Relevant bibliographies by topics / Cisplatin Biochemistry

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Academic literature on the topic 'Cisplatin Biochemistry'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cisplatin Biochemistry"

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Elferink, F., W. J. van der Vijgh, I. Klein, and H. M. Pinedo. "Interaction of cisplatin and carboplatin with sodium thiosulfate: reaction rates and protein binding." Clinical Chemistry 32, no. 4 (April 1, 1986): 641–45. http://dx.doi.org/10.1093/clinchem/32.4.641.

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Abstract Toxicity of cisplatin can be decreased by concomitant administration of sodium thiosulfate, which perhaps chemically inactivates this platinum compound. We studied the disappearance of cisplatin and carboplatin in aqueous solutions of thiosulfate at 37 degrees C by means of liquid chromatography. At initial concentrations that were similar to therapeutic concentrations in plasma, both drugs disappeared, with half-lives of 66 and 537 min for cisplatin and carboplatin, respectively. At higher thiosulfate concentrations, as found in urine, the respective half-lives were 3.7 and 33.8 min. These values suggest that direct chemical interaction in the plasma compartment has limited therapeutic consequences, whereas the anti-toxic effect of thiosulfate might be explained by the rapid inactivation of cisplatin in the kidneys. Reaction products of cisplatin and thiosulfate bound instantaneously and mainly reversibly to plasma proteins. Protein-bound cisplatin was not released by added thiosulfate--which may explain why thiosulfate, to be effective, must be given in advance of and during cisplatin administration.
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Wang, Wenyu, Jihye Im, Soochi Kim, Suin Jang, Youngjin Han, Kyung-Min Yang, Seong-Jin Kim, Danny N. Dhanasekaran, and Yong Sang Song. "ROS-Induced SIRT2 Upregulation Contributes to Cisplatin Sensitivity in Ovarian Cancer." Antioxidants 9, no. 11 (November 16, 2020): 1137. http://dx.doi.org/10.3390/antiox9111137.

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Cisplatin resistance remains a significant obstacle for improving the clinical outcome of ovarian cancer patients. Recent studies have demonstrated that cisplatin is an important inducer of intracellullar reactive oxygen species (ROS), triggering cancer cell death. Sirtuin 2 (SIRT2), a member of class III NAD+ dependent histone deacetylases (HDACs), has been reported to be involved in regulating cancer hallmarks including drug response. In this study, we aimed to identify the role of SIRT2 in oxidative stress and cisplatin response in cancer. Two ovarian cancer cell lines featuring different sensitivities to cisplatin were used in this study. We found different expression patterns of SIRT2 in cisplatin-sensitive (A2780/S) and cisplatin-resistant (A2780/CP) cancer cells with cisplatin treatment, where SIRT2 expression was augmented only in A2780/S cells. Furthermore, cisplatin-induced ROS generation was responsible for the upregulation of SIRT2 in A2780/S cells, whereas overexpression of SIRT2 significantly enhanced the sensitivity of cisplatin-resistant counterpart cells to cisplatin. Our study proposes that targeting SIRT2 may provide new strategies to potentiate platinum-based chemotherapy in ovarian cancer patients.
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Fujimoto, T., H. Maeda, K. Kubo, Y. Sugita, T. Nakashima, E. Sato, Y. Tanaka, M. Madachi, M. Aiba, and Y. Kameyama. "Enhanced Anti-tumour Effect of Cisplatin with Low-voltage Electrochemotherapy in Hamster Oral Fibrosarcoma." Journal of International Medical Research 33, no. 5 (September 2005): 507–12. http://dx.doi.org/10.1177/147323000503300505.

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The aim of this study was to determine the effects of low-voltage electrochemotherapy with intraperitoneal cisplatin on hamster oral fibrosarcoma. Oral fibrosarcoma was transplanted sub-mucosally into the cheek pouch mucosa of 100 hamsters. After transplantation, the hamsters were randomly divided into four equal groups. These groups received no treatment (D-E-); 2 mg/kg body weight cisplatin treatment without electroporation (D+E-); electroporation without cisplatin treatment (D-E+);or 2 mg/kg body weight cisplatin treatment followed by electroporation (D+E+). Electrical pulse treatment together with cisplatin injection markedly reduced the size of the tumour, whereas cisplatin injection or electrical pulse treatment alone did not. These results clearly indicate that the anti-tumour effect of cisplatin on hamster oral fibrosarcoma was considerably potentiated or enhanced by the administration of local electrical pulses at low voltages.
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Murray, Vincent. "Nucleosomes and Cisplatin." Chemistry & Biology 17, no. 12 (December 2010): 1271–72. http://dx.doi.org/10.1016/j.chembiol.2010.12.002.

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Yi, Junyeong, Tae Su Kim, Jhang Ho Pak, and Jong Woo Chung. "Protective Effects of Glucose-Related Protein 78 and 94 on Cisplatin-Mediated Ototoxicity." Antioxidants 9, no. 8 (August 2, 2020): 686. http://dx.doi.org/10.3390/antiox9080686.

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Cisplatin is a widely used chemotherapeutic drug for treating various solid tumors. Ototoxicity is a major dose-limiting side effect of cisplatin, which causes progressive and irreversible sensorineural hearing loss. Here, we examined the protective effects of glucose-related protein (GRP) 78 and 94, also identified as endoplasmic reticulum (ER) chaperone proteins, on cisplatin-induced ototoxicity. Treating murine auditory cells (HEI-OC1) with 25 μM cisplatin for 24 h increased cell death resulting from excessive intracellular reactive oxygen species (ROS) accumulation and caspase-involved apoptotic signaling pathway activation with subsequent DNA fragmentation. GRP78 and GRP94 expression was increased in cells treated with 3 nM thapsigargin or 0.1 μg/mL tunicamycin for 24 h, referred to as mild ER stress condition. This condition, prior to cisplatin exposure, attenuated cisplatin-induced ototoxicity. The involvement of GRP78 and GRP94 induction was demonstrated by the knockdown of GRP78 or GRP94 expression using small interfering RNAs, which abolished the protective effect of mild ER stress condition on cisplatin-induced cytotoxicity. These results indicated that GRP78 and GRP94 induction plays a protective role in remediating cisplatin-ototoxicity.
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Mapuskar, Kranti A., Emily J. Steinbach, Amira Zaher, Dennis P. Riley, Robert A. Beardsley, Jeffery L. Keene, Jon T. Holmlund, et al. "Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury." Antioxidants 10, no. 9 (August 24, 2021): 1329. http://dx.doi.org/10.3390/antiox10091329.

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Cisplatin is a chemotherapy agent commonly used to treat a wide variety of cancers. Despite the potential for both severe acute and chronic side effects, it remains a preferred therapeutic option for many malignancies due to its potent anti-tumor activity. Common cisplatin-associated side-effects include acute kidney injury (AKI) and chronic kidney disease (CKD). These renal injuries may cause delays and potentially cessation of cisplatin therapy and have long-term effects on renal function reserve. Thus, developing mechanism-based interventional strategies that minimize cisplatin-associated kidney injury without reducing efficacy would be of great benefit. In addition to its action of cross-linking DNA, cisplatin has been shown to affect mitochondrial metabolism, resulting in mitochondrially derived reactive oxygen species (ROS). Increased ROS formation in renal proximal convoluted tubule cells is associated with cisplatin-induced AKI and CKD. We review the mechanisms by which cisplatin may induce AKI and CKD and discuss the potential of mitochondrial superoxide dismutase mimetics to prevent platinum-associated nephrotoxicity.
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Xing, Jing-Jing, Jin-Gang Hou, Ying Liu, Ruo-Bing Zhang, Shuang Jiang, Shen Ren, Ying-Ping Wang, et al. "Supplementation of Saponins from Leaves of Panax quinquefolius Mitigates Cisplatin-Evoked Cardiotoxicity via Inhibiting Oxidative Stress-Associated Inflammation and Apoptosis in Mice." Antioxidants 8, no. 9 (September 1, 2019): 347. http://dx.doi.org/10.3390/antiox8090347.

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Background: Although kidney injury caused by cisplatin has attracted much attention, cisplatin-induced cardiotoxicity is elusive. Our previous studies have confirmed that saponins (ginsenosides) from Panax quinquefolius can effectively reduce acute renal injuries. Our current study aimed to identify the potential effects of saponins from leaves of P. quinquefolius (PQS) on cisplatin-evoked cardiotoxicity. Methods: Mice were intragastrically with PQS at the doses of 125 and 250 mg/kg daily for 15 days. The mice in cisplatin group and PQS + cisplatin groups received four times intraperitoneal injections of cisplatin (3 mg/kg) two days at a time from the 7th day, respectively. All mice were killed at 48 h following final cisplatin injection. Body weights, blood and organic samples were collected immediately. Results: Our results showed that cisplatin-challenged mice experienced a remarkable cardiac damage with obvious histopathological changes and elevation of lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB) and cardiac troponin T (cTnT) concentrations and viabilities in serum. Cisplatin also impaired antioxidative defense system in heart tissues manifested by a remarkable reduction in reduced glutathione (GSH) content and superoxide dismutase (SOD) activity, demonstrating the overproduction of reactive oxygen species (ROS) and oxidative stress. Interestingly, PQS (125 and 250 mg/kg) can attenuate cisplatin-evoked changes in the above-mentioned parameters. Additionally, PQS administration significantly alleviated the oxidation resulted from inflammatory responses and apoptosis in cardiac tissues via inhibition of overexpressions of TNF-α, IL-1β, Bax, and Bad as well as the caspase family members like caspase-3, and 8, respectively. Conclusion: Findings from our present research clearly indicated that PQS exerted significant effects on cisplatin-induced cardiotoxicity in part by inhibition of the NF-κB activity and regulation of PI3K/Akt/apoptosis mediated signaling pathways.
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Kohda, Yuka, Yoshiko Kawai, Noriaki Iwamoto, Yoshiko Matsunaga, Hiromi Aiga, Akira Awaya, and Munekazu Gemba. "Serum thymic factor, FTS, attenuates cisplatin nephrotoxicity by suppressing cisplatin-induced ERK activation." Biochemical Pharmacology 70, no. 9 (November 2005): 1408–16. http://dx.doi.org/10.1016/j.bcp.2005.08.002.

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Rodríguez-Ulloa, Arielis, Yassel Ramos, Aniel Sánchez-Puente, Yasser Perera, Alexis Musacchio-Lasa, Jorge Fernández-de-Cossio, Gabriel Padrón, Luis J. G. López, Vladimir Besada, and Silvio E. Perea. "The Combination of the CIGB-300 Anticancer Peptide and Cisplatin Modulates Proteins Related to Cell Survival, DNA Repair and Metastasis in a Lung Cancer Cell Line Model." Current Proteomics 16, no. 4 (April 25, 2019): 338–49. http://dx.doi.org/10.2174/1570164616666190126104325.

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Background: CIGB-300 is a pro-apoptotic peptide that abrogates CK2-mediated phosphorylation, and can elicit synergistic interaction in vitro and in vivo when combined with certain anticancer drugs. Objective: The combination of CIGB-300 with cisplatin is studied through data mining and expressionbased proteomics to reveal the molecular basis of this interaction. Cisplatin resistance-associated proteins, which have also been reported as CK2 substrates, were first identified by bioinformatic analyses. Methods: Data from these analyses suggested that the cisplatin resistance phenotype could be directly improved by inhibiting CK2 phosphorylation on specific substrates. Furthermore, 157 proteins were differentially modulated on the NCI-H125 lung cancer cell line in response to CIGB-300, cisplatin or both drugs as determined by LC-MS/MS. Results: The expression of 28 cisplatin resistance-associated proteins was changed when cisplatin was combined with CIGB-300. Overall, the proteins identified are also related to cell survival, cell proliferation and metastasis. Furthermore, the CIGB-300 regulated proteome revealed proteins that were initially involved in the mechanism of action of CIGB-300 and cisplatin as single agents. Conclusion: This is the first report describing the protein array modulated by combining CIGB-300 and cisplatin that will support the rationale for future clinical settings based on a multi-target cancer therapy.
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Bushau-Sprinkle, Adrienne M., Michelle T. Barati, Yuxuan Zheng, Walter H. Watson, Kenneth B. Gagnon, Syed Jalal Khundmiri, Kathleen T. Kitterman, et al. "Na/H Exchange Regulatory Factor 1 Deficient Mice Show Evidence of Oxidative Stress and Altered Cisplatin Pharmacokinetics." Antioxidants 10, no. 7 (June 28, 2021): 1036. http://dx.doi.org/10.3390/antiox10071036.

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(1) Background: One third of patients who receive cisplatin develop an acute kidney injury. We previously demonstrated the Na/H Exchange Regulatory Factor 1 (NHERF1) loss resulted in increased kidney enzyme activity of the pentose phosphate pathway and was associated with more severe cisplatin nephrotoxicity. We hypothesized that changes in proximal tubule biochemical pathways associated with NHERF1 loss alters renal metabolism of cisplatin or response to cisplatin, resulting in exacerbated nephrotoxicity. (2) Methods: 2–4 month-old male wild-type and NHERF1 knock out littermate mice were treated with either vehicle or cisplatin (20 mg/kg dose IP), with samples taken at either 4, 24, or 72 h. Kidney injury was determined by urinary neutrophil gelatinase-associated lipocalin and histology. Glutathione metabolites were measured by HPLC and genes involved in glutathione synthesis were measured by qPCR. Kidney handling of cisplatin was assessed by a kidney cortex measurement of γ-glutamyl transferase activity, Western blot for γ-glutamyl transferase and cysteine S-conjugate beta lyase, and ICP-MS for platinum content. (3) Results: At 24 h knock out kidneys show evidence of greater tubular injury after cisplatin and exhibit a decreased reduced/oxidized glutathione ratio under baseline conditions in comparison to wild-type. KO kidneys fail to show an increase in γ-glutamyl transferase activity and experience a more rapid decline in tissue platinum when compared to wild-type. (4) Conclusions: Knock out kidneys show evidence of greater oxidative stress than wild-type accompanied by a greater degree of early injury in response to cisplatin. NHERF1 loss has no effect on the initial accumulation of cisplatin in the kidney cortex but is associated with an altered redox status which may alter the activity of enzymes involved in cisplatin metabolism.
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Dissertations / Theses on the topic "Cisplatin Biochemistry"

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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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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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Introduction: 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 successfully filtered the chemotherapeutic Doxorubicin, but had yet to be tested in other chemotherapeutics. This study evaluates binding with new chemotherapeutics: Cisplatin, Carboplatin, and a cocktail comprised of Cisplatin and Doxorubicin.

Materials and Methods: ChemoFilter prototypes based on: 1.) Genomic DNA and 2.) Dowex (ion-exchange) resin, were evaluated for their ability to bind chemotherapy in vitro in phosphate-buffered saline (PBS). ChemoFilter was tested free in solution and encapsulated in nylon or polyester mesh packets of various dimensions. Concentrations were quantified using inductively coupled plasma mass spectrometry (IPC-MS), ultraviolet-visible spectrophotometry (UV-Vis), or fluorospectrometry. 11C, 13C, and/or 14C radiolabeling Carboplatin began for in vitro and in vivo ChemoFilter quantification. In vitro quantification can include scintillation and/or gamma counting. In vivo may include Positron Emission Tomography (PET) imaging, Hyperpolarized 13C Magnetic Resonance Imaging (MRI), and/or Magnetic Resonance Spectroscopy (MRS) for real-time visualization. Reactions were verified using High Performance Liquid Chromatography (HPLC) for chemical species identification.

Results and Discussion: Results indicate significant and nearly complete, ~99% (p<0.01) clearance of Cisplatin using the DNA ChemoFilter sequestered in Nylon mesh, quantified with gold standard ICP-MS (evidenced at 214 and 265 nm). The Ion-exchange ChemoFilter has significant clearance, within seconds, of both Doxorubicin and Cisplatin mixed in a cocktail solution. However, it appears some Cisplatin is binding to the Nylon Mesh itself. Size, shape, and material of the mesh have been optimized. A potential mechanism for 11C, 13C, or 14C radiolabeling of Carboplatin has been developed and early results have been successful. ChemoFilter works much more efficiently when sequestered in nylon packets of specific geometries. Significant improvements have been made to ChemoFilter, moving the device closer to clinical trials.

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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.
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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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)]+ reacts faster with methionine than with cysteine at both pH 4 and 7 at a 1:1:1 ratio. [Pt(N,N,N',N',N"-pentamethyldiethylenetriamine)(NO3)]+ reacts with methionine faster at pH 4 but with cysteine faster at pH 7. This is most likely due to the thiol in the cysteine starting to deprotonate around pH 7. [Pt(Me4en)(NO3)2] (Me4en = N,N,N',N'-tetramethylethylenediamine) forms several products with N-AcCys at both pH 4 and 7, with the amounts of the products varying depending on the ratio of platinum and Cys. Mass spectrometry indicated one product as {[Pt(Me4en)(H2O)]2(N-AcCys)}2+, with two platinum compounds coordinated to a single cysteine. Lastly Pt[(en)(NO3)2] when reacting with N-AcCys at a ratio of 1:1 will coordinate with 2 different Cys molecules. With an excess of Pt the complex prefers to bind to only 1 Cys.
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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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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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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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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.)
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 antimetastatic activity. The majority of anticancer metallodrugs (including NAMI-A and cisplatin) can bind to DNA, which, in many cases, is an important therapeutic target. Much effort has gone into characterizing the DNA binding properties of anticancer metallodrugs. Less study has gone into characterizing the interaction of anticancer mellodrugs with RNA even though RNA is chemically similar to DNA and plays important roles in gene expression and regulation. Focusing on the extensively studied cisplatin, Chapter I covers both what is known about anticancer metallodrug-RNA binding and the information that can be gleaned from DNA binding and drug localization studies. Chapter II provides the details of a kinetic investigation of the in vitro binding of aquated cisplatin to an RNA sequence containing an internal loop derived from the core of the spliceosome, a related RNA hairpin, and the slower reacting DNA hairpin analog. Chapter III follows in cellulo studies with cisplatin-treated S. cerevisiae that demonstrate, using ICP-MS, differences in Pt accumulation in mRNA and rRNA. The effects of cisplatin treatment on S. cerevisiae cell growth and viability were investigated using clonogenic and morphologic assays. In Chapter IV the same protocols were applied in order to investigate Ru accumulation on RNA following S. cerevisiae treatment with NAMI-A. These in cellulo experiments were followed by in vitro binding studies that utilized MALDI-MS to compare Ru interactions with RNA and DNA oligonucleotides following treatment with NAMI-A under different solution conditions, finding enhanced binding in an acidic, reducing environment like that found in tumor tissue. Chapter V pulls together the knowledge gained so far and discusses questions for future investigation. This dissertation includes both previously published and unpublished coauthored material.
Committee in charge: David Tyler, Chairperson; Victoria DeRose, Advisor; Darren Johnson, Member; Andy Berglund, Member; Alice Barkan, Outside Member
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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-fluorophenyl) methylene]-4-piperidinone (EF-24) increases the anti-cancer effects of cisplatin against a human ovarian cancer cell line (A2780) and its cisplatin-resistant counterpart (A2780cis), while preventing cisplatin-mediated side effects in a human kidney cell line (HEK-293T) and a mouse auditory hybridoma cell line (HEI-OC1). The effect of cisplatin and EF-24 on cellular viability was measured using the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. The expression and activity of signal transduction proteins in several apoptotic pathways was measured using caspase luminescence assays. Reactive oxygen species (ROS) production was also measured using flow cytometry. Our data suggest that cisplatin and EF-24 are effective against ovarian cancer cell lines, but both compounds may also have adverse effects on auditory and renal cells. This project provides relevant information that may improve our understanding of how these compounds function in different tissues, facilitating improved cancer treatment and circumvention of side effects commonly associated with cisplatin treatment.
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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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Books on the topic "Cisplatin Biochemistry"

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Lippert, Bernhard. Cisplatin: Chemistry and Biochemistry of a Leading Anticancer Drug. Wiley & Sons, Limited, John, 2006.

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1946-, Lippert Bernhard, ed. Cisplatin: Chemistry and biochemistry of a leading anticancer drug. Zürich: Verlag Helvetica Chimica Acta, 1999.

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Lippert, Bernhard. Cisplatin: Chemistry and Biochemistry of a Leading Anticancer Drug. Wiley-VCH, 1999.

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Ball, Steve, and Sajid Kalathil. Adrenocortical cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0094.

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Adrenocortical cancer (ACC) is rare and associated with poor prognosis. The incidence is estimated at 0.7–2 cases per one million. Overall survival rate at five years for ACC is 37–47%. While the pathogenesis of ACC is incompletely understood, inherited predisposition syndromes are common in childhood ACC. Clinical presentation can be with symptoms and signs of hormone excess (functional tumours), mass effects, or as an incidental radiological finding. A multidisciplinary approach combining radiology, biochemistry, and tissue-based pathology is needed to establish a diagnosis to guide a surgical approach aimed at complete resection of the tumour where possible. At present, recommended first-line therapies for advanced disease are mitotane monotherapy or etopiside, doxorubicin, and cisplatin plus mitotane. Metronomic capecitabine and gemcitabine have been used as alternatives. Adjuvant radiotherapy to the tumour bed should be considered for patients considered to be at high risk of recurrence.
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Conference papers on the topic "Cisplatin Biochemistry"

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Cheng, Xin, Qiuju Lin, and Wenhui Li. "Observation of synergistic effect of End statin and cisplatin On Calu-6 cell." In 2018 International Workshop on Bioinformatics, Biochemistry, Biomedical Sciences (BBBS 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/bbbs-18.2018.4.

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