Relevant bibliographies by topics / Cisplatin

Academic literature on the topic 'Cisplatin'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 June 2024

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Cisplatin":

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

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.
8

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.
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.
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Dissertations / Theses on the topic "Cisplatin":

1

Amaral, Catia Lira do. "Efeito do resveratrol na nefrotoxicidade induzida pela cisplatina em ratos." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-22052007-090133/.

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O resveratrol (Res), um polifenol presente no vinho tinto, é conhecido por possuir potente atividade antioxidante. O efeito do resveratrol (Res) frente à nefrotoxicidade do antineoplásico cisplatina (cDDP) foi avaliado em ratos neste estudo. Os animais foram tratados com Res (25 mg/Kg de peso copóreo, ip., dose única) 30 minutos antes da administração de cisplatina (5 mg/Kg de peso copóreo, ip., dose única) e foram sacrificados depois de 2 ou 5 dias do tratamento. Após 5 dias, o aumento da creatinina sérica, volume urinário e proteinúria, que são marcadores de alterações renais, apresentaram significativa redução (p < 0,05) com a administração de resveratrol. Os ratos tratados com cisplatina apresentaram necrose tubular aguda e maior marcação imuno-histoquímica para células ED1 e linfócitos T no córtex e medula externa renal. Estas alterações foram menos intensas nos animais tratados com resveratrol. Após 2 dias, a administração de cisplatina aos ratos induziu aumento na concentração de malonaldeído (MDA) e reduziu nos níveis de glutationa (GSH) no tecido renal, que não foram amenizadas pelo resveratrol. Os resultados desse estudo indicam que o tratamento com resveratrol atenuou as alterações renais funcionais, histológicas e imuno-histoquímicas induzidas pela cisplatina. O efeito protetor provavelmente está relacionado à diminuição de infiltrado de células inflamatórias no tecido renal
Resveratrol (Res), a polyphenolic present in red wine, is known to possess potent antioxidant properties. The ability of resveratrol to protect against the nephrotoxicity of the antineoplastic agent cisplatin (cDDP) was evaluated in rats. The animals were treated with Res (25 mg/Kg body weight, ip., single dose) 30 minutes before administration of cDDP (5 mg/Kg body weight, ip., single dose) and then, sacrificed in 2 or 5 days followed by the treatment. After 5 days with resveratrol administration, the enhanced serum creatinine levels, urinary volume and urinary protein, which are indicative of renal injury, shown a significant reduction (p < 0.05). The cisplatintreated rats presented a tubular cell necrosis and increase immunostaining for ED1 and T-lymphocytes in the renal cortex and outer medulla. Those alterations were less intense in animals treated with resveratrol. After 2 days, administration of cisplatin to rats induced a higher malondialdehyde levels (MDA), and reduction in glutathione (GSH) concentrations in kidney tissue that were not prevented by resveratrol. In this study, the results indicate that resveratrol treatment attenuated the functional, histological and immunohistochemical renal alterations induced by cisplatin. The protect effect is relatated to the decrease of cells infiltrated at kidney tissue.
2

Santos, Graciela Cristina dos [UNESP]. "Avaliação do efeito protetor do urucum e da bixina sobre a genotoxicidade induzida pelo antitumoral cisplatina em células da linhagem PC12." Universidade Estadual Paulista (UNESP), 2008. http://hdl.handle.net/11449/100973.

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Made available in DSpace on 2014-06-11T19:31:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-12-12Bitstream added on 2014-06-13T18:41:39Z : No. of bitstreams: 1 santos_gc_dr_arafcf.pdf: 2386901 bytes, checksum: b46aa55b36f051a8683831df1b69f150 (MD5)
Universidade Estadual Paulista (UNESP)
A neuropatia induzida por drogas quimioterápicas é uma complicação no tratamento do câncer e outras doenças por ser freqüentemente dolorosa e requerer a interrupção da terapia. O antitumoral cisplatina é comumente usado contra muitas formas de câncer há aproximadamente 40 anos. Entretanto, sua aplicação é associada a muitos efeitos tóxicos, como neurotoxicidade, nefrotoxicidade, perda da audição e vômitos. Estes efeitos adversos têm levado ao desenvolvimento de agentes específicos para amenizar a toxicidade do fármaco. Alguns estudos sugerem que a administração de antioxidantes é capaz de reduzir os danos e proteger os tecidos. Dessa forma, os carotenóides são mais uma opção a ser avaliada, pois são considerados eficazes agentes antioxidantes. O urucum é uma fonte natural de corantes vermelhos e além da bixina (fração lipossolúvel do extrato), estão presentes nas suas sementes, outros carotenóides, como a norbixina, o bcaroteno, a criptoxantina, a luteína e a zeaxantina. Neste estudo, foi avaliada a genotoxicidade e a antigenotoxicidade do urucum e da bixina sobre a toxicidade induzida pelo antitumoral cisplatina em culturas de células PC12. A citotoxicidade foi determinada pelo método do MTT, a frequência de danos cromossômicos pelo Teste do Micronúcleo e a extensão de danos primários ao DNA pelo Ensaio do Cometa. O urucum e a bixina foram avaliados preliminarmente quanto a sua genotoxicidade. O urucum nas concentrações 0,2, 0,5 e 1,0 mg/mL e a bixina nas concentrações 0,05, 0,08 e 0,10 mg/mL não foram citotóxicos e nem genotóxicos às células PC12. Assim, essas concentrações foram utilizadas nos experimentos para verificar a proteção do urucum e da bixina contra os danos induzidos pela cisplatina. Embora o efeito protetor do urucum e da bixina não tenha sido evidente nos resultados obtidos pelo Ensaio do Cometa, eles se mostraram...
The neuropathy induced by chemotherapeutic drugs is a complication in the treatment of cancer and other diseases, because it is often painful and requires discontinuation of the therapy. Cisplatin has been commonly used against many forms of cancer for approximately 40 years. However, its application is associated with many toxic effects such as neurotoxicity, nephrotoxicity, hearing loss and vomiting. These adverse effects have led to the development of specific agents to lessen the toxicity of the drug. Some studies have suggested that the administration of antioxidants is able to reduce the damage and protect the tissues. Thus, the carotenoids are one more option to be evaluated, because they are considered to be effective antioxidants. Annatto is a natural source of red dyes and pigments and in addition to bixin (liposoluble fraction of the extract), other carotenoids are present in its seeds, such as norbixin, B-carotene, cryptoxanthin, lutein and zeaxanthin. In the present study, the genotoxicity and antigenotoxicity of annatto and bixin on the cisplatin induced-toxicity in PC12 cell cultures was assessed. Cytotoxicity was determined by the MTT assay, chromosomal damage by the Micronucleus test and the extent of primary damage to the DNA by the Comet assay. Annatto and bixin were first assessed with respect to their genotoxicity. Annatto concentrations of 0.2, 0.5 and 1.0 mg/ml and bixin concentrations of 0.05, 0.08 and 0.10 mg/ml were neither cytotoxic nor genotoxic to the PC12 cells. Thus, these concentrations were used in experiments to verify the protective effect of annatto and bixin against damage induced by cisplatin. Although the protective effect of annatto and bixin was not evident in the results obtained by the Comet assay, effective inhibition of the chromosomal damage (Micronucleus test) induced by cisplatin was shown. Annatto and bixin protected... (Complete abstract click electronic access below)
3

Santos, Graciela Cristina dos. "Avaliação do efeito protetor do urucum e da bixina sobre a genotoxicidade induzida pelo antitumoral cisplatina em células da linhagem PC12 /." Araraquara : [s.n.], 2008. http://hdl.handle.net/11449/100973.

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Resumo: A neuropatia induzida por drogas quimioterápicas é uma complicação no tratamento do câncer e outras doenças por ser freqüentemente dolorosa e requerer a interrupção da terapia. O antitumoral cisplatina é comumente usado contra muitas formas de câncer há aproximadamente 40 anos. Entretanto, sua aplicação é associada a muitos efeitos tóxicos, como neurotoxicidade, nefrotoxicidade, perda da audição e vômitos. Estes efeitos adversos têm levado ao desenvolvimento de agentes específicos para amenizar a toxicidade do fármaco. Alguns estudos sugerem que a administração de antioxidantes é capaz de reduzir os danos e proteger os tecidos. Dessa forma, os carotenóides são mais uma opção a ser avaliada, pois são considerados eficazes agentes antioxidantes. O urucum é uma fonte natural de corantes vermelhos e além da bixina (fração lipossolúvel do extrato), estão presentes nas suas sementes, outros carotenóides, como a norbixina, o bcaroteno, a criptoxantina, a luteína e a zeaxantina. Neste estudo, foi avaliada a genotoxicidade e a antigenotoxicidade do urucum e da bixina sobre a toxicidade induzida pelo antitumoral cisplatina em culturas de células PC12. A citotoxicidade foi determinada pelo método do MTT, a frequência de danos cromossômicos pelo Teste do Micronúcleo e a extensão de danos primários ao DNA pelo Ensaio do Cometa. O urucum e a bixina foram avaliados preliminarmente quanto a sua genotoxicidade. O urucum nas concentrações 0,2, 0,5 e 1,0 mg/mL e a bixina nas concentrações 0,05, 0,08 e 0,10 mg/mL não foram citotóxicos e nem genotóxicos às células PC12. Assim, essas concentrações foram utilizadas nos experimentos para verificar a proteção do urucum e da bixina contra os danos induzidos pela cisplatina. Embora o efeito protetor do urucum e da bixina não tenha sido evidente nos resultados obtidos pelo Ensaio do Cometa, eles se mostraram... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The neuropathy induced by chemotherapeutic drugs is a complication in the treatment of cancer and other diseases, because it is often painful and requires discontinuation of the therapy. Cisplatin has been commonly used against many forms of cancer for approximately 40 years. However, its application is associated with many toxic effects such as neurotoxicity, nephrotoxicity, hearing loss and vomiting. These adverse effects have led to the development of specific agents to lessen the toxicity of the drug. Some studies have suggested that the administration of antioxidants is able to reduce the damage and protect the tissues. Thus, the carotenoids are one more option to be evaluated, because they are considered to be effective antioxidants. Annatto is a natural source of red dyes and pigments and in addition to bixin (liposoluble fraction of the extract), other carotenoids are present in its seeds, such as norbixin, B-carotene, cryptoxanthin, lutein and zeaxanthin. In the present study, the genotoxicity and antigenotoxicity of annatto and bixin on the cisplatin induced-toxicity in PC12 cell cultures was assessed. Cytotoxicity was determined by the MTT assay, chromosomal damage by the Micronucleus test and the extent of primary damage to the DNA by the Comet assay. Annatto and bixin were first assessed with respect to their genotoxicity. Annatto concentrations of 0.2, 0.5 and 1.0 mg/ml and bixin concentrations of 0.05, 0.08 and 0.10 mg/ml were neither cytotoxic nor genotoxic to the PC12 cells. Thus, these concentrations were used in experiments to verify the protective effect of annatto and bixin against damage induced by cisplatin. Although the protective effect of annatto and bixin was not evident in the results obtained by the Comet assay, effective inhibition of the chromosomal damage (Micronucleus test) induced by cisplatin was shown. Annatto and bixin protected... (Complete abstract click electronic access below)
Orientador: Maria de Lourdes Pires Bianchi
Coorientador: Antonio Cardozo dos Santos
Banca: Alessandro de Oliveira Rios
Banca: Daisy Maria Fávero Salvadori
Banca: João Bosco Faria
Banca: Cecilia Rodrigues Silva
Doutor
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Kullmann, Maximilian [Verfasser]. "Identifying intracellular cisplatin interaction partners and assessing their contribution to cisplatin resistance / Maximilian Kullmann." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/111988876X/34.

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Hadi, Sutopo. "The chemistry of cisplatin metabolites /." [St. Lucia, Qld.], 2007. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19800.pdf.

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Zhang, Jin-Gang. "Cisplatin nephrotoxicity : mechanisms and antidotes." Thesis, University of Liverpool, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307635.

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Castro, João Humberto Teotônio de [UNESP]. "Avaliação do espermograma de cães submetidos à administração de cisplatina." Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/89030.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
A correta orientação do Médico Veterinário, aos proprietários de cães, usados com finalidades reprodutivas, submetidas à quimioterapia com cisplatina, é importante na medida que este agente citostático age nas células em constante divisão, podendo ser citotóxicos para as células germinativas testiculares. O objetivo desse trabalho foi avaliar a qualidade espermática através do espermograma de cães que receberam cisplatina em diferentes momentos de análise espermática. A dose utilizada foi de 70 mg/mø, em intervalos de 21 dias, totalizando 4 infusões. Os cães foram divididos em dois grupos de 4 animais cada, sendo que um dos grupos recebeu a quimioterapia e o protocolo de diurese para proteção renal, já o grupo controle não recebeu a cisplatina, estando sujeito apenas aos fatores ambientais. Os resultados obtidos demonstraram que a cisplatina influenciou na qualidade espermática de cães, pois elevou as patologias maiores e totais acima do aceitável para cães aptos a reprodução. Portanto, infere-se que este citostático possa acarretar alterações morfofuncionais nos túbulos seminíferos e conduto epididimário.
The correct veterinary`s orientation for male dogs` owners used for reproduction goals, undergone cisplatin administration, is important because of this cistostatic act in cell with frequently proliferation, and could to cause germ cell injury. The objections of this experiment was to analysis the sperm quality through dogs` spermogram that received cisplatin`s infusions. The dose used was 70 mg/mø in 21 days periods, with 4 infusion in total. The dogs were divided in 2 groups with 4 animal each one. One of the groups received all the diuresys protocol (to protect the kidney) and the citostatic. And the other control group just didn`t receive the cisplatin infusion to know the real action of cisplatin effects without environmental stresses. The results show that cisplatin influence at the sperm quality in the dogs, because it elevated the major and total defects above that would be acceptable for competent dog to reproduct. It could deduct that cisplatin cause phisiologic alteration in the testis and epididymis.
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Oliva, Carlos Alfredo Calpa [UNESP]. "Hemograma e teores séricos de Na, K, Mg, Ca e P de cães hígidos submetidos à administração de cisplatina." Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/89087.

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A cisplatina é um fármaco antineoplásico utilizado como adjuvante no tratamento de diversas neoplasias. Neste estudo foram avaliados o hemograma e os teores de sódio, potássio, magnésio, cálcio e fósforo do soro sanguíneo de cães submetidos à terapia com cisplatina. Foram utilizados oito cães, machos, sem raça definida, com 10 a 15 kg de peso, clinicamente sadios. Os cães foram distribuídos em dois grupos, contendo 4 animais cada, sendo que os animais do grupo 1 receberam cisplatina e aqueles do grupo 2 não receberam cisplatina. Os cães do grupo 1 receberam quimioterapia e protocolo de diurese para proteção renal, já o grupo controle 2 não recebeu a cisplatina, estando sujeito apenas aos fatores ambientais. Os animais do grupo 1 foram submetidos a quatro sessões de quimioterapia com cisplatina na dose de 70mg/mø, administrada por via intravenosa, durante 20 minutos, no intervalo de 21 dias. Antes da administração da cisplatina, realizou-se fluidoterapia com solução fisiológica a 0,9% na dose de 25mL/kg/hora, por via intravenosa, durante duas horas, e depois por mais uma hora. Todos os animais receberam metoclopramida na dose de 2mg/kg, por via intravenosa, 15 minutos antes da administração da cisplatina e furosemida na dose de 2 mg/kg, por via intravenosa, 5 minutos após administração de metoclopramida. As amostras foram processadas e analisadas antes de cada sessão de quimioterapia. Os resultados mostraram que não houve diferença significativa entre os grupos para as contagens de hemácias, concentração de hemoglobina, hematócrito e contagem de leucócitos, mesmo assim as concentrações séricas de eletrólitos mantiveram-se dentro dos padrões da normalidade. Os resultados obtidos podem ser indicativos de que o protocolo empregado para o grupo 1 se mostrou efetivo para manter as características do hemograma e a concentração sérica dos eletrólitos.
The cisplatin is an antineoplasic drug used like adjunct treatment of various neoplasms. In this study, one evaluated the hemogram and sodium, potassium, magnesium, calcium and phosphorus levels in the dogs` blood under administration of cisplatin. One used 8 male dogs, with no definite race, weighing from 10 to 15 kilograms, and clinically healthy. The dogs were divided into two groups of 4 animals each, being group 1 treated with cisplatin and group 2 with no cisplatin. Group 1 received chemotherapy and the diurese protocol for kidney protection, group 2 did not receive cisplatin, being exposed only to the environmental factors. The animals from group 1 were submitted to four chemotherapy sessions with cisplatin 70mg/m2 administered intravenously for 20 minutes, in a 21 days interval before the cisplatin administration, one carried out a fluidotherapy with physiologic solution 0,9% on a dosage of 25mg/kg/hour intravenously during 2 hours, and posteriorly for one more hour. All the animals received methoclopramid intravenously on a dosage of 2mg/kg, 15 minutes before the cisplatin and furosemide administration on a 2mg/kg dosage, 5 minutes before the cisplatin infusion. The evaluation of the hemogram and the electrolytes levels above mentioned were done before each chemotherapy session. The results demonstrate that there were no significant differences among the groups for red blood cells counting, hemoglobin concentration, hematocrit and leucocytes counting, but still, the electrolytes seric concentration maintained itself in a normal standard. The results obtained may indicate that the protocol employed for group 1 showed efficiency to maintain the characteristics of the hemogram and the electrolytes seric concentration.
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Li, Yan Julia. "Cisplatin-induced cytotoxicity in MDCK cells." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6408.

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Background. The mechanism of cisplatin-induced nephrotoxicity is not well understood. The distal tubules are affected in both human and animal studies, although the majority of cisplatin-induced renal damage is in proximal tubules. Platinum (Pt) forms intra- and interstrand cross-links with DNA in cancer cells. Hypothesis. A mechanism of cisplatin-induced cytotoxicity in MDCK cells relates to its ability to bind to DNA and interfere with its synthesis. Methods. The canine distal renal tubular epithelial cell line, MDCK was used as an in vitro model to investigate the mechanism of cisplatin-induced nephrotoxicity. The intracellular Pt accumulation and Pt binding with DNA were assayed by atomic absorption spectrophotometry. DNA synthesis was measured by BrdU labeling and fluorescence microscopy at the concentrations from 0 to 100 muM. The alkaline comet assay with 10 Gy radiation was used to measure Pt DNA interstrand cross-links after a one hour cisplatin exposure from 0 to 100 muM at both zero and sixteen hour time points. According to the principles of alkaline comet assay, the tail moment is inversely related with the amount of Pt interstrand cross-links. (Abstract shortened by UMI.)
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Brock, Penelope. "Cisplatin toxicity in infants and children /." Leuven : Leuven University Press, 1994. http://www.gbv.de/dms/bs/toc/190814756.pdf.

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Books on the topic "Cisplatin":

1

Ozols, Robert F. High-dose Platinol (cisplatin for infection) in hypertonic saline. Syracuse, N.Y: Bristol-Myers Oncology Division, 1985.

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Chu, Wendy. Mechanism of cisplatin resistance inhuman malignant melanoma. Ottawa: National Library of Canada, 1998.

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Yoshihiro, Kikuchi, ed. Mechanism of cisplatin resistance and its circumvention. Commack, NY: Nova Science Publishers, 1998.

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Merazga, Yamina. Aspects of the interaction between cisplatin and renal glutathione. Uxbridge: Brunel University, 1990.

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

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Morley, Christopher. Analogues of cisplatin from diamino carbohydrates and related compounds. Norwich: University of East Anglia, 1986.

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Evans, Dyfed Llyr. The induction of apoptosis by the anticancer agent cisplatin. Manchester: Universityof Manchester, 1994.

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Laurell, Göran. Ototoxicity of the anticancer drug cisplatin: Clinical and experimental aspects. Stockholm, Sweden: Distributed by Almqvist & Wiksell Periodical Co., 1991.

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Institut für Qualität und Wirtschaftlichkeit im Gesundheitswesen. Pembrolizumab (nicht kleinzelliges Lungenkarzinom: Nutzenbewertung gemäß § 35a SGB V. Köln: Institut für Qualität und Wirtschaftlichkeit im Gesundheitswesen, 2017.

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Bryant, Eric Edward. Systems Genetics of DNA Damage Tolerance – Cisplatin, RAD5 & CRISPR-mediated Nonsense. [New York, N.Y.?]: [publisher not identified], 2019.

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Book chapters on the topic "Cisplatin":

1

Rosenberg, Barnett. "Platinum Complexes for the Treatment of Cancer: Why the Search Goes On." In Cisplatin, 1–27. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch1.

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Ano, Susan O., Zsuzsanna Kuklenyik, and Luigi G. Marzilli. "Structure and Dynamics of Pt Anticancer Drug Adducts from Nucleotides to Oligonucleotides as Revealed by NMR Methods." In Cisplatin, 247–91. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch10.

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Chen, Yu, Zijian Guo, and Peter J. Sadler. "195Pt- and 15N-NMR Spectroscopic Studies of Cisplatin Reactions with Biomolecules." In Cisplatin, 293–318. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch11.

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Bau, Robert, and Michal Sabat. "Structural Aspects of Pt-Purine Interactions: From Models to DNA." In Cisplatin, 319–37. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch12.

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Reedijk, Jan, and Jan Maarten Teuben. "Platinum-Sulfur Interactions Involved in Antitumor Drugs, Rescue Agents, and Biomolecules." In Cisplatin, 339–62. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch13.

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Appleton, Trevor G. "Diammine- and Diamineplatinum Complexes with Non-Sulfur-Containing Amino Acids and Peptides." In Cisplatin, 363–76. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch14.

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Lippert, Bernhard. "Platinum Blues: On the Way toward Unraveling a Mystery." In Cisplatin, 377–403. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch15.

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Randaccio, Lucio, and Ennio Zangrando. "Heteronuclear PtII Complexes with Pyrimidine Nucleobases." In Cisplatin, 405–28. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch16.

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Natile, Giovanni, Francesco P. Intini, and Concetta Pacifico. "Diplatinum(III) Complexes: Chemical Species More Widely Spread Than Suspected." In Cisplatin, 429–53. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch17.

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Matsumoto, Kazuko. "Inorganic and Organometallic Chemistry of Cisplatin-Derived Diplatinum(III) Complexes." In Cisplatin, 455–75. Zürich: Verlag Helvetica Chimica Acta, 2006. http://dx.doi.org/10.1002/9783906390420.ch18.

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Conference papers on the topic "Cisplatin":

1

Absar, Saheem, Mujibur Khan, Kyle Edwards, and David Calamas. "Electrospinning of Cisplatin-Loaded Cellulose Nanofibers for Cancer Drug Delivery." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-37182.

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Cellulosic nanofibers have been electrospun with an antitumor agent Cisplatin. Cellulose acetate (CA) and Cisplatin were co-electrospun using a coaxial electrospinning system. For the outer sheath, a solution of 7.5wt% CA in Acetone and DMAc (2:1) was used. The inner core consisted of Cisplatin dissolved in DMF at a concentration of 5mg/ml. Drug-loaded nanofibers from Cellulose pulp (2wt%) dissolved in NMMO. H2O were also produced. The solutions were electrospun in a high voltage electric field of 25–30 kV. Characterization of neat and drug-loaded nanofibers was performed using Scanning electron microscopy (SEM) and Energy Dispersive X-Ray Spectroscopy (EDS). The characterization studies have shown the formation of nanofibers having both sporadic beads with internal agglomeration and conjugation of Cisplatin on the nanofiber surfaces.
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Camargo, Luana Cristina, Joao Paulo Figueiro Longo, Karen Letycia Rodrigues de Paiva, Marina Mesquita Simões, Thais Bergmann, and Victor Carlos Mello da Silva. "Immunotherapy vaccines for triple-negative breast cancer and its influence on the tumor microenvironment." In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1024.

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Objective: Cancer is still a complex and debilitating disease even though advances in treatment have occurred. Triplenegative breast cancer (TNBC) is an aggressive subtype of breast cancer with a poor prognosis and occurs more frequently in young women. Due to its metastatic features and unique tumor microenvironment, TNBC treatment is limited. In this study, we evaluated how three chemotherapy drugs could be used to produce vaccines with cells under immunogenic cell death. Methodology: For that, 4T1-luc2 cells were treated with cisplatin (100 μM), mitoxantrone (MTX) (15 μM), and doxorubicin (DOX) (50 μM) for 24 h. Then, the treated cells were injected subcutaneously in tumor-bearing Balb/c female mice, after the tumor challenge. The treatment occurred three times, once a week. During and after the treatment, primary tumor and metastatic progression were followed using the chemiluminescence technique. After 5 weeks of the tumor challenge, mice were euthanized and organs (liver, tumor, lungs, and spleen) were collected for analysis. Additionally, the spleens were processed for flow cytometry for regulatory T lymphocyte and myeloid-derived suppressor cells analysis. Results: Cisplatin and MTX vaccines slowed the primary and metastatic tumor growth as well as the decreased tumor, liver, and spleen weight, while the DOX vaccine slowed the metastatic tumor progression in the lungs but did not alter tumor and other organs’ weight. Moreover, cisplatin and MTX vaccine increased the ratio of lymphocytes in the spleen but not the DOX vaccine. All comparison was done regarding the tumor-bearing mice treated with PBS. Conclusion: Taken together, both MTX and cisplatin vaccines treated primary and secondary tumors probably by the increase of lymphocyte recruitment, and the cisplatin vaccine also has an influence on the tumor microenvironment. Finally, the therapeutical vaccine might be an interesting approach as a treatment for TNBC due to its positive effect on metastasis and tumor microenvironment, especially with cisplatin.
3

Lau, KingWun. "Brief summary of cisplatin nephrotoxicity." In International Conference on Biological Engineering and Medical Science (ICBIOMed2022), edited by Gary Royle and Steven M. Lipkin. SPIE, 2023. http://dx.doi.org/10.1117/12.2669859.

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Soodvilai, Sirima, Sunhapas Soodvilai, Warayuth Sajomsang, Theerasak Rojanarata, Prasopchai Patrojanasophon, and Praneet Opanasopit. "Chitosan Polymeric Micelles for Prevention of Cisplatin-Induced Nephrotoxicity and Anticancer Activity of Cisplatin." In ICBET 2020: 2020 10th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3397391.3397438.

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Lee, Chunman, Masao Sasai, and Yoshiki Sawa. "Abstract 4452: Controlled release complex of cisplatin for mesothelioma: gamma-PGA/Cisplatin complex formulation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4452.

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Liang, Xiaobing, Michael D. Mueller, and Jing Jie Yu. "Abstract 2982: Activation of checkpoint kinase Chk2 by cisplatin and its role in cisplatin resistance." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2982.

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Abdullah, N., N. Al Balushi, S. Al-Bahlani, S. Dobretsov, I. Hassan, T. Sang, Y. Tamimi, and I. Burney. "EP765 The effect of malformina1 on cisplatin-sensitive and cisplatin-resistant ovarian cancer cell lines." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.816.

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Larisch, C., T. Markowiak, S. Golovchenko, P. Bednarski, K. Müller, C. Großer, H.-S. Hofmann, and M. Ried. "Dosis-abhängige Cisplatin-Konzentration und -Eindringtiefe in humanes Lungengewebe bei Inkubation in hyperthermer Cisplatin-Lösung." In 32. Jahrestagung der Deutschen Gesellschaft für Thoraxchirurgie. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1771119.

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Gupta, Vikas, Ashok Kumar Chauhan, Paramjeet Kaur, Anil Khurana, Yashpal Verma, and Nupur Bansal. "Comparative evaluation of concomitant chemoradiation with weekly cisplatin and gemcitabine versus weekly cisplatin in the management of locally advanced carcinoma of uterine cervix." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685264.

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Aim: To evaluate feasibility of concomitant chemoradiation with weekly cisplatin and gemcitabine, and comparing the advantage of using this regimen over cisplatin alone in terms of disease control and toxicities in management of locally advanced carcinoma cervix. Materials and Methods: The study has been conducted on fifty previously untreated, histopathologically proven FIGO stage II B - IV A patients of carcinoma cervix, attending the Department of Radiotherapy, Post Graduate Institute of Medical Sciences, Rohtak for definitive treatment by radiation therapy. The patients were divided randomly in two groups of 25 patients each. Group I received cisplatin 40 mg/m2 and gemcitabine 125 mg/m2 with concomitant external beam radiotherapy 50 Gy/25 fractions/5 weeks, followed by intracavitary high dose rate brachytherapy 7 Gy to point A, for 3 times, once in a week. Group II received concomitant chemotherapy with cisplatin 40 mg/m2 weekly alone while radiotherapy schedule were same as in group I. Results: Total treatment duration in group I and II were 9-11 and 8-10 weeks respectively. Complete response rate in group I and II were 92% and 80%. Grade III skin and mucosal reactions was 20% in group I and none in group II. Diarrhoea was 24% in group I & 8% in group II. Grade II & III leucopenia was seen in 28% and 4% cases of group I & group II respectively. Upper gastrointestinal and renal toxicities were comparable in both arms. After six month of follow up, no evidence of disease was seen in 92% and 80% cases of group I and group II. Conclusion: If the toxicity is managed adequately in platinum based doublet group, it may produce improvement in response. Study is ongoing.
10

Richards, Elizabeth J., William O. Cookson, Sanjay Popat, and Miriam F. Moffatt. "Transcriptome Changes Accompanying Induced Cisplatin Resistance." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4918.

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Reports on the topic "Cisplatin":

1

Turchi, John J. Proteomic Analysis of Cisplatin-Resistant Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada425620.

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Turchi, John. Proteomic Analysis of Cisplatin-Resistant Ovarian Concers. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada462560.

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Turchi, John J. Proteomic Analysis of Cisplatin-Resistant Ovarian Concers. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada463194.

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Balaji, Kethandapatti C. MT 2A Phosphorylation by PKC Mu/PKD Influences Chemosensitivity to Cisplatin in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2008. http://dx.doi.org/10.21236/ada495664.

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Allworth, Ann E. The Role of Terbium and Gadolinium in Reversal of Cisplatin Resistance in Cultured Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada414791.

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Miao, Fang, Yaru Guo, Yan Yuan, Juzhou Chen, and Yong Xin. Bevacizumab combined with pemetrexed plus carboplatin or cisplatin in the treatment of malignant pleural effusion of lung cancer : A meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0096.

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Wang, Dandan, Shuaihang Hu, Kangdi Cao, Chenxi Qiao, Zhuo Wang, and Wei Hou. Clinical efficacy and safety of Chinese herb injections combination with Docetaxel combined with cisplatin (DP) chemotherapy for advanced non-small cell lung cancer: A protocol for Bayesian network meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0081.

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Li, Qian, Hua Xiao, Ren-long Liang, Qian-ru Yu, De-qing Tian, Li-na Zhao, Wen-wen Wang, and Xiao-jia Yong. Efficacy and safety of Cinobufacini injection combined with vinorelbine and cisplatin regimen chemotherapy for stage III/IV non-small cell lung cancer A protocol for systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0091.

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Health hazard evaluation report: HETA-2009-0121-3106, evaluation of exposures to healthcare personnel from cisplatin during a mock interperitoneal operation, University Medical Center, Las Vegas, Nevada. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, March 2010. http://dx.doi.org/10.26616/nioshheta200901213106.

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