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Journal articles on the topic 'Cisplatin'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Ozdemir-sanci, Tuba, and Ebru Alimogullari. "Effect of naringin and cisplatin combination on cell viability and cell death in bladder cancer cells." Journal of Research in Pharmacy 29, no. 2 (2025): 673–81. https://doi.org/10.12991/jrespharm.1664894.

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Bladder cancer is a prevalent malignancy characterized by high recurrence rates and limited therapeutic options, particularly due to resistance and toxicity associated with cisplatin therapy. Bladder cancer remains a significant global health concern, and while cisplatin is a cornerstone of treatment, its efficacy is often limited by resistance and toxicity. Therefore, there is a critical need for novel agents that can enhance cisplatin's effects while mitigating its drawbacks. This study investigates the potential of naringin, a natural flavonoid, to exhibit antiproliferative and proapoptotic

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2

Demirel, Özge, and Serap Şahin. "Duloksetin Hidroklorür’ün DU-145 İnsan Prostat Kanser Hücreleri Üzerine Sitotoksik Etkisinin Araştırılması." Black Sea Journal of Health Science 8, no. 4 (2025): 132–38. https://doi.org/10.19127/bshealthscience.1649481.

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Prostat kanseri (PKa), Dünya çapında en yaygın kanserlerden birisi olup kansere bağlı ölümlerin büyük bir kısmını oluşturmaktadır. Bir serotonin-nöradrenalin geri alım intibitörü (SNGI) olan duloksetin, hem norepinefrin hem de serotoninin geri alımının inhibisyonu yoluyla antidepresan bir rol oynamaktadır. Duloksetin hidroklorürün DU-145 prostat kanser hücrelri üzerine sitotoksik etkisi ile ilgili çalışma bulunmamaktadır. Çalışmamızda, duloksetin hidroklorür ve cisplatinin DU-145 prostat kanseri ve L-929 sağlıklı fare fibroblast hücreleri üzerine sitotoksik etkileri 3-[4,5-Dimetiltiyazol-2-İl]

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3

ATAMAN, J. E., and D. BAXTER-GRILLO. "MORPHOLOGICAL EVALUATION OF CISPLATIN-INDUCED TESTICULAR DAMAGE IN WISTAR RATS." Nigerian Journal of Life Sciences (ISSN: 2276-7029) 4, no. 1 (2022): 16–25. http://dx.doi.org/10.52417/njls.v4i1.151.

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Twenty-one Wistar rats weighing 200 - 250 mg were categorized into three treatment groups- the control, saline and the cisplatin groups, each comprising of seven rats per group, to assess the effects of cisplatin-induced testicular damage in Wistar rats. The control group received feed mash and water ad libitum, the saline group received equal volumes of physiological saline intraperitoneally with normal feeds and water, while the cisplastin group received 8 mg/kg body weight of cisplastin only for five days and had normal feeds and water for twelve weeks before sacrifice. The effects of these

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4

Monroe, Jerry D., Denis Hodzic, Matthew H. Millay, Blaine G. Patty, and Michael E. Smith. "Anti-Cancer and Ototoxicity Characteristics of the Curcuminoids, CLEFMA and EF24, in Combination with Cisplatin." Molecules 24, no. 21 (2019): 3889. http://dx.doi.org/10.3390/molecules24213889.

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In this study, we investigated whether the curcuminoids, CLEFMA and EF24, improved cisplatin efficacy and reduced cisplatin ototoxicity. We used the lung cancer cell line, A549, to determine the effects of the curcuminoids and cisplatin on cell viability and several apoptotic signaling mechanisms. Cellular viability was measured using the MTT assay. A scratch assay was used to measure cell migration and fluorescent spectrophotometry to measure reactive oxygen species (ROS) production. Western blots and luminescence assays were used to measure the expression and activity of apoptosis-inducing f

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Heiserman, James Patrick, Zenab Minhas, Elahe Nikpayam, and Dong-Joo Cheon. "Targeting Heat Shock Protein 27 and Fatty Acid Oxidation Augments Cisplatin Treatment in Cisplatin-Resistant Ovarian Cancer Cell Lines." International Journal of Molecular Sciences 24, no. 16 (2023): 12638. http://dx.doi.org/10.3390/ijms241612638.

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Most ovarian cancer patients develop recurrent cancers which are often resistant to commonly employed chemotherapy agents, such as cisplatin. We have previously shown that the inhibition of heat shock protein 27 (HSP27) or fatty acid oxidation (FAO) sensitizes cisplatin-resistant ovarian cancer cell lines to cisplatin and dual inhibition of both HSP27 and FAO induces substantial cell death in vitro. However, it is unclear how HSP27 and FAO promote cisplatin resistance, and if dual inhibition of both HSP27 and FAO would augment cisplatin treatment in vivo. Here we showed that HSP27 knockdown in

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6

CHEN, PING, QING-SHENG WU, YA-PING DING, and ZI-CHUN ZHU. "PREPARATION OF CISPLATIN COMPOSITE MICRO/NANOFIBERS AND ANTITUMOR ACTIVITY IN VITRO AGAINST HUMAN TUMOR spc-a-1 CELLS." Nano 06, no. 04 (2011): 325–32. http://dx.doi.org/10.1142/s1793292011002688.

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In this paper, the cisplatin composite micro/nanofibers were prepared by electrospinning. Average diameter of the typical products was about 700 nm, and cisplatins were incorporated in biodegradable poly (L-lactic acid) fibers. The controlled release of cisplatin can be gained for long time. The possible mechanisms of cisplatin release in the PBS and the PBS with proteinase K were discussed. 3-(4, 5)-dimethylthiahiazo-(-z-y1)-3, 5-di-phenytetrazoliumromide (MTT) method was used to test antitumor activities in vitro against human lung tumor spc-a-1 cells. When incubation time was 24 h, the same

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7

Moon, Hyeon-Min, Jin-Sung Park, Il-Buem Lee, et al. "Cisplatin fastens chromatin irreversibly even at a high chloride concentration." Nucleic Acids Research 49, no. 21 (2021): 12035–47. http://dx.doi.org/10.1093/nar/gkab922.

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Abstract Cisplatin is one of the most potent anti-cancer drugs developed so far. Recent studies highlighted several intriguing roles of histones in cisplatin's anti-cancer effect. Thus, the effect of nucleosome formation should be considered to give a better account of the anti-cancer effect of cisplatin. Here we investigated this important issue via single-molecule measurements. Surprisingly, the reduced activity of cisplatin under [NaCl] = 180 mM, corresponding to the total concentration of cellular ionic species, is still sufficient to impair the integrity of a nucleosome by retaining its c

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8

Karayay, Betül, Heidi Olze, and Agnieszka J. Szczepek. "Degranulation of Murine Resident Cochlear Mast Cells: A Possible Factor Contributing to Cisplatin-Induced Ototoxicity and Neurotoxicity." International Journal of Molecular Sciences 24, no. 5 (2023): 4620. http://dx.doi.org/10.3390/ijms24054620.

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Permanent hearing loss is one of cisplatin’s adverse effects, affecting 30–60% of cancer patients treated with that drug. Our research group recently identified resident mast cells in rodents’ cochleae and observed that the number of mast cells changed upon adding cisplatin to cochlear explants. Here, we followed that observation and found that the murine cochlear mast cells degranulate in response to cisplatin and that the mast cell stabilizer cromoglicic acid (cromolyn) inhibits this process. Additionally, cromolyn significantly prevented cisplatin-induced loss of auditory hair cells and spi

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Bridget, SAMUEL1 Victor SAMUEL2* Otuamiobhedio Messiah WILFRED3 Victor Nnaemeka OGBONNA4 Igbanam Michael URANGIKOR5 Eugene ITIRI6 Emeka Emmanuel EZEALISIOBI7 Chinemerem Ulu IKPE8 Bliss ANYALEBECHI9 Benita Basil EGBE10. "CISPLATIN-INDUCED NEPHROTOXICITY IN WISTAR RATS." ISRG Journal of Clinical Medicine and Medical Research [ISRGJCMMR] II, no. II (2025): 5–9. https://doi.org/10.5281/zenodo.14955099.

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<strong>Abstract</strong> <em>This study examined the morphological changes in the kidneys of Wistar rats exposed to cisplatin over short-term (14 days) and long-term (28 days) periods. We randomly assigned 25 albino rats to three groups: a control group (Group A) receiving distilled water and rat pellets, a low-dose cisplatin group (Group B) receiving 7.5mg/ml of cisplatin twice weekly, and a high-dose cisplatin group (Group C) receiving 16mg/ml of cisplatin twice weekly. 24 hours after the last treatment, animals were sacrificed and kidneys were collected into sterile bottles for histologica

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Kasturi Pangarkar. "Development of cisplatin as an anti-cancer drug." GSC Advanced Research and Reviews 23, no. 1 (2025): 005–11. https://doi.org/10.30574/gscarr.2025.23.1.0101.

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Cisplatin, a platinum-based chemotherapeutic agent, has been a cornerstone in the treatment of various cancers since its FDA approval in 1978. It is particularly effective against cancers such as ovarian, colorectal, prostate, bladder, and non-small cell lung cancer (NSCLC). Cisplatin exerts its anticancer effects by forming platinum-DNA adducts that inhibit DNA replication and transcription, leading to cell cycle arrest and apoptosis. However, its clinical application is limited by severe side effects, including renal toxicity, nausea, vomiting, and the development of drug resistance. To miti

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Subandi, Subandi, Fredlina Balindra, Aura Gizta, Husnul Khotimah, and Kusworini Handono. "Nano Liposomal Curcumin as an Adjuvant: Enhancing Cisplatin Anticancer Effects in HeLa Cells." Sciences of Pharmacy 4, no. 2 (2025): 96–102. https://doi.org/10.58920/sciphar0402347.

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Cervical cancer, mainly driven by oncogenic HPV infections, remains a global health burden. Cisplatin is standard chemotherapy for advanced cases but is limited by toxicity. Nano liposomal curcumin, with improved bioavailability, may enhance cisplatin’s efficacy. This study investigated the combination’s effect on HeLa cells by analyzing Cyclin E1 and Bcl-2 expression. Nano liposomal curcumin was synthesized using thin-film hydration, yielding stable 32 nm nanoparticles. HeLa cells were divided into control and treatment groups, and varying doses of nano liposomal curcumin with cisplatin were

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ATAMAN, J. E., and A. A. A. OSINUBI. "EFFECTS OF ETHANOLIC LEAF EXTRACT OF NEWBOULDIA LAEVIS (P. BEAUV) ON CISPLATIN-INDUCED CHANGES ON TESTICULAR AND BLOOD PARAMETERS OF WISTAR RATS." Nigerian Journal of Life Sciences (ISSN: 2276-7029) 4, no. 1 (2022): 26–36. http://dx.doi.org/10.52417/njls.v4i1.152.

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Thirty-five Wistar rats weighing 200 - 250 mg were categorized into five treatment groups- the control, saline, cisplatin, pre-cisplatin and the post-cisplatin groups, each comprising of seven rats per group, to assess the effects of ethanolic leaf extract of Newbouldia laevis on cisplatin-induced testicular damage in Wistar rats. The control group received feed mash and water ad libitum, the saline group received equal volumes of physiological saline intraperitoneally with normal feeds and water. The pre-cisplatin group was treated with 100mg/kg body weight of ethanolic leaf extract of Newbou

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13

Solanki, Malvika H., Prodyot K. Chatterjee, Madhu Gupta, et al. "Magnesium protects against cisplatin-induced acute kidney injury by regulating platinum accumulation." American Journal of Physiology-Renal Physiology 307, no. 4 (2014): F369—F384. http://dx.doi.org/10.1152/ajprenal.00127.2014.

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Despite its success as a potent antineoplastic agent, ∼25% of patients receiving cisplatin experience acute kidney injury (AKI) and must discontinue therapy. Impaired magnesium homeostasis has been linked to cisplatin-mediated AKI, and because magnesium deficiency is widespread, we examined the effect of magnesium deficiency and replacement on cisplatin-induced AKI in physiologically relevant older female mice. Magnesium deficiency significantly increased cisplatin-associated weight loss and markers of renal damage (plasma blood urea nitrogen and creatinine), histological changes, inflammation

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14

Kumar, Gopal, Malvika H. Solanki, Xiangying Xue, et al. "Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity." American Journal of Physiology-Renal Physiology 313, no. 2 (2017): F339—F350. http://dx.doi.org/10.1152/ajprenal.00688.2016.

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Approximately 30% of all cancer patients treated with cisplatin, a widely used broad-spectrum chemotherapeutic agent, experience acute kidney injury (AKI). Almost all patients receiving cisplatin have magnesium (Mg) losses, which are proposed to aggravate AKI. Currently, there are no methods to successfully treat or prevent cisplatin-AKI. Whereas Mg supplementation has been shown to reduce AKI in experimental models and several small clinical trials, the effects of Mg status on tumor outcomes in immunocompetent tumor-bearing mice and humans have not been investigated. The purpose of this study

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15

Abedini Nazari, Najmeh, Behnam Omidi Sarajar, Seyedeh Zohreh Azarshin, Fatemeh Javani Jouni, Zahra Razzaghi, and Jaber Zafari. "Overcoming Cisplatin’s Challenges: A Promising Future in Cancer Care; A Comprehensive Review." International Journal of Medical Toxicology and Forensic Medicine 13, no. 04 (2024): 43478. http://dx.doi.org/10.32598/ijmtfm.v13i4.43478.

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Background: Cisplatin’s common use as an anti-neoplastic drug poses significant challenges due to its adverse effects, including renal disorders, neuropathies, hearing impairment, and gastrointestinal issues. Methods: A comprehensive search was done across major bibliographic databases, including PubMed, Embase, Web of Science, Google Scholar, and Scopus on cisplatin’s application in various cancer treatments. A manual examination of article reference lists was conducted, collecting data from 1990 to October 2023 for up-to-date research analysis. Results: Cisplatin primarily acts by binding to

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Orasan, Alexandru, Mihaela-Cristina Negru, Anda Ioana Morgovan, et al. "Strategies to Mitigate Cisplatin-Induced Ototoxicity: A Literature Review of Protective Agents, Mechanisms, and Clinical Gaps." Audiology Research 15, no. 2 (2025): 22. https://doi.org/10.3390/audiolres15020022.

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Background: Cisplatin, a widely used chemotherapeutic agent, is associated with significant ototoxicity, leading to progressive and irreversible sensorineural hearing loss in up to 93% of patients. Cisplatin generates reactive oxygen species (ROS) in the cochlea, activating apoptotic and necroptotic pathways that result in hair cell death. Inflammatory processes and nitrative stress also contribute to cochlear damage. Methods: This literature review was conducted to explore the mechanisms underlying cisplatin-induced ototoxicity and evaluate protective strategies, including both current and em

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17

Kantapan, Jiraporn, Nuttawadee Intachai, Nopawit Khamto, et al. "Pentagalloyl Glucose and Cisplatin Combination Treatment Exhibits a Synergistic Anticancer Effect in 2D and 3D Models of Head and Neck Carcinoma." Pharmaceuticals 15, no. 7 (2022): 830. http://dx.doi.org/10.3390/ph15070830.

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Although cisplatin is a first-line chemotherapy drug for head and neck squamous cell carcinoma (HNSCC), its therapeutic efficacy is limited owing to serious side effects and acquired drug resistance. This study determined whether combining pentagalloyl glucose (PGG) and cisplatin enhanced their anti-tumor activities on HNSCC cell lines. We investigated the anticancer effect of PGG combined with cisplatin in 2D and 3D multicellular spheroid cell culture. The results revealed that PGG combined with cisplatin inhibited cell viability and produced synergistic effects. PGG potentiates the anticance

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Al-Gholam, Marwa A., Asmaa S. Moaty, Ahmed M. Zein-Elabedein, and Asmaa S. Essawy. "Possible ameliorative effects of pentoxifylline on cisplatin-induced ototoxicity in rats: a study with hearing test, light, and scanning electron microscopy." European Journal of Anatomy 26, no. 1 (2022): 95–106. http://dx.doi.org/10.52083/dqjc4772.

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Cisplatin is an antineoplastic drug widely used to treat various types of cancer. Ototoxicity is still cisplatin’s most critical side-effect. Some patients may experience dose limitations due to hearing loss. Pentoxifylline (PX) exhibits powerful antioxidant, anti-inflammatory, and immune-regulatory effects. Our study was designed to investigate the protective effects of pentoxifylline on cisplatin-induced ototoxicity. Forty adult male healthy Sprague-Dawley rats were used through the entire experiment. Four groups of animals were categorized: Group I (control group); Group II (PX group) recei

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Dhima, Irida, Stelios Zerikiotis, Panagiotis Lekkas, et al. "Curcumin Acts as a Chemosensitizer for Leiomyosarcoma Cells In Vitro But Fails to Mediate Antioxidant Enzyme Activity in Cisplatin-Induced Experimental Nephrotoxicity in Rats." Integrative Cancer Therapies 18 (January 2019): 153473541987281. http://dx.doi.org/10.1177/1534735419872811.

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Background. Cisplatin (cis-diamminedichloroplatinum) is a widely used chemotherapeutic agent for the treatment of various cancers. Although it represents an effective regimen, its application is accompanied by side effects to normal tissues, especially to the kidneys. Cisplatin generates free radicals and impairs the function of antioxidant enzymes. Modulation of cisplatin-induced oxidative stress by specific antioxidant molecules represents an attractive approach to minimize side effects. Methods. We studied the ability of curcumin to sensitize leiomyosarcoma (LMS) cells to cisplatin. Assays

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Caramalis, A., S. Nissel-Horowitz, U. Iqbal, et al. "Weekly chemotherapy with platinum as radio-sensitizer during concomitant chemoradiotherapy for squamous cell head and neck cancer." Journal of Clinical Oncology 25, no. 18_suppl (2007): 16541. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.16541.

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16541 Background: CRT protocols for locally advanced HNC commonly utilize single agent cisplatinum as the radiation- sensitizing chemotherpy. This is typically administered in q 3 weekly doses of 100 mg/sq m concomitantly with XRT. However, many pts are not candidates for this dose and schedule of cisplatinum delivery due to co-morbidities. Limited data are available regarding the efficacy of alternate dosing of platinum analogues.We therefore analysed our experience with alternate dosing of cisplatin or carboplatin administered concomitantly with XRT. Methods: IRB approval was obtained for th

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Telgenhoff, D. J., and S. K. Aggarwal. "Transmission Electron Microscopy of Rat Kupffer Cell Activation After Cisplatin Treatment: an in Vivo Study." Microscopy and Microanalysis 3, S2 (1997): 83–84. http://dx.doi.org/10.1017/s1431927600007303.

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Cisplatin (cis-diamminedichloroplatinum II) is a broad spectrum anti-cancer agent. Its main limitations are its severe toxic side effects. Cisplatin’s major mechanisms of action include inhibition of DNA synthesis by interstrand and intrastrand crosslinking, inhibition of cytokinesis, and macrophage activation. Cisplatin acts through the activation of the immune system by inducing macrophages to form cytoplasmic extensions which seek out and phagocytose tumor cells. More recently, cisplatin has been shown to activate Kupffer cells (macrophages in the liver) by increasing their number and cytop

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&NA;. "Cisplatin see Carboplatin/cisplatin." Reactions Weekly &NA;, no. 372 (1991): 3. http://dx.doi.org/10.2165/00128415-199103720-00015.

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&NA;. "Cisplatin see Fluorouracil + cisplatin." Reactions Weekly &NA;, no. 382 (1991): 6. http://dx.doi.org/10.2165/00128415-199103820-00022.

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&NA;. "Cisplatin see Epirubicin/cisplatin." Reactions Weekly &NA;, no. 304 (1990): 6. http://dx.doi.org/10.2165/00128415-199003040-00011.

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&NA;. "Cisplatin see Bleomycin/cisplatin." Reactions Weekly &NA;, no. 312 (1990): 5. http://dx.doi.org/10.2165/00128415-199003120-00022.

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&NA;. "Cisplatin see Carboplatin/cisplatin." Reactions Weekly &NA;, no. 317 (1990): 4. http://dx.doi.org/10.2165/00128415-199003170-00012.

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Couillard-Montminy, Valérie, Pierre-Yves Gagnon, Sebastien Fortin, and Jimmy Côté. "Effectiveness of adjuvant carboplatin-based chemotherapy compared to cisplatin in non-small cell lung cancer." Journal of Oncology Pharmacy Practice 25, no. 1 (2017): 44–51. http://dx.doi.org/10.1177/1078155217724595.

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Background Cisplatin and vinorelbine given intravenously is a well-established adjuvant chemotherapy regimen after surgery for early non-small cell lung cancer. However, few validated alternatives exist when cisplatin is not indicated or tolerated. Carboplatin is frequently used in this setting. We evaluated the 5-year overall survival, progression-free survival and toxicity in patients treated for stage IB to IIIB resected non-small cell lung cancer receiving adjuvant carboplatin-based chemotherapy compared to cisplatin in association with vinorelbine. Methods Single-center retrospective stud

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Fritzsche, Saskia, Christian Strauss, Christian Scheller, and Sandra Leisz. "Nimodipine Treatment Protects Auditory Hair Cells from Cisplatin-Induced Cell Death Accompanied by Upregulation of LMO4." International Journal of Molecular Sciences 23, no. 10 (2022): 5780. http://dx.doi.org/10.3390/ijms23105780.

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Ototoxicity is one of the main dose-limiting side effects of cisplatin chemotherapy and impairs the quality of life of tumor patients dramatically. Since there is currently no established standard therapy targeting hearing loss in cisplatin treatment, the aim of this study was to investigate the effect of nimodipine and its role in cell survival in cisplatin-associated hearing cell damage. To determine the cytotoxic effect, the cell death rate was measured using undifferentiated and differentiated UB/OC−1 and UB/OC−2 cells, after nimodipine pre-treatment and stress induction by cisplatin. Furt

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von Fournier, Armin, Erik Würflein, Helena Moratin, et al. "Cisplatin-Mediated IL-6 and IDO1 Suppression in Mesenchymal Stromal Cells: Implications for Tumor Microenvironment Modulation In Vitro." Current Issues in Molecular Biology 47, no. 4 (2025): 231. https://doi.org/10.3390/cimb47040231.

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Mesenchymal stromal cells (MSCs) influence tumor biology and immunology by releasing cytokines, chemokines and growth factors. Currently, cisplatin is an integral part of drug-based tumor therapy, for example, in head and neck squamous cell carcinoma (HNSCC). Cisplatin treatment induces apoptosis as a primary mechanism of action; however, additional immunomodulatory effects of cisplatin are gaining interest. The aim of this study is to evaluate the possible immunomodulatory effects of cisplatin in human MSCs (hMSCs). The MSCs, obtained from human bone marrow, were characterized by analyzing pl

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Zhang, Weiqi, and Ching-Hsuan Tung. "Redox-responsive cisplatin nanogels for anticancer drug delivery." Chemical Communications 54, no. 60 (2018): 8367–70. http://dx.doi.org/10.1039/c8cc01795f.

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Naghashpour, Mahsa, Dian Dayer, Hadi Karami, et al. "Evaluating the Magnolol Anticancer Potential in MKN-45 Gastric Cancer Cells." Medicina 59, no. 2 (2023): 286. http://dx.doi.org/10.3390/medicina59020286.

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Background and Objectives: Combination therapy improves the effect of chemotherapy on tumor cells. Magnolol, used in treating gastrointestinal disorders, has been shown to have anti-cancer properties. We investigated the synergistic effect of cisplatin and magnolol on the viability and maintenance of MKN-45 gastric cancer cells. Materials and Methods: The toxicity of magnolol and/or cisplatin was determined using the MTT technique. The trypan blue method was used to test magnolol and/or cisplatin’s effect on MKN-45 cell growth. Crystal violet staining was used to assess the treated cells’ tend

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&NA;. "Cisplatin see Bleomycin/cisplatin/vinblastine." Reactions Weekly &NA;, no. 292 (1990): 5. http://dx.doi.org/10.2165/00128415-199002920-00012.

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&NA;. "Cisplatin see Vincristine/cisplatin/bleomycin." Reactions Weekly &NA;, no. 334 (1991): 6. http://dx.doi.org/10.2165/00128415-199103340-00024.

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&NA;. "Cisplatin see Bleomycin/cisplatin/methotrexate." Reactions Weekly &NA;, no. 341 (1991): 4. http://dx.doi.org/10.2165/00128415-199103410-00020.

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&NA;. "Cisplatin see Bleomycin/cisplatin/etoposide." Reactions Weekly &NA;, no. 365 (1991): 5. http://dx.doi.org/10.2165/00128415-199103650-00015.

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Ivanova, Stefka. "Comparative assessment of clinical trials, indications, pharmacokinetic parameters and side effects of approved platinum drugs." Pharmacia 69, no. 1 (2022): 1–7. http://dx.doi.org/10.3897/pharmacia.69.e78813.

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Platinum complexes are among the most commonly applied anticancer agents. The aim of current work is collection, analysing and comparative estimation of clinical trials and pharmacological indications of currently approved for application platinum detivatives: Cisplatin, Carboplatin, Oxaliplatin, Nedaplatin (Japan), Lobaplatin (China), Heptaplatin (North Korea), and Satraplatin. The other aim of the study includes the summarizing of the hystoric data for the stages of the developlement of these drugs, and the comparison of pharmacokimetic parameters, side effecs and the dose-liniting factors o

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Ivanova, Stefka. "Comparative assessment of clinical trials, indications, pharmacokinetic parameters and side effects of approved platinum drugs." Pharmacia 69, no. (1) (2022): 1–7. https://doi.org/10.3897/pharmacia.69.e78813.

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Platinum complexes are among the most commonly applied anticancer agents. The aim of current work is collection, analysing and comparative estimation of clinical trials and pharmacological indications of currently approved for application platinum detivatives: Cisplatin, Carboplatin, Oxaliplatin, Nedaplatin (Japan), Lobaplatin (China), Heptaplatin (North Korea), and Satraplatin. The other aim of the study includes the summarizing of the hystoric data for the stages of the developlement of these drugs, and the comparison of pharmacokimetic parameters, side effecs and the dose-liniting factors o

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Wang, Chong-Zhi, Daniel Basila, Han H. Aung, et al. "Effects of Ganoderma lucidum Extract on Chemotherapy-Induced Nausea and Vomiting in a Rat Model." American Journal of Chinese Medicine 33, no. 05 (2005): 807–15. http://dx.doi.org/10.1142/s0192415x05003429.

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Chemotherapy is highly cytotoxic, causing a number of severe adverse effects such as nausea and vomiting. Herbal medicines, which can often be used on a daily basis for prolonged treatment, may be clinically beneficial. Ganoderma lucidum or Lingzhi mushroom has been recognized as a remedy in treating a number of medical conditions, including balancing immunity and decreasing drug-induced side effects. It has been shown that rats react to emetic stimuli, like the chemotherapy agent cisplatin, by increased consumption of kaolin, known as pica; and this rat model has been utilized to evaluate nov

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Lutze, Richard, Matthew Ingersoll, Regina Kelmann, and Tal Teitz. "Trametinib, a MEK1/2 Inhibitor, Protects Mice from Cisplatin- and Noise-Induced Hearing Loss." Pharmaceuticals 17, no. 6 (2024): 735. http://dx.doi.org/10.3390/ph17060735.

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Hearing loss is one of the most common types of disability; however, there is only one FDA-approved drug to prevent any type of hearing loss. Treatment with the highly effective chemotherapy agent, cisplatin, and exposure to high-decibel noises are two of the most common causes of hearing loss. The mitogen-activated protein kinase (MAPK) pathway, a phosphorylation cascade consisting of RAF, MEK1/2, and ERK1/2, has been implicated in both types of hearing loss. Pharmacologically inhibiting BRAF or ERK1/2 is protective against noise- and cisplatin-induced hearing loss in multiple mouse models. T

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Ali H. Saliem and Sarmad Mohammed Hashim. "Evaluation the Protective Effect of Capparis spinosa Fruits Hydroalcoholic Extract Against Nephrotoxicity Induced by Cisplatin in Rats." University of Thi-Qar Journal of agricultural research 11, no. 2 (2022): 25–35. http://dx.doi.org/10.54174/utjagr.v11i2.178.

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The present study was carried out to evaluate the kidney abnormality changes, and nephrotoxicity after using the cisplatine and investigate the protective effect of capparis spinosa fruit extract against these effects and evaluate the kidney function test urea, cratenine, total protein tests and histopathological changes of kidney . Twenty one (21) male rats were randomly divided into three groups (7 rats/ each). First group was received distilled water orally for 10 days and served as control group. Second group was received cisplatin only (10 mg/kg, i.p.) as a single dose at day 8 and served

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1389 (2012): 17. http://dx.doi.org/10.2165/00128415-201213890-00054.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1395 (2012): 15. http://dx.doi.org/10.2165/00128415-201213950-00050.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 694 (1998): 7–8. http://dx.doi.org/10.2165/00128415-199806940-00019.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 707 (1998): 9. http://dx.doi.org/10.2165/00128415-199807070-00029.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 729 (1998): 7. http://dx.doi.org/10.2165/00128415-199807290-00018.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 751 (1999): 7. http://dx.doi.org/10.2165/00128415-199907510-00023.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1161 (2007): 8–9. http://dx.doi.org/10.2165/00128415-200711610-00023.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1167 (2007): 11. http://dx.doi.org/10.2165/00128415-200711670-00033.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1175 (2007): 11–12. http://dx.doi.org/10.2165/00128415-200711750-00036.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1177 (2007): 9–10. http://dx.doi.org/10.2165/00128415-200711770-00023.

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