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Relevant bibliographies by topics / Cisplatin Biochemistry / Dissertations / Theses

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Dissertations / Theses on the topic 'Cisplatin Biochemistry'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Holding, Jeremy David. "Cisplatin : protein binding and biological activity." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257185.

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2

Fisher, Joshua. "In Vitro Binding Kinetics of ChemoFilter with Cisplatin." Thesis, University of California, San Francisco, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10165379.

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<p> <b>Introduction:</b> Endovascular chemotherapy treatment allows localized delivery adjacent to the target tumor; allowing an increased dosage and decreased leakage to other areas. It also allows for the opportunity to filter chemotherapy escaping the target tumor and entering the bloodstream. The ChemoFilter - a temporarily deployable, endovascular device will do just that; reducing systemic toxicity thus reducing adverse side effects from chemotherapy treatment. This will allow further increased dosage, increased tumor suppression, and increased tolerance to treatment. ChemoFilter has suc

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3

Filipski, Kelly K. "Contribution of organic cation transporter 2 (OCT2) to cisplatin-induced nephrotoxicity." View the abstract Download the full-text PDF version, 2009. http://etd.utmem.edu/ABSTRACTS/2009-022-Filipski-index.htm.

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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2009.<br>Title from title page screen (viewed on August 6, 2009). Research advisor: Alex Sparreboom, Ph.D. Document formatted into pages (ix, 79 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 74-78).

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4

Smith, Adam C. R. "The Effects of Carrier Ligands on Cisplatin Binding to Cysteine and Methionine." TopSCHOLAR®, 2017. http://digitalcommons.wku.edu/theses/1969.

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We have reacted several derivatives of the anticancer drug cisplatin with N-acetyl-Lcysteine (N-AcCys) and N-acetyl-L-methionine (N-AcMet), which are two of the primary amino acid targets of platinum. NMR spectroscopy was used to monitor the reactions and determine the effect the different ligands would have on the platinum reactivity. Several of the platinum compounds were tested at pH of 4 and 7, and with platinum:amino acid ratios of 1:1, 2:1 and 1:2. Competition reactions between cysteine and methionine were done to confirm which would react with the platinum compound first. [Pt(dien)(NO3)

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5

Dangeti, Venkata Srinivas Mohan Nimai. "Processing of Cisplatin Interstrand crosslinks (ICLs) by DNA repair proteins." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1352833172.

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6

Hira, Akshay. "TIP60 regulation of DNp63a is associated with cisplatin resistance." Wright State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright1566585763492406.

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7

Tacka, Kirk A. Dabrowiak James C. "I. Kinetic study of the reactions of glutathione and thiol drugs with cyclophosphamide. II. Quanitative studies of cisplatin-induced cell death." Related electronic resource: Current Research at SU : database of SU dissertations, recent titles available full text, 2004. http://wwwlib.umi.com/cr/syr/main.

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8

Hostetter, Alethia A. 1981. "In vitro and in cellulo interactions of platinum and ruthenium anticancer metallodrugs with RNA." Thesis, University of Oregon, 2011. http://hdl.handle.net/1794/11254.

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xviii, 125 p. : ill. (some col.)<br>Since its approval by the FDA in 1978 cisplatin (cis-diamminedichloroplatinum(II)) has revolutionized the treatment of several cancer types, particularly testicular cancer which now has a cure rate greater than 90%. Following the example set by its success, a broad range of antitumor metallodrugs is being developed. One of the most promising of these drugs, currently in Phase Two of clinical trials, is the Ru-based NAMI-A (imadozolium trans -[tetrachloro(dimethylsulfoxide)(imidazole)ruthenate(III)]) which displays low systemic toxicity and strong antimetasta

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9

Hodzic, Denis. "Effects of EF-24 and Cisplatin on Cancer, Renal, and Auditory Cells." TopSCHOLAR®, 2019. https://digitalcommons.wku.edu/theses/3110.

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Cisplatin is a chemotherapy drug effective against several forms of cancer, but can also cause serious side-effects, including nephrotoxicity and ototoxicity. Curcumin, a natural plant compound, can increase cisplatin’s anti-cancer activity and counteract cisplatin’s deleterious effect on the auditory and renal systems. Unfortunately, curcumin exhibits poor bioavailability, which has promoted interest in the development of synthetic curcumin analogs (curcuminoids) that are soluble, target cancer, and do not cause side effects. This study investigated whether the curcuminoid (3E,5E)-3,5-bis[(2-

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10

Sawant, Akshada S. "The Role of Base Excision Repair and Mismatch Repair Proteins in the Processing of Cisplatin Interstrand Cross-Links." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1404407224.

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11

Lutterman, Daniel Aaron. "Investigation of transition metal complexes with potential photochemical applications." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1184601514.

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12

Chapman, Erich G. 1984. "Platinum coordination to RNA." Thesis, University of Oregon, 2010. http://hdl.handle.net/1794/11072.

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xix, 111 p. : ill. (some col.)<br>Since discovery of its biological effects in the late 1960's, cisplatin (cis-diamminedichloroplatinum( II)) has become one of the most broadly-prescribed cancer drugs in use today. A majority of efforts to understand the metallobiochemistry of this drug have focused on describing the interactions of cisplatin-derived Pt(II) complexes with DNA. Drug binding to this "high value" cellular target is believed to trigger the apoptotic pathways that underlie cisplatin's cytotoxic effects. Although RNA is chemically similar to DNA and responsible for accurately transf

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13

Nielsen, Frederick A. "Harnessing Macrophage Polarization for Platinum-based Immunochemotherapy." Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1525778398029577.

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14

Liu, Renyan. "Synergistic growth inhibition and enhancement of cell death by combination of Melanoma Differentiation Associated gene-7 (MDA-7/IL-24) and cisplatin in ovarian cancer cell lines." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/7.

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Ovarian cancer is the most lethal gynecological malignancy among women. The current first-line treatments for ovarian cancer are cisplatin, carboplatin and paclitaxel. However, resistance to these platinum-based drugs occurs in the large majority of initially responsive tumors, resulting in fully chemoresistant, fatal disease. Therefore, the resistance to cisplatin therapy has been a critical hurdle in the management of recurrent ovarian cancer. The mechanisms responsible for cisplatin resistance are not completely understood. In the search for new therapies to overcome/bypass cisplatin resist

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15

Puckett, Nathan. "Effects of Binding Affinity between Bovine Serum Albumin and Platinum Drugs." TopSCHOLAR®, 2017. http://digitalcommons.wku.edu/theses/1977.

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Platinum complex drugs such as cisplatin have been used as highly successful chemotherapy drugs since the 1970s. We are interested in how the ligands attached to cisplatin analogs influences their reactivity with biologically relevant targets along with time and amount. For this study, reactions were conducted to determine the reactivity between different platinum compounds and the protein bovine serum albumin. Various platinum compounds with different ligands were reacted in varying amounts with albumin in ammonium acetate buffer for either 1 hour, 4 hours, or 24 hours. Each reaction was quen

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16

Fourrier-Bauchet, Laurence. "Mécanisme d'action de la drogue anticancéreuse cis-dichlorodiammineplatine (II) : étude de l'interaction entre les protéines de réparation des mésappariements et l'ADN platiné." Phd thesis, Université d'Orléans, 2003. http://tel.archives-ouvertes.fr/tel-00483029.

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Le système de réparation des mésappariements de l'ADN (MMR) est impliqué dans la cytotoxicité du cisplatine, puissante drogue anticancéreuse qui interagit avec l'ADN. Nous avons étudié in vitro certaines étapes clé des mécanismes moléculaires qui relient le fonctionnement du système de réparation MMR avec la cytotoxicité de cette drogue. Notre étude s'est focalisée sur l'interaction entre l'ADN platiné et la protéine MutS du système MMR impliquée dans les étapes d'initiation de la réparation. Trois points ont été abordés dans cette étude : i) la reconnaissance par MutS des lésions du cisplatin

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17

Michels, Judith. "Les Inhibiteurs de PARP dans le Traitement des Cancers Chimio-Résistants. Etude pré-clinique sur la Dépendance à PARP." Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-01063796.

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Introduction Le cancer bronchique est un problème de santé publique en étant la première cause de décès par cancer dans le monde. Il reste de mauvais pronostic avec une résistance au Cisplatine qui est inéluctable dans l'histoire naturelle de la maladie. Nous nous sommes intéressés à l'association du CDDP aux inhibiteurs de la Poly(ADP-ribose) polymérase. Les inhibiteurs pharmacologiques de PARP sont source d'optimisme en oncologie clinique en monothérapie pour des tumeurs déficientes pour une voie de réparation de l'ADN et en association aux cytotoxiques classiques.Matériel et méthodes Nous a

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18

Mishra, Akaash K. "Developing small molecule inhibitors targeting Replication Protein A for platinum-based combination therapy." Thesis, 2014. http://hdl.handle.net/1805/6466.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>All platinum (Pt)-based chemotherapeutics exert their efficacy primarily via the formation of DNA adducts which interfere with DNA replication, transcription and cell division and ultimately induce cell death. Repair and tolerance of Pt-DNA lesions by nucleotide excision repair and homologous recombination (HR) can substantially reduce the effectiveness of the Pt therapy. Inhibition of these repair pathways, therefore, holds the potential to sensitize cancer cells to Pt treatment and increase clinical efficacy. Replication Protein

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