Thematische Bibliographien / Oxaliplatin

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Auswahl der wissenschaftlichen Literatur zum Thema „Oxaliplatin“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 10. März 2023

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Zeitschriftenartikel zum Thema "Oxaliplatin"

Ain, Noor ul, Nusrat Bano, Anwar Ejaz Beg, Kamran Hameed, Talha Bin Fayyaz und Rafia Sadaf. „HEMATOLOGICAL TOXICITY IN RATS;“. Professional Medical Journal 24, Nr. 02 (14.02.2017): 342–46. http://dx.doi.org/10.29309/tpmj/2017.24.02.525.

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Objectives: Oxaliplatin causes hematological toxicities in clinical setting whichlimits its efficacy. The aim of this study is to investigate the therapeutic effects of Andrographispaniculata against hematological toxicity caused by oxaliplatin. Study design: Experimentalanimal study. Period: Study takes 8 month from March 2015 to Oct 2015. Setting: Dow universityanimal house. Method: Wistar albino male rats, divided into 3 equals groups (n=6): GroupN* was a control group (0.9% normal saline), Group NP0 was Oxaliplatin treated group andGroup NP1 was prophylactically treated with Andrographis paniculata followed by Oxaliplatinin order to assess the protective effects of Andrographis paniculata against the hematologictoxicity caused by Oxaliplatin. Results: Prophylactic treatment with Andrographis paniculata(NP1) significantly increases the levels of platelets and neutrophile count compared with thestandard (NP0) (p<0.01) and increases the RBCs count and levels of hemoglobin comparedwith the standard (NP0). Conclusion: Prophylactic treatment with Andrographis paniculata(NP1) was effective in reducing risk of thrombocytopenia, anemia and neutropenia associatedwith Oxaliplatin.

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Grothey, A., D. A. Nikcevich, J. A. Sloan, J. W. Kugler, P. T. Silberstein, T. Dentchev, D. B. Wender, H. E. Windschilt, X. Zhao und 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, Nr. 15_suppl (20.05.2009): 4025. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.4025.

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4025 Background: Cumulative sNT is the dose-limiting toxicity of oxaliplatin which commonly leads to early discontinuation of oxaliplatin-based therapy in the palliative and adjuvant setting. We recently demonstrated the protective effect of CaMg against oxaliplatin-induced sNT as assessed by NCI-CTC (Nikcevich ASCO 2008). It is unclear, though, if CaMg reduced acute and/or chronic, cumulative sNT. Methods: 104 pts with colon cancer undergoing adjuvant therapy with FOLFOX were randomized to IV CaMg (1g calcium gluconate plus 1g magnesium sulfate pre- and post-oxaliplatin) or placebo (PL) in a double-blinded manner. NCI-CTC, an oxaliplatin-specific sNT scale and patient-reported outcome (PRO) questionnaires were used to differentially assess the effect of CaMg on acute (effect on sNT on days 1–4 after oxaliplatin) and chronic sNT (area between curves over whole course of therapy). Results: A total of 102 pts (50 CaMg, 52 PL; 96 mFOLFOX6, 6 FOLFOX4) were available for analysis. Apart from a strong reduction in muscle cramps with CaMg (p=0.002), no difference was found between CaMg and PL in PRO with regard to items reflecting acute sNT (e.g. sensitivity to cold, swallowing of cold liquids, throat discomfort) on days 1–4 after oxaliplatin of any treatment cycle. In contrast, CaMg was able to significantly reduce cumulative sNT in form of numbness in fingers (p=0.02), impaired ability to button shirts (p=0.05), tingling in fingers (p=0.06), and muscle cramps over the course of therapy (p=0.01). Conclusions: In our phase III, placebo-controlled trial, CaMg was able to significantly reduce chronic, cumulative sNT related to oxaliplatin as evaluated by specific PRO questionnaires. No effect was noted on phenomena associated with acute sNT. CaMg can be recommended as neuroprotectant against oxaliplatin-related chronic sNT, oxaliplatin's dose-limiting toxicity. [Table: see text]

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Pires, Lívia Márcia Vidal, und 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, Nr. 35 (23.09.2021): 382–97. http://dx.doi.org/10.24276/rrecien2021.11.35.382-397.

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O objetivo deste estudo foi realizar um mapeamento dos fatores clínicos preditivos da Neuropatia Sensorial Periférica induzida pela Oxaliplatina. Para tanto, foi realizada uma revisão sistemática, elaborada a partir das recomendações da diretriz PRISMA. A estratégia PICO também foi utilizada para formular a questão de pesquisa e orientar a busca nas bases de dados: PubMed, Embase, Scopus, BVS/IBECS e CINAHL. Foram selecionadas 26 publicações para análise final e inclusão na revisão. As publicações foram classificadas quanto ao nível de evidência e grau de recomendação, de acordo com o sistema JBI. Na análise das publicações foram mapeados 15 fatores preditivos, com maior destaque para a dose cumulativa de Oxaliplatina utilizada. O reconhecimento dos fatores clínicos preditivos da Neuropatia Sensorial Periférica, independente da precocidade que possa ser feito, são importantes para a elaboração de estratégias mensuráveis no exercício do cuidado colaborativo e multidimensional.Descritores: Toxicidade, Quimioterapia Combinada, Enfermagem Baseada em Evidências, Cuidados de Enfermagem, Neoplasias Colorretais. Mapping of clinical factors predictive of oxaliplatin-induced peripheral sensory neuropathy: systematic reviewAbstract: The aim of this study was to map the predictive clinical factors of Oxaliplatin-induced Peripheral Sensory Neuropathy. For that, a systematic review was carried out, based on the recommendations of the PRISMA guideline. The PICO strategy was also used to formulate the research question and guide the search in the databases: PubMed, Embase, Scopus, BVS/IBECS and CINAHL. 26 publications were selected for final analysis and inclusion in the review. The publications were classified according to the level of evidence and degree of recommendation, according to the JBI system. In the analysis of the publications, 15 predictive factors were mapped, with greater emphasis on the cumulative dose of Oxaliplatin used. The recognition of clinical predictive factors for Peripheral Sensory Neuropathy, regardless of the precocity that can be done, are important for the development of measurable strategies in the exercise of collaborative and multidimensional care.Descriptors: Toxicity, Combined Chemotherapy, Evidence-Based Nursing, Nursing Care, Colorectal Neoplasms. Mapeo de factores clínicos predictivos de neuropatía sensorial periférica inducida por oxaliplatino: revisión sistemáticaResumen: El objetivo de este estudio fue mapear los factores clínicos predictivos de la Neuropatía Sensorial periférica inducida por oxaliplatino. Para ello se realizó una revisión sistemática, con base en las recomendaciones de la guía PRISMA. También se utilizó la estrategia PICO para formular la pregunta de investigación y orientar la búsqueda en las bases de datos: PubMed, Embase, Scopus, BVS/IBECS y CINAHL. Se seleccionaron 26 publicaciones para su análisis final e inclusión en la revisión. Las publicaciones se clasificaron según el nivel de evidencia y grado de recomendación, según el sistema JBI. En el análisis de las publicaciones se mapearon 15 factores predictivos, con mayor énfasis en la dosis acumulada de Oxaliplatino utilizada. El reconocimiento de factores clínicos predictivos de la Neuropatía Sensorial Periférica, independientemente de la precocidad que se pueda realizar, es importante para el desarrollo de estrategias medibles en el ejercicio de la atención colaborativa y multidimensional.Descriptores: Toxicidad, Quimioterapia Combinada, Enfermería Basada en Evidencias, Cuidado de Enfermera, Neoplasias Colorrectales.

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&NA;. „Oxaliplatin“. Reactions Weekly &NA;, Nr. 1378 (November 2011): 27. http://dx.doi.org/10.2165/00128415-201113780-00098.

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&NA;. „Oxaliplatin“. Reactions Weekly &NA;, Nr. 1384 (Januar 2012): 43. http://dx.doi.org/10.2165/00128415-201213840-00174.

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&NA;. „Oxaliplatin“. Reactions Weekly &NA;, Nr. 1385 (Januar 2012): 35. http://dx.doi.org/10.2165/00128415-201213850-00129.

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&NA;. „Oxaliplatin“. Reactions Weekly &NA;, Nr. 1388 (Februar 2012): 24. http://dx.doi.org/10.2165/00128415-201213880-00093.

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&NA;. „Oxaliplatin“. Reactions Weekly &NA;, Nr. 1389 (Februar 2012): 34. http://dx.doi.org/10.2165/00128415-201213890-00124.

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&NA;. „Oxaliplatin“. Reactions Weekly &NA;, Nr. 1390 (Februar 2012): 28–29. http://dx.doi.org/10.2165/00128415-201213900-00109.

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&NA;. „Oxaliplatin“. Reactions Weekly &NA;, Nr. 1390 (Februar 2012): 29. http://dx.doi.org/10.2165/00128415-201213900-00112.

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Dissertationen zum Thema "Oxaliplatin"

Xiaoqing, Liu. „Dose-banding studies on oxaliplatin“. Thesis, University of Plymouth, 2016. http://hdl.handle.net/10026.1/8081.

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Oxaliplatin is an anticancer drug widely used in cancer chemotherapy. This thesis evaluates whether a specific dose-banding scheme for oxaliplatin could replace the individual dosing method that is currently used in the oxaliplatin administration. Dose-banding was introduced into UK clinical practice in 2001, as it reduces delays in patients receiving their treatment and, through quality control and end-product testing, safeguards the infusion quality and patient safety. A range of studies were included in this thesis: an extended stability study on oxaliplatin infusions using a sequential temperature cycling design; studies on oxalate, a potential degradation product and metabolite of oxaliplatin which has been linked to oxaliplatin neurotoxicity and the development of an ex vivo pharmacokinetic (PK) simulation model to compare the effect of different oxaliplatin dosing methods on its therapeutic outcomes. The shelf-life of oxaliplatin infusions over a concentration range of 0.2 mg/mL – 0.7 mg/mL is extended to 84 days when stored at 2 – 8℃ plus a further 7 days after being left at room temperature (25℃) for 24 hours. This ensures the unused oxaliplatin infusions are safe to be re-issued to patients, which could reduce drug wastage. The oxalate study suggests that the dose-limiting neurotoxicity of oxaliplatin is unlikely to be directly related to the oxalate produced from oxaliplatin degradation in infusions or from the non-enzymic transformation of oxaliplatin in vivo because the oxalate levels from these routes are minor compared to the endogenous level. The safety and efficacy of dose-banding schemes was demonstrated by comparing the simulated PK characteristics gained from the ex vivo model. Dose-banding with the +10% maximum deviation was selected as the most promising dosing scheme for oxaliplatin. Finally, recommendations are made concerning the introduction of oxaliplatin dose-banding scheme into clinical practice, and on the benefits of harmonised dose-banding schemes.

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Vincent, Jacob Adam. „Sensorimotor Deficits Following Oxaliplatin Chemotherapy“. Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1496136263522854.

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Wieczerzak, Krystyna Blanka. „Sensorimotor Analysis of Oxaliplatin Treated Rats“. Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1432856752.

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Robinson, Stuart Michael. „The pathogenesis of oxaliplatin induced sinusoidal obstruction syndrome“. Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/1942.

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Oxaliplatin based chemotherapy has demonstrated remarkable efficacy in down staging colorectal liver metastases such that patients initially considered to have inoperable disease are able to undergo a potentially curative resection. In addition the use of neoadjuvant Oxaliplatin based chemotherapy has been shown to improve progression free survival following liver resection. Taken together this means that ever increasing numbers of patients are presenting for liver resection having received multiple cycles of chemotherapy. Whilst this approach has many advantages the use of pre-operative chemotherapy has been associated with the development of sinusoidal obstruction syndrome (SOS) in the liver parenchyma in up to 40% of patients. It is thought that the presence of SOS significantly increase the risks associated with major liver resection. More recent data also suggests that the presence of SOS within the liver may result in poorer disease specific outcomes in the long term and in particular a higher risk of early intra-hepatic recurrence. At present the pathogenesis of SOS in this context is not understood and no treatment exists to either prevent its development or reverse the histological changes in the liver associated with it. The aim of the current study was to develop a reproducible in vivo experimental model of Oxaliplatin induced SOS and to interrogate this to identify the pathophysiological mechanisms which underpin its development. With this knowledge it was hoped that potential therapeutic strategies could be suggested to ameliorate the development of SOS in patients treated with Oxaliplatin based chemotherapy. C57BL/6J mice treated with weekly intraperitoneal injections of Oxaliplatin and 5- FU/Leucovorin for 5 weeks develop histological changes of SOS when maintained on a iv purified, but not chow, diet. This is associated with increased expression of key matrix remodelling genes within the liver parenchyma such as MMP2, MMP9, TIMP1, TGFβ and Procollagen I. The development of these gene expression changes is accelerated in the presence of tumour within the liver perhaps as a consequence of increased production of inflammatory mediators such as CXCL1. The presence of SOS is associated with a dramatic increase in expression of the serine protease family member PAI-1 which is involved in a variety of processes including matrix remodelling, thrombus formation and cellular senescence. Immunohistochemistry revealed endothelial cells in areas of sinusoidal injury stained positive for the cell cycle inhibitor p21CIP1/WAF1 in keeping with senescence in these cells. This process was associated with depletion of hepatic glutathione and decreased expression of the antioxidant transcription factor NRF2 suggesting a role for oxidative stress in the pathogenesis of SOS. To explore this further the experiment was repeated but this time using dietary supplementation with either the thiol donor N-Acetylcysteine (NAC) or the NRF2 activator butyrated hydroxyanisole (BHA) alongside FOLFOX treatment. Whilst supplementation with NAC had no effect on the development of SOS its development was completely prevented by supplementation with BHA suggesting that NRF2 activating antioxidants may be a useful therapeutic strategy in preventing the development of SOS. In conclusion this study has described the first reproducible experimental model of Oxaliplatin induced SOS which accurately reflects the pathogenesis of the disease in humans. Through interrogation of this it has been possible to identify therapeutic strategies which may be of value in preventing the development of SOS in patients with colorectal liver metastases.

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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.

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L’oxaliplatino (OHP) è un composto del platino di terza generazione, usato in combinazione con 5-fluorouracile e leucovorin per il trattamento del tumore al colon-retto metastatico. L’assunzione di OHP è in grado di indurre l’insorgenza di due fenomeni di tossicità, acuto e cronico. La tossicità acuta è caratterizzata da disestesie e parestesie transitorie esacerbate dal contatto col freddo. La gravità di questi sintomi è predittiva per lo sviluppo della neuropatia sensoriale cronica. Sebbene i meccanismi patogenetici alla base della tossicità acuta non siano stati del tutto chiariti, l’ipotesi più accreditata supporta un maggiore coinvolgimento dei canali del sodio voltaggio-dipendenti. Tuttavia, gli studi sino ad ora condotti si sono focalizzati solo su aspetti specifici della risposta elettrofisiologica cellulare ed hanno utilizzato concentrazioni di OHP molto elevate producendo risultati a volte controversi. Per questi motivi, il nostro obiettivo è stato quello di valutare gli effetti di una concentrazione di OHP più fisiologica sulle proprietà elettriche di diversi modelli di neuroni sensoriali. Poiché i neuroni dei gangli della radice dorsale (DRG) rappresentano il principale bersaglio farmacologico dei composti del platino, i nostri studi sono stati condotti incubando con OHP (7.5 μM) cellule F-11 differenziate. Abbiamo quindi studiato le possibili alterazioni prodotte dal farmaco sul potenziale di riposo (Vrest), sulle caratteristiche del potenziale d’azione (AP) e sulle proprietà biofisiche dei canali voltaggio-dipendenti di sodio e potassio. Le loro proprietà elettrofisiologiche sono state studiate con la tecnica del patch-clamp in configurazione whole-cell. Il cisplatino (CDDP 15 μM) è stato usato come composto di controllo per verificare l'esclusività degli effetti indotti da OHP. Inoltre, al fine di convalidare i risultati raccolti sulle cellule F-11 differenziate, i nostri esperimenti sono stati riprodotti su culture primarie di neuroni sensoriali derivati da DRG di embrioni di ratto o di ratti adulti. Rispetto alle cellule non trattate, l’incubazione con OHP ha determinato una depolarizzazione del Vrest, una riduzione della frequenza di scarica di AP, un aumento della densità di corrente di sodio e una riduzione della densità di corrente dei canali del potassio ERG. Tuttavia, la somministrazione di OHP non ha avuto alcuna influenza sui canali del potassio delayed-rectifier e sulla durata di AP indotti. Inoltre, OHP ha determinato uno spostamento delle curve di attivazione e di inattivazione delle correnti di sodio TTX-sensibili verso potenziali più negativi ed un aumento della risultante corrente finestra. Un comportamento simile è stato osservato anche per i canali ERG. Al contrario, il trattamento con CDDP non ha determinato variazioni del Vrest ed ha causato una riduzione della frequenza di scarica, un aumentato della durata di PA ed una riduzione della densità di corrente di potassio delayed-rectifier, di ERG e di sodio. Nelle colture primarie di neuroni sensoriali embrionali, l'incubazione con OHP ha indotto un aumento della frazione di neuroni in grado di generare PA multipli evocati ed un aumento delle densità di corrente di sodio e di potassio. Infine, i dati raccolti dalle colture primarie di neuroni derivati da ratti adulti hanno mostrato che la somministrazione di OHP per 24 ore aumenta la densità di corrente di sodio, mentre non ha alcun effetto sugli altri parametri studiati. In conclusione, i nostri risultati hanno messo in luce diversi target di OHP a livello dei neuroni sensoriali, agendo sia sui canali del sodio che del potassio. Inoltre i dati raccolti, suggeriscono che le cellule F-11 differenziate rappresentano un buon modello cellulare per lo sviluppo di strategie farmacologiche volte a prevenire l'insorgenza di neurotossicità causata da un’alterazione della funzionalità dei canali del sodio.
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.

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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.

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Les chimiothérapies à base de sels de platine exercent leurs effets anti-tumoraux en compromettant l'intégrité de l'ADN. Cette cytotoxicité conduit à une augmentation du stress oxydant qui, à son tour, favorise les processus de mort cellulaire. L'oxaliplatine indiquée dans les cancers métastatiques secondaires du colon et dans les cancers colorectaux, induit une augmentation des espèces réactives de l’oxygène en diminuant le glutathion réduit dans les cellules cancéreuses. Similairement aux autres chimiothérapies à base de sels de platine, elle doit être utilisée avec précaution. En effet, la majorité des patients recevant de l'oxaliplatine développent des neuropathies périphériques. Cette neurodégénérescence est un facteur limitant de cette chimiothérapie puisqu'elle peut nécessiter une réduction du dosage ou même une interruption du traitement si cet effet secondaire atteint une sévérité de grade 3. Les toxicités neurologiques peuvent se manifester dans les heures suivant l'injection sous forme aiguë. La forme chronique résulte d'injections cumulées de doses élevées. La forme aiguë, caractérisée par une paresthésie transitoire et une myotonie, est réversible et se résout généralement en quelques jours tandis que la forme chronique présente une paresthésie et une thermoalgie persistantes résultant de la dégradation axonale distale et de la démyélinisation des fibres nerveuses de gros diamètre. Les voies inflammatoires ont été incriminées dans l'étiologie de cette neurodégénérescence. Le niclosamide, un ténicide modulant les voies Stat3, Wnt, Notch et Beta-caténine, a été étudié in vitro et in vivo. Ayant déjà démontré les propriétés anti-inflammatoires de ce composé dans la sclérodermie systémique, nous avons cherché à déterminer si le niclosamide pourrait également prévenir la neurotoxicité de l'oxaliplatine. Le niclosamide a démontré une neuroprotection à la fois in vitro sur les neurones traités par l'oxaliplatine et in vivo dans les modèles de neuropathies périphériques induites par l'oxaliplatine. Le niclosamide est déjà utilisé en clinique avec des effets secondaires limités. L'association de cette molécule avec l'oxaliplatine pourrait augmenter l'indice thérapeutique de cette chimiothérapie. La benztropine est un inhibiteur des récepteurs muscariniques M1 et M3 possédant un potentiel de remyélinisation démontré dans le système nerveux central en favorisant la différenciation et la prolifération des cellules précurseurs des oligodendrocytes. La répartition différentielle entre les sous-types de récepteurs peut permettre le ciblage spécifique des cellules tumorales, notamment par l'inhibition de la signalisation autocrine de l'acétylcholine. La benztropine est un composé bien toléré qui ne provoque aucune réaction immunologique lors de son administration. Cette molécule présente un effet neuroprotecteur in vitro sur les neurones traités par l'oxaliplatine au cours d’études de viabilité cellulaire ainsi qu’in vivo dans les modèles murins de neuropathies périphériques induites par l'oxaliplatine et le diabète. L'association de cette molécule avec l'oxaliplatine pourrait augmenter l'indice thérapeutique de cette chimiothérapie, en potentialisant ses effets antitumoraux tout en diminuant la neurotoxicité. L’ubiquité des propriétés neuroprotectrices de la benztropine a été démontrée sur des neuropathies périphériques résultants d’autres étiologies. Nous avons ici décrit deux molécules permettant de conserver l’efficacité antitumorale du traitement par oxaliplatine tout en limitant ses effets neurotoxiques. Nous avons décrit les mécanismes par lesquels ces molécules exercent leur neuroprotection. Les résultats prometteurs obtenus au cours de ces travaux permettent d’envisager l’utilisation en clinique de ces molécules afin de prévenir non seulement les neuropathies périphériques induites par l'oxaliplatine, mais aussi les neuropathies périphériques résultant d'autres étiologies
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

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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.

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Oxaliplatin as an effective chemotherapeutic agent in FOLFOX regimens is using to treat colorectal cancer. In this study we investigate cytotoxicity of Oxaliplatin as single chemotherapeutic agent toHCT116P53+/- to identify molecular mechanism of Oxaliplatin action in induction of apoptosis pathway. Oxaliplatin exposure to HCT116P53+/- colorectal cell lines with deficiency of mismatch repair characteristic resulted to decrease the number of viable cells through apoptosis. Effective Oxaliplatin concentrations (IC50) which inhibit 50% of cell viability were determined using XTT method. Standard curve and time-dependent assay performed to confirm IC50 concentration. Western blot analysis demonstrated relocalization of Bax to mitochondria and induction of intrinsic apoptosis pathway resulted Oxaliplatin exposure. Inactivation of Bax in HCT116P53+/- will result significant reduction in number of viable cells following treatment with Oxaliplatin

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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.

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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.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2006.
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.

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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.

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La tossicità dei farmaci antitumorali rappresenta una delle principali limitazioni nella pratica clinica. Tra gli effetti collaterali dei farmaci chemioterapici, la neurotossicità periferica è uno dei più invalidanti per i pazienti malati di cancro. Oxaliplatino (OHP), un composto ampiamente usato per il trattamento del carcinoma del colon-retto metastatico, è uno dei farmaci antineoplastici più neurotossici. I pazienti possono sviluppare due forme clinicamente distinte di neuropatia periferica: una forma acuta aggravata dal freddo ed una neuropatia sensoriale distale cronica. A causa della mancanza di efficaci terapie farmacologiche in grado di prevenire e/o alleviare i sintomi neuropatici, la riduzione o l'interruzione della dose di OHP è spesso necessaria. Nonostante approfondite ricerche, la patogenesi della neurotossicità periferica indotta da OHP (OIPN) è ancora in gran parte sconosciuta. In letteratura sono descritti numerosi studi preclinici in vivo, diversi tra loro per la schedula di trattamento con OHP utilizzata, tuttavia la caratterizzazione della neurotossicità periferica è limitata. Infatti, per verificare l'insorgenza della OINP, oltre alla valutazione del dolore neuropatico, dovrebbero essere effettuate analisi neurofisiologiche ed istopatologiche. La disfunzione mitocondriale è stata recentemente suggerita come possibile meccanismo coinvolto nell'insorgenza della neurotossicità periferica indotta dai farmaci chemioterapici. Il primo obiettivo di questo lavoro è stato confrontare tre modelli murini di OIPN pubblicati con il modello murino di OIPN attualmente in uso nel nostro laboratorio, mediante una valutazione multimodale. Inoltre, dato il potenziale ruolo dello stress ossidativo nella patogenesi della neuropatia periferica, è stata analizzata la possibilità che il trattamento con OHP potesse indurre stress ossidativo e disfunzione mitocondriale. I risultati di questo studio indicano che una singola dose di OHP 5 mg/kg somministrata per via endovenosa è in grado di riprodurre le caratteristiche cliniche della forma acuta della OIPN. D'altra parte, al fine di riprodurre le caratteristiche cliniche della OIPN cronica, è necessario un trattamento prolungato con OHP. Sono state osservate alterazioni delle ampiezze dei nervi caudali e digitali, allodinia meccanica ed una riduzione della densità delle fibre nervose intraepidermiche solo dopo 4 settimane di OHP 5 mg/kg somministrato per via endovenosa due volte a settimana, schedula attualmente utilizzata nel nostro laboratorio. Pertanto, il nostro modello di laboratorio OHP è quello che meglio mima le caratteristiche della OIPN. Per quanto riguarda l'aspetto patogenetico, questo studio non ha ben chiarito il ruolo della disfunzione dei mitocondri e dello stress ossidativo nell'insorgenza della OIPN. I livelli di stress ossidativo, dosando i TBARS, non sono aumentati considerevolmente nei DRG e nei nervi caudali dopo il trattamento con OHP con qualsiasi schedula utilizzata, mentre i nervi sciatici hanno mostrato un aumento dei livelli di TBARS a 2 settimane dopo una dose cumulativa di 20 mg/kg (endovena) ed a 4 settimane dopo 30 mg/kg (intraperitoneale). Inoltre, un aumento significativo dei livelli del complesso I della catena respiratoria ed una riduzione della forma fosforilata di DRP1 sono stati rilevati nei DRG prelevati dagli animali trattati con la nostra schedula di trattamento per 4 e 2 settimane, rispettivamente. In conclusione, un modello animale affidabile dovrebbe essere in grado di valutare la neurotossicità acuta e cronica al fine di studiare i meccanismi alla base della OIPN. Definire un metodo di valutazione standard sarebbe utile per ottenere risultati coerenti tra diversi gruppi di lavoro. Inoltre, la disfunzione mitocondriale e lo stress ossidativo possono essere implicati nell'insorgenza della OIPN, ma sono necessarie ulteriori indagini.
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.

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Bücher zum Thema "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.

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M, Lloyd Jones, und National Co-ordinating Centre for HTA (Great Britain), Hrsg. 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.

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Lloyd, Jones M., National Co-ordinating Centre for HTA (Great Britain) und Health Technology Assessment Programme, Hrsg. 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.

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R, Kelland Lloyd, und Farrell Nicholas 1948-, Hrsg. Platinum-based drugs in cancer therapy. Totowa, N.J: Humana Press, 2000.

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Schmoll, H. J. Eloxatin (Oxaliplatin. S Karger Pub, 2003.

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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.

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Schmoll, H. J. Oxaliplatin (eloxatin): Fortschritte In Der Tumortherapie 2004 (Onkologie). S Karger Pub, 2004.

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Schmoll, H. J. Oxaliplatin (Eloxatin): Fortschritte in Der Tumortherapie (Onkologie). S Karger Pub, 2000.

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McLeon, Kelly. Oxaliplatin, Fluorouracil, and Leucovorin as Adjuvant Treatment for Colon Cancer. Herausgegeben von SreyRam Kuy und Miguel A. Burch. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199384075.003.0011.

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The landmark MOSAIC trial examined whether the addition of oxaliplatin to a postoperative adjuvant treatment regimen of fluorouracil and leucovorin affected disease-free survival from colon cancer. The MOSAIC trial established the efficacy of FOLFOX over 5-FU/LV as adjuvant treatment for stage III colon cancer and established FOLFOX4 as the reference standard for adjuvant treatment for stage III disease. This chapter describes the basics of the study, including funding, year study began, year study was published, study location, who was studied, who was excluded, how many patients, study design, study intervention, follow-up, endpoints, results, and criticism and limitations. The chapter briefly reviews other relevant studies and information, gives a summary and discusses implications, and concludes with a relevant clinical case.

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Publications, ICON Health. Oxaliplatin - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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Buchteile zum Thema "Oxaliplatin"

Mader, Ines, Patrizia Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola und 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.

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Mader, Ines, Patrizia Fürst-Weger, Robert Mader, Elisabeth Nogler-Semenitz und 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.

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Mader, Ines, Patrizia E. Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola und 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.

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Bonetti, Andrea, und 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.

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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.

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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.

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Aschele, Carlo, Elisa Bennicelli und 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.

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Jacobson, Stacy D., Steven R. Alberts und 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.

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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.

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Gatti, Laura, und 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.

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Konferenzberichte zum Thema "Oxaliplatin"

Jungwirth, Ute, Petra Heffeter, Johannes Gojo, Sergey Abramkin, Kristof Meelich, Michael Galanski, Wilfried Körner, Michael M. Micksche, Bernhard K. Keppler und 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.

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Kuang, Yuting, Anthony El-Khoueiry, Pietro Taverna, Mats Ljungman und 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.

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Chen, Yufeng, Zhaoliang Yu, Peng Deng und 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.

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Wu, Xiaojun, E. Yiwen, Xinlong Xu und 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.

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Fortuna, M., P. Tavcar, M. Sonc, I. Virant, M. Kovacevic, S. Rozman, A. Eberl und 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.

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McIntyre, Alexander, Fiammetta Falcone, Patrick G. Johnston, Daniel B. Longley und 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.

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Huang, Huakang, und 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.

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Sorensen, Kathleen, Jennifer Jess, Susan Goosen, Guillermo Flores, Zach Madaj, Elissa Bogulaslawski und 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.

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Yamano, Tomoki, Shuji Kubo, Aya Yano und 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.

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Chen, Chi-Long, Yu-Chan Chang und 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.

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Berichte der Organisationen zum Thema "Oxaliplatin"

Si, Yue, Yan Yuan, Yihua Zou, Haiyan Wang und 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, Januar 2023. http://dx.doi.org/10.37766/inplasy2023.1.0064.

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Zhou, Tong, Shuo Wang, Lanxin Zhang, Yuerong Gui, Jun Dong, Dandan Wang und 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.

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Jing, Hailiang, Jianing Jian, Hong Liu, Hairuo Chen, Xi Fu, Zhuohong Li, Qiaoling Wang, Linjiong Li, Fengming You und 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, Dezember 2020. http://dx.doi.org/10.37766/inplasy2020.12.0124.

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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, Oktober 2020. http://dx.doi.org/10.37766/inplasy2020.10.0050.

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