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Journal articles on the topic 'Cisplatin'

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Author: Grafiati

Published: 4 June 2021

Last updated: 6 July 2024

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1

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 (March 17, 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 treatments on total sperm count, sperm motility, percentage live:dead sperm and on testicular and epididymal morphology of the Wistar rats were assessed. The results revealed total sperm count in the cisplatin group as significantly different from control (p<0.001), and the motile sperm count in the cisplatin group was also significantly different from control (p<0.001). Also, there was a greater percentage of dead sperm and more morphologically abnormal forms in the cisplatin group, compared to control. The testicular and epididymal sections of the saline treatment showed normal progression of the spermatogenic germ cell series and normal testicular interstitium. The sections of the testes from the cisplatin group had seminiferous tubules with atrophic changes, detached basement membrane from the seminiferous epithelium, inflammed interstitium with oedema, paucity of Leydig cells, vascular congestion and haemorrhage. The epididymis showed lumen with empty or scanty spermatozoa, necrosis and haemorrhage. These findings affirms the reality of severe gonadotoxicity associated with use of cisplatin as chemotherapeutic agent, especially in the male.

2

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 (October 29, 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 factor (AIF), caspases-3/7, -8, -9, and -12, c-Jun N-terminal kinases (JNK), mitogen-activated protein kinase (MAPK), and proto-oncogene tyrosine-protein kinase (Src). A zebrafish model was used to evaluate auditory effects. Cisplatin, the curcuminoids, and their combinations had similar effects on cell viability (IC50 values: 2–16 μM) and AIF, caspase-12, JNK, MAPK, and Src expression, while caspase-3/7, -8, and -9 activity was unchanged or decreased. Cisplatin increased ROS yield (1.2-fold), and curcuminoid and combination treatments reduced ROS (0.75–0.85-fold). Combination treatments reduced A549 migration (0.51–0.53-fold). Both curcuminoids reduced auditory threshold shifts induced by cisplatin. In summary, cisplatin and the curcuminoids might cause cell death through AIF and caspase-12. The curcuminoids may potentiate cisplatin’s effect against A549 migration, but may counteract cisplatin’s effect to increase ROS production. The curcuminoids might also prevent cisplatin ototoxicity.

3

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 (August 10, 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 two cisplatin-resistant ovarian cancer cell lines (A2780CIS and PEO4) resulted in more ROS production upon cisplatin treatment. HSP27-knockdown cancer cells exhibited decreased levels of reduced glutathione (GSH) and glucose6phosphate dehydrogenase (G6PD), a crucial pentose phosphate pathway enzyme. ROS depletion with the compound N-acetyl cysteine (NAC) attenuated cisplatin-induced upregulation of HSP27, FAO, and markers of apoptosis and ferroptosis in cisplatin-resistant ovarian cancer cell lines. Finally, inhibition of HSP27 and FAO with ivermectin and perhexiline enhanced the cytotoxic effect of cisplatin in A2780CIS xenograft tumors in vivo. Our results suggest that two different cisplatin-resistant ovarian cancer cell lines upregulate HSP27 and FAO to deplete cisplatin-induced ROS to attenuate cisplatin’s cytotoxic effect.

4

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 (August 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 content of cisplatin from virgin cisplatin and the composite fibers has almost equal antitumor activity in vitro. However, when incubation time was 48 h, the composite fibers show much higher antitumor activity than the virgin cisplatin. The system may be useful in the postoperative local chemotherapy and have clinical applications as an implantable drug for tumor in the future.

5

Moon, Hyeon-Min, Jin-Sung Park, Il-Buem Lee, Young-Im Kang, Hae Jun Jung, Dongju An, Yumi Shin, et al. "Cisplatin fastens chromatin irreversibly even at a high chloride concentration." Nucleic Acids Research 49, no. 21 (November 23, 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 condensed structure firmly, even against severe mechanical and chemical disturbances. Our finding suggests that such cisplatin-induced fastening of chromatin can inhibit nucleosome remodelling required for normal biological functions. The in vitro chromatin transcription assay indeed revealed that the transcription activity was effectively suppressed in the presence of cisplatin. Our direct physical measurements on cisplatin-nucleosome adducts suggest that the formation of such adducts be the key to the anti-cancer effect by cisplatin.

6

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 (February 27, 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 spiral ganglion neurons. Our study provides the first evidence for the possible mast cell participation in cisplatin-induced damage to the inner ear.

7

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 (March 17, 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 Newbouldia laevis for twelve weeks before being treated with 8mg/kg of cisplatin intraperitoneally for five days. Sacrifice was done after another twelve weeks. Cisplatin group received 8 mg/kg body weight of cisplastin for five days without any extract treatment, but had normal feeds and water for twelve weeks before sacrifice. The post-cisplatin group had 8mg/kg body weight of cisplatin for five days before being treated with 100mg/kg of ethanolic leaf extract of Newbouldia laevis for twelve weeks before sacrifice. The extract group received only the 100mg/kg of ethanolic leaf extract of Newbouldia laevis for twelve weeks without any other treatment before sacrifice. The effects of these treatments on body weight, testicular and epididymal weight, testicular volume, total and motile sperm count, sperm motility, percentage live:dead sperm, hormonal and haematological parameters as well effects on testicular and epididymal cytoarchitecture of the Wistar rats were assessed.There were significant (p<0.05) changes in body weight, testicular and epididymal weight, testicular volume, sperm, hormonal and haematological parameters in the treatments, compared to control. The pre-cisplatin treatment group showed significant (p<0.05) improvement in the induced changes caused by cisplatin, compared to the post-cisplatin group. The findings of this investigation confirms the protective effects of ethanolic leaf extract of Newbouldia laevis on cisplatin-induced gonadotoxicity in male Wistar rats.

8

Kumar, Gopal, Malvika H. Solanki, Xiangying Xue, Rachel Mintz, Swati Madankumar, Prodyot K. Chatterjee, and Christine N. Metz. "Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity." American Journal of Physiology-Renal Physiology 313, no. 2 (August 1, 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 was to further examine the effects of Mg deficiency (±Mg supplementation) on cisplatin-mediated AKI and tumor killing in immunocompetent mice bearing CT26 colon tumors. Using a model where cisplatin alone (20 mg/kg cumulative dose) produced minimal kidney injury, Mg deficiency significantly worsened cisplatin-mediated AKI, as determined by biochemical markers (blood urea nitrogen and plasma creatinine) and histological renal changes, as well as markers of renal oxidative stress, inflammation, and apoptosis. By contrast, Mg supplementation blocked cisplatin-induced kidney injury. Using LLC-PK1renal epithelial cells, we observed that Mg deficiency or inhibition of Mg uptake significantly enhanced cisplatin-induced cytotoxicity, whereas Mg supplementation protected against cytotoxicity. However, neither Mg deficiency nor inhibition of Mg uptake impaired cisplatin-mediated killing of CT26 tumor cells in vitro. Mg deficiency was associated with significantly larger CT26 tumors in BALB/c mice when compared with normal-fed control mice, and Mg deficiency significantly reduced cisplatin-mediated tumor killing in vivo. Finally, Mg supplementation did not compromise cisplatin’s anti-tumor efficacy in vivo.

9

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 (January 28, 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 DNA in the cell nucleus and disrupting DNA transcription and replication, leading to cytotoxicity and malignant cell destruction. Mechanisms of resistance included altered drug absorption, increased efflux and detoxification, modified targets, and increased DNA repair. Interactions with matrix proteins, pH changes, and food affect cisplatin effectiveness. Cisplatin-induced DNA damage mainly forms DNA adducts, causing intra- and inter-strand cross-links. Despite its therapeutic benefits, inevitable adverse effects, like nephrotoxicity, ototoxicity, gastrointestinal diseases, hepatotoxicity, cardiovascular issues, and neuropathy exist. Strategies to mitigate these include hydration therapy, thiol-containing agents, antioxidants, and modulators. Combination therapy enhances cisplatin efficacy. Conclusion: Cisplatin is a potent anticancer tool marked by challenges from adverse effects and emerging resistance. Ongoing research focuses on combined therapeutic approaches and supports interventions to enhance efficacy and reduce adverse effects, fostering optimism for better cancer treatments.

10

Solanki, Malvika H., Prodyot K. Chatterjee, Madhu Gupta, Xiangying Xue, Andrei Plagov, Margot H. Metz, Rachel Mintz, Pravin C. Singhal, and Christine N. Metz. "Magnesium protects against cisplatin-induced acute kidney injury by regulating platinum accumulation." American Journal of Physiology-Renal Physiology 307, no. 4 (August 15, 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, and renal cell apoptosis and modulated signaling pathways (e.g., ERK1/2, p53, and STAT3). Conversely, these damaging effects were reversed by magnesium. Magnesium deficiency alone significantly induced basal and cisplatin-mediated oxidative stress, whereas magnesium replacement attenuated these effects. Similar results were observed using cisplatin-treated LLC-PK1 renal epithelial cells exposed to various magnesium concentrations. Magnesium deficiency significantly amplified renal platinum accumulation, whereas magnesium replacement blocked the augmented platinum accumulation after magnesium deficiency. Increased renal platinum accumulation during magnesium deficiency was accompanied by reduced renal efflux transporter expression, which was reversed by magnesium replacement. These findings demonstrate the role of magnesium in regulating cisplatin-induced AKI by enhancing oxidative stress and thus promoting cisplatin-mediated damage. Additional in vitro experiments using ovarian, breast, and lung cancer cell lines showed that magnesium supplementation did not compromise cisplatin's chemotherapeutic efficacy. Finally, because no consistently successful therapy to prevent or treat cisplatin-mediated AKI is available for humans, these results support developing more conservative magnesium replacement guidelines for reducing cisplatin-induced AKI in cancer patients at risk for magnesium deficiency.

11

Kantapan, Jiraporn, Nuttawadee Intachai, Nopawit Khamto, Puttinan Meepowpan, Padchanee Sangthong, Kittichai Wantanajittikul, Nathupakorn Dechsupa, and Imjai Chitapanarux. "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 (July 4, 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 anticancer effect of cisplatin by promoting apoptosis and inhibiting cell migration. The western blot and molecular docking analysis revealed that the synergistic effect of the combination treatment may be related to the PGG-mediated reduced expression of phosphorylated STAT3 and phosphorylated Akt. Furthermore, we found that the combined treatment of PGG and cisplatin’s effect on 3D multicellular spheroid size was more potent than the monotherapies. Our findings indicated that the combination therapy of PGG and cisplatin synergistically inhibited HNSCC cancer cell viability and induced apoptosis in 2D and 3D models. The present results suggested that PGG may be a promising adjunct drug used with cisplatin for a practical therapeutic approach to head and neck cancer.

12

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

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13

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

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14

&NA;. "Cisplatin see Epirubicin/cisplatin." Reactions Weekly &NA;, no. 304 (June 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 (August 1990): 5. http://dx.doi.org/10.2165/00128415-199003120-00022.

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16

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

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17

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 (January 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) received 25 mg/kg/day of oral PX by gavage for 8 consecutive days; Group III (Cisplatin group) received cisplatin single intraperitoneal dose of 10 mg/kg; Group IV (PX + Cisplatin group) received 25 mg/kg/day of oral PX by gavage for 8 successive days and a single intraperitoneal dose of 10 mg/kg cisplatin at the 4th day. First and 9th-day Distortiondistortion-product otoacoustic emissions (DPOAE) tests were conducted. An intracardiac blood sample was collected for total antioxidant capacity (TAC) measurement, and the cochleae of rats were examined histopathologically. A significant reduction in serum TAC value was detected in the cisplatin group, while PX treatment significantly reduced TAC. Cisplatin decreased the DPOAE amplitudes in rats; conversely, the PX+cisplatin group showed a significant increase at all frequencies. Upon histopathological examination, the Ciplastin group revealed perturbation of the normal architecture of the organ of Corti, increased collagen deposition and marked expression of caspase-3, while the PX+cisplatin group revealed preserved architecture of the organ of Corti, minimal collagen deposition and downregulation of Caspase-3 expression. As evidenced by our findings and results from DPOAE results, biochemical findings, histological and ultrastructural analyses, PX significantly protects rats against ototoxicity caused by cisplatin.

18

Dhima, Irida, Stelios Zerikiotis, Panagiotis Lekkas, Yannis V. Simos, Maria Gkiouli, Patra Vezyraki, Evangelia Dounousi, 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 for cell proliferation, mitochondrial function, induction of apoptosis, and cell cycle arrest were performed using various concentrations of cisplatin and a concentration of curcumin that caused a nonsignificant reduction in cell viability. Moreover, the effect of curcumin was examined against cisplatin-induced experimental nephrotoxicity. Renal injury was assessed by measuring serum creatinine, blood urea nitrogen (BUN), and the kidney’s relative weight. Oxidative stress was measured by means of enzymatic activities of superoxide dismutase and glutathione peroxidase in the rats’ blood and malondialdehyde levels in rats’ urine. Results. In our study, we found that curcumin sensitizes LMS cells to cisplatin by enhancing apoptosis and impairing mitochondrial function. In an in vivo model of cisplatin-induced experimental nephrotoxicity, intraperitoneal administration of curcumin failed to preserve blood’s antioxidant enzyme activity and decrease lipid peroxidation. Nevertheless, curcumin was able to protect nephrons’ histology from cisplatin’s toxic effect. Conclusion. Our results showed that curcumin can act as chemosensitizer, but its role as an adjunctive cisplatin-induced oxidative stress inhibitor requires further dose-finding studies to maximize the effectiveness of chemotherapy.

19

Caramalis, A., S. Nissel-Horowitz, U. Iqbal, R. Roy, N. Radhakrishnan, A. Thomas, J. Pollack, Y. Lebowicz, and B. Mehrotra. "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 (June 20, 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 this retrospective analysis. Tumor registry and pharmacy data were reviewed to identify eligible pts. between 2004–2006 who were treated with alternate dosing of platinum with XRT. Pt characteristics recorded included: age, gender, stage, site of disease, type of chemotherpeutic agent used carboplatin or cisplatinum, number of doses administered, local disease free survival and overall survival. Results: Eleven pts were identified. Median age: 64 years (44–75); Gender: M:F::8:3; Sites: Oral cavity: n=2; Pharynx: n=11; Stage III: n=3; Stage IVa &b: n=8. Cisplatin weekly (doses 30–40mg/sqm): n=8; Carboplatin weekly AUC=2: n=3; Cisplatin weekly, changed to carboplatin: n=1. Nine of 11 pts achieved a local CR (82%); one pt has achieved a near CR and one pt achieved a PR and required salvage laryngectomy. At a median follow up of 14 mos (range: 4–34), all pts remain alive. In addition to the pt that achieved a PR after initial treatment, one other pt has required surgical salvage at 23 mos post CRT. No treatment related mortality occurred in this series. Conclusions: Weekly administration of cisplatin and carboplatin appears to be a feasible alternative to standard dose and schedule of cisplatin with acceptable efficacy. Future studies should compare targetted therapies such as cetuximab with or in combination with weekly platinum regimens during CRT for pts not eligible for standard dose cisplatinum. No significant financial relationships to disclose.

20

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 (August 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 cytoplasmic extensions. Electron microscopic analysis of cisplatin treated rat liver in vivo was performed to examine these extensions in greater detail and relate these to other changes in the liver cells.Wistar rats (100-130 g) were given intraperitoneal injections of cisplatin (9 mg/kg in 0.9% sodium chloride) over a five day period. Controls were treated with equal amounts of the vehicle of injection. After 9 days the rats were sacrificed. Segments of liver were fixed in 2% glutaraldehyde in 0.1 M cacodylate buffer (pH 7.3).

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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 (August 21, 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 study of patients having received adjuvant chemotherapy between January 2004 and December 2013 at the oncology clinic at Institut Universitaire de Cardiologie et de Pneumologie de Québec (Canada). Three sub-groups, cisplatin/vinorelbine, carboplatin/vinorelbine and the substitution of cisplatin/vinorelbine for carboplatin/vinorelbine (cisplatin/vinorelbine/carboplatin/vinorelbine), were studied during treatment. Results One hundred twenty-seven patients were included in this study. The median PFS was not significantly different, with 50.4 months for cisplatin/vinorelbine, 57.3 months for cisplatin/vinorelbine/carboplatin/vinorelbine and not yet achieved for the carboplatin/vinorelbine group ( p = 0.80). Overall survival also did not differ significantly between the three groups. The 5-year overall survival rates were 66% in cisplatin/vinorelbine group, 55% in carboplatin/vinorelbine group and 70% in cisplatin/vinorelbine/carboplatin/vinorelbine group ( p = 0, 95). No differences were noted between groups concerning high-grade hematologic toxicity. Conclusions Although the effectiveness and hematologic toxicity are comparable between cisplat in and carboplatin in the adjuvant treatment of resected non-small cell lung cancer, the results obtained corroborate the practice used at our oncology clinic. Nevertheless, more prospective studies would be needed to confirm these results.

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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 (May 21, 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. Furthermore, immunoblot analysis and intracellular calcium measurement were performed to investigate anti-apoptotic signaling, which was associated with a reduced cytotoxic effect after nimodipine pre-treatment. Cisplatin’s cytotoxic effect was significantly attenuated by nimodipine up to 61%. In addition, nimodipine pre-treatment counteracted the reduction in LIM Domain Only 4 (LMO4) by cisplatin, which was associated with increased activation of Ak strain transforming/protein kinase B (Akt), cAMP response element-binding protein (CREB), and signal transducers and activators of transcription 3 (Stat3). Thus, nimodipine presents a potentially well-tolerated substance against the ototoxicity of cisplatin, which could result in a significant improvement in patients’ quality of life.

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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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&NA;. "Cisplatin see Bleomycin/cisplatin/vinblastine." Reactions Weekly &NA;, no. 292 (March 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 (January 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 (March 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 (August 1991): 5. http://dx.doi.org/10.2165/00128415-199103650-00015.

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Naghashpour, Mahsa, Dian Dayer, Hadi Karami, Mahshid Naghashpour, Mahin Taheri Moghadam, Seyed Mohammad Jafar Haeri, and Katsuhiko Suzuki. "Evaluating the Magnolol Anticancer Potential in MKN-45 Gastric Cancer Cells." Medicina 59, no. 2 (February 1, 2023): 286. http://dx.doi.org/10.3390/medicina59020286.

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Abstract:

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’ tendency for colony formation. The expression of genes linked to apoptosis, cell cycle arrest, and cell migration was examined using the qPCR method. Results: According to MTT data, using magnolol and/or cisplatin significantly reduced cell viability. The ability of the treated cells to proliferate and form colonies was also reduced considerably. Magnolol and/or cisplatin treatment resulted in a considerable elevation in Bax expression. However, the level of Bcl2 expression was dramatically reduced. p21 and p53 expression levels were significantly increased in the treated cells, while MMP-9 expression was significantly reduced. Conclusions: These findings show that magnolol has a remarkable anti-tumor effect on MKN-45 cells. In combination with cisplatin, magnolol may be utilized to overcome cisplatin resistance in gastric cancer cells.

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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 (January 5, 2022): 1–7. http://dx.doi.org/10.3897/pharmacia.69.e78813.

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Abstract:

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 of the drugs. The observational study on pharmacokinetic parameters shows that protein binding decreases in order: 95% (Cisplatn); 90% (Oxaliplatin); 50% (Nedaplatin); low (Carboplatin). For every of Cisplatin, Carboplatin, Oxaliplatin have been reported more than 1000 clinical trials; for Lobaplatin, Nedaplatin, Satraplatin - about 10 trials. The differenses in dose-limiting effects are: neuro-, nephro-, ototoxicity (Cisplatin); neurotoxicity (Oxaliplatin); nephrotoxicity (Heptaplatin); myelosuppression: thrombocytopenia, neutropenia, leukopenia (Carboplatin, Nedaplatin, Satraplatin).

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Wang, Chong-Zhi, Daniel Basila, Han H. Aung, Sangeeta R. Mehendale, Wei-Tien Chang, Eryn McEntee, Xiongfei Guan, and Chun-Su Yuan. "Effects of Ganoderma lucidum Extract on Chemotherapy-Induced Nausea and Vomiting in a Rat Model." American Journal of Chinese Medicine 33, no. 05 (January 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 novel anti-emetic compounds. In this study, we evaluated the effects of a G. lucidum extract (SunRecome®, the most commonly used Lingzhi mushroom extract in China) in attenuating cisplatin-induced nausea and vomiting in the rat pica model. We observed that intraperitoneal cisplatin injection caused a significant increase in kaolin intake at 24, 48, 72 and 96 hours, reflecting cisplatin's nausea and vomiting action. This cisplatin-induced kaolin intake dose-dependently decreased after 1, 3 and 10 mg/kg G. lucidum extract injection ( p < 0.01). In addition, there was a significant reduction of food intake after cisplatin. The cisplatin-induced food intake reduction improved significantly after G. lucidum extract administrations in a dose-related manner ( p < 0.01), suggesting a supportive effect of the extract on general body condition. Future controlled clinical trials are needed to evaluate the safety and effectiveness of this herbal medication.

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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 (June 5, 2024): 735. http://dx.doi.org/10.3390/ph17060735.

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Abstract:

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. Trametinib, a MEK1/2 inhibitor, protects from cisplatin-induced outer hair cell death in mouse cochlear explants; however, to the best of our knowledge, inhibiting MEK1/2 has not yet been shown to be protective against hearing loss in vivo. In this study, we demonstrate that trametinib protects against cisplatin-induced hearing loss in a translationally relevant mouse model and does not interfere with cisplatin’s tumor-killing efficacy in cancer cell lines. Higher doses of trametinib were toxic to mice when combined with cisplatin, but lower doses of the drug were protective against hearing loss without any known toxicity. Trametinib also protected mice from noise-induced hearing loss and synaptic damage. This study shows that MEK1/2 inhibition protects against both insults of hearing loss, as well as that targeting all three kinases in the MAPK pathway protects mice from cisplatin- and noise-induced hearing loss.

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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 (September 29, 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 as a cisplatin treated group. Third group, was received capparis spinosa fruit extract (100 mg/kg B.W) for 10 days and 10 mg/kg cisplatin as a single dose at day 8 . The results showed that the animals that treated with cisplatine alone were severed from histopathological changes and significantly increasing in the level of (Urea, Cr and Total protein ). While the third group (that treated with hydroalcoholic extract of capparis spiosa fruit ethanol 70% ) showed decreasing in the histopathplogical changes in kidney , also significantly decrease in the level of (Urea, Cr and Total protein ). In this study csplatine induced histopathplogical changes, alteration and increasing in the level of (Urea, Cr and Total protein ), while the ( hydroalcoholic extract of capparis spiosa fruit ethanol 70% ) was have ability to maintain kidney function test .

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

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

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

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

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

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

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

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

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

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

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1178 (November 2007): 15. http://dx.doi.org/10.2165/00128415-200711780-00044.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1179 (November 2007): 12. http://dx.doi.org/10.2165/00128415-200711790-00035.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1127 (November 2006): 9–10. http://dx.doi.org/10.2165/00128415-200611270-00028.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1142 (March 2007): 12–13. http://dx.doi.org/10.2165/00128415-200711420-00029.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1148 (April 2007): 13. http://dx.doi.org/10.2165/00128415-200711480-00043.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1355 (June 2011): 13. http://dx.doi.org/10.2165/00128415-201113550-00041.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1365 (August 2011): 13. http://dx.doi.org/10.2165/00128415-201113650-00042.

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&NA;. "Cisplatin." Reactions Weekly &NA;, no. 1368 (September 2011): 13. http://dx.doi.org/10.2165/00128415-201113680-00043.

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