Academic literature on the topic 'Oxaliplatin'
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Journal articles on the topic "Oxaliplatin":
Ain, Noor ul, Nusrat Bano, Anwar Ejaz Beg, Kamran Hameed, Talha Bin Fayyaz, and Rafia Sadaf. "HEMATOLOGICAL TOXICITY IN RATS;." Professional Medical Journal 24, no. 02 (February 14, 2017): 342–46. http://dx.doi.org/10.29309/tpmj/2017.24.02.525.
Grothey, A., D. A. Nikcevich, J. A. Sloan, J. W. Kugler, P. T. Silberstein, T. Dentchev, D. B. Wender, H. E. Windschilt, X. Zhao, and C. L. Loprinzi. "Evaluation of the effect of intravenous calcium and magnesium (CaMg) on chronic and acute neurotoxicity associated with oxaliplatin: Results from a placebo-controlled phase III trial." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 4025. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.4025.
Pires, Lívia Márcia Vidal, and Patrícia Dos Santos Claro Fuly. "Mapeamento de fatores clínicos preditivos da neuropatia sensorial periférica induzida por oxaliplatina: revisão sistemática." Revista Recien - Revista Científica de Enfermagem 11, no. 35 (September 23, 2021): 382–97. http://dx.doi.org/10.24276/rrecien2021.11.35.382-397.
&NA;. "Oxaliplatin." Reactions Weekly &NA;, no. 1378 (November 2011): 27. http://dx.doi.org/10.2165/00128415-201113780-00098.
&NA;. "Oxaliplatin." Reactions Weekly &NA;, no. 1384 (January 2012): 43. http://dx.doi.org/10.2165/00128415-201213840-00174.
&NA;. "Oxaliplatin." Reactions Weekly &NA;, no. 1385 (January 2012): 35. http://dx.doi.org/10.2165/00128415-201213850-00129.
&NA;. "Oxaliplatin." Reactions Weekly &NA;, no. 1388 (February 2012): 24. http://dx.doi.org/10.2165/00128415-201213880-00093.
&NA;. "Oxaliplatin." Reactions Weekly &NA;, no. 1389 (February 2012): 34. http://dx.doi.org/10.2165/00128415-201213890-00124.
&NA;. "Oxaliplatin." Reactions Weekly &NA;, no. 1390 (February 2012): 28–29. http://dx.doi.org/10.2165/00128415-201213900-00109.
&NA;. "Oxaliplatin." Reactions Weekly &NA;, no. 1390 (February 2012): 29. http://dx.doi.org/10.2165/00128415-201213900-00112.
Dissertations / Theses on the topic "Oxaliplatin":
Xiaoqing, Liu. "Dose-banding studies on oxaliplatin." Thesis, University of Plymouth, 2016. http://hdl.handle.net/10026.1/8081.
Vincent, Jacob Adam. "Sensorimotor Deficits Following Oxaliplatin Chemotherapy." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1496136263522854.
Wieczerzak, Krystyna Blanka. "Sensorimotor Analysis of Oxaliplatin Treated Rats." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1432856752.
Robinson, Stuart Michael. "The pathogenesis of oxaliplatin induced sinusoidal obstruction syndrome." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/1942.
MONZA, LAURA. "In vitro models for studying oxaliplatin neurotoxic effects." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2019. http://hdl.handle.net/10281/241333.
Chemotherapy-induced peripheral neurotoxicity is one of the most common and often dose limiting side effects of anticancer drugs. Among others, oxaliplatin (OHP) is a third generation platinum compound used in combination with 5-fluorouracil and leucovorin as an efficient treatment for metastatic colorectal cancer. Unlike other compounds of the same class, oxaliplatin may also cause an acute syndrome characterized by transient cold-induced dysesthesias and paresthesias located at limb extremities and at perioral area. The severity of these symptoms is predictive of the development of chronic and cumulative sensory neuropathy. Hence, unraveling the mechanisms underlying the acute syndrome should not be considered a secondary aim. Since Adelsberger et al. (Eur J Pharmacol 406:25-32, 2000) first described the effects of OHP on voltage-dependent sodium channels, many in vitro studies on different animal models supported the hypothesis of a major involvement of these channels in the acute syndrome. However, all of these works used very high OHP concentrations and focused on single aspects of the overall electrophysiological cellular response to OHP administration and gave controversial results. For these reasons, our aim was to study the effects of an OHP concentration comparable to the one estimated in patients’ blood on the electrical properties of different models of sensory neurons. We thus investigated the possible alterations produced by the drug on membrane resting potential (Vrest), on the main action potential (AP) features and on the biophysical properties of voltage-dependent sodium and potassium channels. Since dorsal root ganglion (DRG) neurons represent the main pharmacological target of platinum compounds, we incubated differentiated F-11 cells (rat DRG neurons x mouse neuroblastoma N18TG-2 cell line) for 24 or 48 h with 7.5 µM OHP. Their electrophysiological properties were investigated by the patch-clamp technique in the whole-cell configuration. Cisplatin (CDDP 15 µM) was used as reference compound to verify the exclusivity of OHP-induced effects. Finally, in order to validate the results collected with the differentiated F-11 cells, our experiments were reproduced on primary sensory neurons deriving from the dissociation of isolated embryonic and adult rat DRGs. Compared to untreated cells, treated F-11 cells displayed depolarized Vrest, decreased firing frequency, increased sodium current density and reduced ERG (ether-à-go-go-related gene) potassium current density. However, OHP administration did not affect the delayed rectifying potassium channels and the duration of induced APs. In TTX-sensitive sodium currents, OHP shifted both steady-state activation and inactivation curves towards more negative potentials and caused an expansion of the window current. A similar shift of both activation and inactivation curves was observed for ERG channels. In contrast, CDDP caused no effect on Vrest, decreased firing frequency, increased AP duration, and reduced sodium, ERG and delayed rectifier potassium current densities. In embryonic primary DRG neuron cultures, OHP incubation induced a significant increase of the fraction of sensory neurons able to generate multiple evoked APs and of voltage-dependent sodium and potassium current densities. Vrest and the firing frequency were not affected by the treatment. Lastly, data collected on primary DRG neuron cultures derived from adult rats showed that administration of OHP for 24h significantly increased sodium current density while no effects were produced on the other parameters of interest. In conclusion, the collected data indicate that OHP has different targets on DRG neurons, acting on both sodium and potassium channels, and suggest that differentiated F-11 cells represent a good cellular model for the development of pharmacological strategies aimed at preventing the onset of neurotoxicity caused by sodium channel dysfunction.
Cerles, Olivier. "Prévention des neuropathies périphériques induites par les chimiothérapies par une modulation pharmacologique des dérives des formes réactives de l'oxygène et des récepteurs muscariniques." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB106.
Platinum-based chemotherapies have been shown to elicit their anti-tumoral effects by compromising DNA integrity. These impairments ultimately lead to a burst in oxidative stress which in turn promotes cell death processes. Oxaliplatin, a platinum-based antineoplastic drug is usually indicated in secondary metastatic colon cancers and colorectal cancers and mediates a rise in reactive oxygen species through the depletion of reduced glutathione in cancerous cells. This chemotherapy is indicated as a frontline and an adjuvant treatment and similarly to other platinum-based chemotherapies, it warrants for particular caution. Most patients receiving oxaliplatin develop peripheral neuropathies. This neurodegeneration is a limiting factor of this chemotherapy since it may require the lowering of dosage or even the interruption of the treatment if this side-effect is assessed as a grade 3 peripheral neuropathy. Neurological toxicities may manifest within hours of injection as an acute form or as a chronic form resulting from cumulated high-dosage injections. The acute form, characterized by transient paresthesia and myotonia, is reversible and usually resolves within days while the chronic form presents persistent paresthesia and thermoalgia resulting from distal axonal degradation and demyelination of large fibers. Inflammatory pathways have also been incriminated in the etiology of this neurodegeneration. Niclosamide, a teniacide known to downregulate Stat3, Wnt, Notch and Beta-catenin pathways was investigated in vitro and in vivo. Having previously demonstrated this compound’s anti-inflammatory properties in systemic sclerosis, we sought to investigate whether niclosamide could also prevent oxaliplatin’s neurotoxicity. Niclosamide demonstrated neuroprotection both in vitro on oxaliplatin-treated neurons and in vivo in models of oxaliplatin-induced peripheral neuropathies. Niclosamide is used in humans with limited side-effects. The association of this molecule with oxaliplatin could increase the therapeutic index of this chemotherapy. Benztropine is an inhibitor of muscarinic M1 and M3 receptors with known remyelinating potential in the central nervous system by promoting oligodendrocytes precursor cells differentiation and proliferation. The differential distribution between subtypes of receptors can allow the specific targeting of tumor cells, namely through the inhibition of autocrine acetylcholine signaling. This compound is well tolerated and does not elicit any immunological reaction upon its administration. These observations of potential for both, preventing neurotoxicity as well as increasing the efficacy profile of neurotoxic chemotherapies, prompted us to investigate this M1 and M3 receptors inhibitor. Benztropine demonstrated neuroprotection in vitro on oxaliplatin-treated neurons as demonstrated by viability assays studies as well as in vivo in models of oxaliplatin-induced as well as diabetic peripheral neuropathies. The association of this molecule with oxaliplatin could increase the therapeutic index of this chemotherapy, potentiate this chemotherapy’s antitumoral effects against certain cancers as well as decrease the occurrence of diabetic neuropathies, a prevalent complication of diabetes. We have herein described two molecules which allow oxaliplatin treatment to exert its cytotoxic effects without eliciting its neurotoxicity. Furthermore, we have described the mechanisms by which these molecules exert their neuroprotection. The neuroprotective abilities of one of these molecules have also been broadened by the study of other types of peripheral neuropathies, namely diabetic neuropathies. The promising results obtained over the course of these works allow for optimism in the prospect of finding therapies to counteract not only oxaliplatin-induced peripheral neuropathies but peripheral neuropathies resulting from other etiologies
Azarm, Asieh. "Effect of oxaliplatin on HCT116 P53+/- colon cancer cells." Thesis, Högskolan i Skövde, Institutionen för vård och natur, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-5451.
Golf, Alexander. "Eine randomisierte Phase-II-Studie mit Capecitabin/Oxaliplatin versus Gemcitabin/Capecitabin versus Gemcitabin/Oxaliplatin bei Patienten mit lokal fortgeschrittenem inoperablem oder metastasiertem Pankreaskarzinom." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-108951.
Gong, Peng Chaney Stephen G. "Modeling conformational dynamics of cisplatin and oxaliplatin adducts with DNA." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,496.
Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Biomedical Engineering." Discipline: Biomedical Engineering; Department/School: Medicine.
POZZI, ELEONORA. "OXALIPLATIN-INDUCED PERIPHERAL NEUROTOXICITY IN MOUSE MODELS: DIFFERENT TREATMENT SCHEDULES AND FOCUS ON OXIDATIVE STRESS." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/261949.
The toxicity of anticancer drugs represents one of the major limitation in their clinical use. Among the side effects of chemotherapy, peripheral neurotoxicity is one of the most disabling for cancer patients. Oxaliplatin (OHP) is one of the most neurotoxic antineoplastic drug widely used for the treatment of metastatic colorectal cancer. Patients undergoing OHP-regimen experience two clinically distinct forms of peripheral neuropathy: an acute cold-enhanced form and a chronic distal sensory neuropathy. Due to the lack of effective pharmacological therapies in preventing and/or alleviating neuropathic symptoms, OHP dose reduction or interruption is often mandatory. Despite extensive investigation, the pathogenesis of OHP-induced peripheral neurotoxicity (OIPN) is still largely unknown. In literature several preclinical in vivo studies, different from each other in schedules of OHP treatment, are described but the characterization of peripheral neurotoxicity is limited. In fact, to verify the OINP onset, in addition to the evaluation of neuropathic pain, neurophysiological and histopathological analyses should be assessed. Mitochondrial dysfunction has recently been suggested as putative mechanisms possibly involved in the onset and development of chemotherapy-induced peripheral neurotoxicity. Mitochondrial dysfunction and associated oxidative stress may result in chronic neuronal energy impairment leading to neuropathic symptoms. The first aim of this study was to compare OIPN mouse models reported in three published studies with OIPN mouse model currently used in our laboratory, using a multimodal assessment. Moreover, given the potential role of oxidative stress in the pathogenesis of peripheral neuropathy, the possibility that OHP treatment could induce oxidative stress and eventually mitochondrial dysfunctions has also been analysed. Taken together, the results of this study indicate that a single dose of OHP 5 mg/kg administrated in tail vein is able to reproduce the clinical features of acute OIPN. On the other hand, to reproduce the clinical features of chronic OIPN, prolonged OHP treatment is required. In fact, alterations in caudal and digital nerves amplitudes and mechanical allodynia together with a reduction in intraepidermal nerve fiber density were observed only after 4 weeks of OHP 5 mg/kg administrated intravenously twice a week, the schedule currently used in our laboratory. Changes in DRG morphometry were instead more commonly observed also in the other OHP schedules reproduced in this study. As a whole, these results suggested that our laboratory OHP model is the one which better mimic the OIPN features. Regarding the pathogenic aspect, this study is far from clarifying the role of mitochondrial dysfunction and oxidative stress in the onset of OIPN, even if some results have been obtained. In general, oxidative stress levels measured with TBARS assay did not increase considerably in DRG and caudal nerves following OHP treatment with any schedule used, whereas sciatic nerves showed an increase in TBARS level at 2 weeks after a cumulative dose at 20 mg/kg (intravenous administration) and at 4 weeks after 30 mg/kg (intraperitoneal administration). Furthermore, a significant increase in protein expression levels of respiratory chain complex I in DRG collected from the animals treated for 4 weeks with our OHP schedule was detected. In the same samples, a decrease in phosphoryled form of DRP1 was observed closely approximating significance after 2 weeks of OHP treatment, indicating reduced mitochondrial fission process. In conclusion, a reliable animal model should be able to evaluate acute and chronic neurotoxicity in order to study the mechanism underlying OIPN. Setting a standard method of evaluation would be useful to obtain consistent results among different workgroups. Moreover, mitochondrial dysfunction and oxidative stress may be implicated in the onset of OIPN but further investigations are required.
Books on the topic "Oxaliplatin":
National Institute for Clinical Excellence. Guidance on the use of irinotecan, oxaliplatin and raltitrexed for the treatment of advanced colorectal cancer. London: NICE, 2002.
M, Lloyd Jones, and National Co-ordinating Centre for HTA (Great Britain), eds. A rapid and systematic review of the evidence for the clinical effectiveness and cost-effectiveness of irinotecan, oxaliplatin and raltitrexed for the treatment of advanced colorectal cancer. Alton: Core Research on behalf of NCCHTA, 2001.
Lloyd, Jones M., National Co-ordinating Centre for HTA (Great Britain), and Health Technology Assessment Programme, eds. A Rapid and systematic review of the evidence for the clinical effectiveness and cost-effectiveness of irinotecan, oxaliplatin and raltitrexed for the treatment of advanced colorectal cancer. Southampton: NCCHTA, 2001.
R, Kelland Lloyd, and Farrell Nicholas 1948-, eds. Platinum-based drugs in cancer therapy. Totowa, N.J: Humana Press, 2000.
Schmoll, H. J. Eloxatin (Oxaliplatin. S Karger Pub, 2003.
Marshall, John L. The Clinical Use of Oxaliplatin: Case Studies and Roundtable Discussion, Including a Clinical Discussion on Audio CD. Cmp United Business Media, 2004.
Schmoll, H. J. Oxaliplatin (eloxatin): Fortschritte In Der Tumortherapie 2004 (Onkologie). S Karger Pub, 2004.
Schmoll, H. J. Oxaliplatin (Eloxatin): Fortschritte in Der Tumortherapie (Onkologie). S Karger Pub, 2000.
McLeon, Kelly. Oxaliplatin, Fluorouracil, and Leucovorin as Adjuvant Treatment for Colon Cancer. Edited by SreyRam Kuy and Miguel A. Burch. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199384075.003.0011.
Publications, ICON Health. Oxaliplatin - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.
Book chapters on the topic "Oxaliplatin":
Mader, Ines, Patrizia Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola, and Sabine M. Wassertheurer. "Oxaliplatin." In Paravasation von Zytostatika, 210–12. Vienna: Springer Vienna, 2002. http://dx.doi.org/10.1007/978-3-7091-3799-4_40.
Mader, Ines, Patrizia Fürst-Weger, Robert Mader, Elisabeth Nogler-Semenitz, and Sabine Wassertheurer. "Oxaliplatin." In Extravasation of Cytotoxic Agents, 298–303. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-88893-3_47.
Mader, Ines, Patrizia E. Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola, and Sabine M. Wassertheurer. "Oxaliplatin." In Extravasation of Cytotoxic Agents, 195–97. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-3710-9_40.
Bonetti, Andrea, and Furini Lara. "Oxaliplatin-Based Chemotherapy for Colon Cancer." In Platinum and Other Heavy Metal Compounds in Cancer Chemotherapy, 271–84. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-459-3_31.
Stein, Alexander. "Oxaliplatin, Clinical Use in Cancer Patients." In Encyclopedia of Metalloproteins, 1615–22. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_563.
Taguchi, T. "Clinical Trials of Oxaliplatin and DWA2114R." In Platinum and Other Metal Coordination Compounds in Cancer Chemotherapy 2, 199–203. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0218-4_19.
Aschele, Carlo, Elisa Bennicelli, and Amalia Milano. "Should Oxaliplatin Be Added to Preoperative Chemoradiation?" In Multidisciplinary Management of Rectal Cancer, 263–72. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-43217-5_35.
Jacobson, Stacy D., Steven R. Alberts, and Richard M. Goldberg. "Oxaliplatin in the Treatment of Colorectal Cancer." In Colorectal Cancer, 525–66. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-160-2_29.
Aschele, Carlo. "Should Oxaliplatin Be Added to Preoperative Chemoradiation?" In Multidisciplinary Management of Rectal Cancer, 173–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-25005-7_18.
Gatti, Laura, and Paola Perego. "Cellular Resistance to Oxaliplatin and Drug Accumulation Defects." In Platinum and Other Heavy Metal Compounds in Cancer Chemotherapy, 115–24. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-459-3_16.
Conference papers on the topic "Oxaliplatin":
Jungwirth, Ute, Petra Heffeter, Johannes Gojo, Sergey Abramkin, Kristof Meelich, Michael Galanski, Wilfried Körner, Michael M. Micksche, Bernhard K. Keppler, and Walter Berger. "Abstract C93: Novel monosubstituted oxaliplatin analogs with improved characteristics." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c93.
Kuang, Yuting, Anthony El-Khoueiry, Pietro Taverna, Mats Ljungman, and Nouri Neamati. "Abstract 2533: SGI-110 priming sensitizes hepatocellular carcinoma cells to oxaliplatin." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2533.
Chen, Yufeng, Zhaoliang Yu, Peng Deng, and Xiaojian Wu. "Abstract 972: Pharmacological targeting CDC7 sensitizes oxaliplatin treatment in colorectal cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-972.
Wu, Xiaojun, E. Yiwen, Xinlong Xu, and Li Wang. "Interaction between DNA and Oxaliplatin in Aqueous Solution Studied Using THz-TDS." In Laser and Tera-Hertz Science and Technology. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/ltst.2012.sf2a.3.
Fortuna, M., P. Tavcar, M. Sonc, I. Virant, M. Kovacevic, S. Rozman, A. Eberl, and J. Dolenc. "5PSQ-056 Evaluation of oxaliplatin-specific neurotoxicity based on total cumulative dose." In Abstract Book, 23rd EAHP Congress, 21st–23rd March 2018, Gothenburg, Sweden. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/ejhpharm-2018-eahpconf.410.
McIntyre, Alexander, Fiammetta Falcone, Patrick G. Johnston, Daniel B. Longley, and Simon S. McDade. "Abstract LB-016: Nutlin and oxaliplatin induce p53-dependent addiction to FLIP." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-016.
Huang, Huakang, and Daniel W. Rosenberg. "Abstract 3608: Prostaglandin E-2 promotes resistance to oxaliplatin in colorectal cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3608.
Sorensen, Kathleen, Jennifer Jess, Susan Goosen, Guillermo Flores, Zach Madaj, Elissa Bogulaslawski, and Patrick J. Grohar. "Abstract 5817: Oxaliplatin and ATR inhibitors show strong synergy in Ewing sarcoma cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5817.
Yamano, Tomoki, Shuji Kubo, Aya Yano, and Naohiro Tomita. "Abstract 5453: Different mechanism of Oxaliplatin resistance in human colorectal cancer cell lines." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5453.
Chen, Chi-Long, Yu-Chan Chang, and Michael Hsiao. "Abstract 1520: RAB31 triggers oxaliplatin resistance in colorectal cancer via epithelial-mesenchymal transition." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1520.
Reports on the topic "Oxaliplatin":
Si, Yue, Yan Yuan, Yihua Zou, Haiyan Wang, and Yong Xin. S-1 or Capecitabine in combination with Oxaliplatin for Gastric Cancer：A meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0064.
Zhou, Tong, Shuo Wang, Lanxin Zhang, Yuerong Gui, Jun Dong, Dandan Wang, and Bingjie Fan. Efficacy and Safety of Compound Kushen Injection Combined With Oxaliplatin-Based Chemotherapy in the Treatment of Advanced Colorectal Cancer: a Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0059.
Jing, Hailiang, Jianing Jian, Hong Liu, Hairuo Chen, Xi Fu, Zhuohong Li, Qiaoling Wang, Linjiong Li, Fengming You, and Wenyuan Li. The effect of oral Chinese herbal medicine on Oxaliplatin-induced Peripheral Neuropathy in patients with advanced colorectal cancer treated with FOLFOX: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2020. http://dx.doi.org/10.37766/inplasy2020.12.0124.
Wang, Shuo, Xueqian Wang, Tong Zhou, Shuaihang Hu, Peiyu Tian, Zheng Li, Yuxiao Li, et al. Efficacy of Chinese herbal injections combined with fluoropyrimidine and oxaliplatin-based chemotherapy for advanced colorectal cancer: a protocol for systematic review and meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0050.