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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"

1

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 (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.

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Wang, Wenyu, Jihye Im, Soochi Kim, et al. "ROS-Induced SIRT2 Upregulation Contributes to Cisplatin Sensitivity in Ovarian Cancer." Antioxidants 9, no. 11 (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 s

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Fujimoto, T., H. Maeda, K. Kubo, et al. "Enhanced Anti-tumour Effect of Cisplatin with Low-voltage Electrochemotherapy in Hamster Oral Fibrosarcoma." Journal of International Medical Research 33, no. 5 (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 toget

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4

Murray, Vincent. "Nucleosomes and Cisplatin." Chemistry & Biology 17, no. 12 (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 (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 apo

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6

Mapuskar, Kranti A., Emily J. Steinbach, Amira Zaher, et al. "Mitochondrial Superoxide Dismutase in Cisplatin-Induced Kidney Injury." Antioxidants 10, no. 9 (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 k

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Xing, Jing-Jing, Jin-Gang Hou, Ying Liu, 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 (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 in

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Kohda, Yuka, Yoshiko Kawai, Noriaki Iwamoto, et al. "Serum thymic factor, FTS, attenuates cisplatin nephrotoxicity by suppressing cisplatin-induced ERK activation." Biochemical Pharmacology 70, no. 9 (2005): 1408–16. http://dx.doi.org/10.1016/j.bcp.2005.08.002.

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9

Rodríguez-Ulloa, Arielis, Yassel Ramos, Aniel Sánchez-Puente, et al. "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 (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 di

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Bushau-Sprinkle, Adrienne M., Michelle T. Barati, Yuxuan Zheng, et al. "Na/H Exchange Regulatory Factor 1 Deficient Mice Show Evidence of Oxidative Stress and Altered Cisplatin Pharmacokinetics." Antioxidants 10, no. 7 (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 trea

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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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<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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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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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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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.)<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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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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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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2

1946-, Lippert Bernhard, ed. Cisplatin: Chemistry and biochemistry of a leading anticancer drug. 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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4

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 surgic

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Conference papers on the topic "Cisplatin Biochemistry"

1

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). Atlantis Press, 2018. http://dx.doi.org/10.2991/bbbs-18.2018.4.

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