA does not change the behavior of the cells inside the three dimensional microstructures while TSA and Scriptaid evoked striking changes in the cells morphology. TSA and Scriptaid drugs cause the cells to stretch inside the isotropic microchambers to avoid contact with curved sidewalls in contrast to their originally rounded shape. The proposed microstructures can be used to evaluate mechanical properties and the pathological grade of various cancer cell lines after different conditions i.e. drug exposure.
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J., Alex Mathew y Nixon Raj N. "Insilico Docking Studies on Anticancer Drugs for Breast Cancer". En 2009 International Association of Computer Science and Information Technology - Spring Conference. IEEE, 2009. http://dx.doi.org/10.1109/iacsit-sc.2009.12.

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Shrestha, Gajendra, Michael Xiao, Richard Robison, Larry L. St Clair y Kim O'Neill. "Abstract 3220: Lichen derived polyphenols as potential anticancer drugs". En 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.am2014-3220.

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Ribeiro, Tatiane. "23 Evidence-based medicine challenges in new anticancer drugs". En EBM Live Abstracts, July 2019, Oxford, UK. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/bmjebm-2019-ebmlive.104.

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Informes sobre el tema "Anticancer drugs"

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Howard, David, Peter Bach, Ernst Berndt y Rena Conti. Pricing in the Market for Anticancer Drugs. Cambridge, MA: National Bureau of Economic Research, enero de 2015. http://dx.doi.org/10.3386/w20867.

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Zhang, Jian-Ting. Molecular Study of Interactions between P-Glycoprotein and Anticancer Drugs. Fort Belvoir, VA: Defense Technical Information Center, agosto de 1995. http://dx.doi.org/10.21236/ada300162.

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Biswas, Kaustav y Samuel J. Danishefsky. Synthesis of Epothilone Analogs: Toward the Development of Potent Anticancer Drugs. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2002. http://dx.doi.org/10.21236/ada409475.

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Inoue, Takashi y Mamoru Narukawa. Anti-tumor efficacy of anti-PD-1/PD-L1 antibodies in combination with other anticancer drugs in solid tumors: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, octubre de 2022. http://dx.doi.org/10.37766/inplasy2022.10.0004.

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Review question / Objective: The aim of this systematic review is to compare the combination of PD-1/PD-L1 inhibitors plus other anticancer drugs and monotherapies of PD-1/PD-L1 inhibitors in terms of antitumor efficacy in the solid tumors to better inform clinical practice. To this end, the proposed systematic review will address the following question: Which is the best choice to enhance response rate in subjects with solid tumors, PD-1/PD-L1 inhibitors plus cytotoxic agents or PD-1/PD-L1 inhibitors plus other targeted anticancer drugs? Condition being studied: Cancer is the leading cause of death worldwide, accounting to approximately 9.6 million deaths worldwide in 2018. The clinical efficacy of immune checkpoint inhibitors (CPIs) including PD-1/PD-L1 inhibitors has been proven; however, it is also known that their efficacy as monotherapy is limited, with a response rate of 20% or less in solid tumors. The combination of CPIs and anticancer agents has been actively attempted in solid tumors area.
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Feltmate, Colleen. Application of Nanotechnology in the Targeted Release of Anticancer Drugs in Ovarian Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2007. http://dx.doi.org/10.21236/ada486569.

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Feltmate, Colleen. Application of Nanotechnology in the Targeted Release of Anticancer Drugs in Ovarian Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2006. http://dx.doi.org/10.21236/ada481424.

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Beerman, Terry A. Discovery of DNA Binding Anticancer Drugs That Target Oncogenic Transcription Factors Associated With Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, octubre de 2001. http://dx.doi.org/10.21236/ada403322.

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Venedicto, Melissa y Cheng-Yu Lai. Facilitated Release of Doxorubicin from Biodegradable Mesoporous Silica Nanoparticles. Florida International University, octubre de 2021. http://dx.doi.org/10.25148/mmeurs.009774.

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Cervical cancer is one of the most common causes of cancer death for women in the United States. The current treatment with chemotherapy drugs has significant side effects and may cause harm to healthy cells rather than cancer cells. In order to combat the potential side effects, nanoparticles composed of mesoporous silica were created to house the chemotherapy drug doxorubicin (DOX). The silica network contains the drug, and a pH study was conducted to determine the conditions for the nanoparticle to disperse the drug. The introduction of disulfide bonds within the nanoparticle created a framework to efficiently release 97% of DOX in acidic environments and 40% release in neutral environments. The denotation of acidic versus neutral environments was important as cancer cells are typically acidic. The chemistry was proved with the incubation of the loaded nanoparticle into HeLa cells for a cytotoxicity report and confocal imaging. The use of the framework for the anticancer drug was shown to be effective for the killing of cancerous cells.
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Macedo, Luciana y Linda Malkas. The Human Breast Cancer DNA Synthesome Can Serve as a Novel In Vitro Model System for Studying the Mechanism of Action of Anticancer Drugs. Fort Belvoir, VA: Defense Technical Information Center, julio de 2000. http://dx.doi.org/10.21236/ada393926.

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Jiang, Haiyan. The Human Breast Cancer Cell DNA Synthesome Can Serve as a Novel in Vitro Model System for Studying the Mechanism of Action of Anticancer Drugs. Fort Belvoir, VA: Defense Technical Information Center, julio de 1999. http://dx.doi.org/10.21236/ada384124.

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