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Preventive effect and safety of pregabalin on FOLFOX-related peripheral neurotoxicity for patients with advanced and recurrent colorectal cancer

ABSTRACT: Interventions: In case of FOLFOX related-peripheral neurotoxicity (Grade1), pregabalin is administered. Primary outcome(s): Neurotoxicity frequency of cumulative dose 500mg/m2 of oxaliplatin (Grade2 and more) Study Design: Single arm Non-randomized

DISEASE(S): Colorectal Cancer

PROVIDER: 2628289 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Preventive effect of pregabalin on oxaliplatin-related neurotoxicity for patients with advanced/recurrent colorectal cancer: a prospective phase 2 study

Project description:Interventions: Pregabalin is administered during FOLFOX or XELOX therapy. Initial dose:75mg twice daily(150mg/day),increased to 300 - 600mg/day if there was persistent paresthesia or functional impariment(Grade2 or more). Primary outcome(s): Neurotoxicity frequency of accumulation dose 500mg/m2 of L-OHP (Grade2 or more) Study Design: Single arm Non-randomized

| 2624861 | ecrin-mdr-crc

Preventive effect of shakuyaku-kanzo-to on neurotoxicity of FOLFOX plus bevacizumab for patients with metastatic colorectal cancer: a prospective phase II study

Project description:Interventions: Patients receive FOLFOX4 plus bevacizumab or modified FOLFOX6 plus bevacizumab and take shakuyaku-kanzo-to (7.5g/day) orally every day during FOLFOX plus bevacizumab treatment. Primary outcome(s): Neurotoxicity frequency of accumulation dose 500mg/m2 of oxaliplatin Study Design: Single arm Non-randomized

| 2617341 | ecrin-mdr-crc

Lead exposure induced transgenerational developmental neurotoxicity by altering genome methylation in Drosophila

Project description:Heavy metal toxicity is a worldwide health problem. Lead exposure is of particular concern due to the adverse effects of low concentrations on cognitive development in children. Although the mechanism of lead neurotoxicity has been well studied, the analysis and molecular mechanism of the transgenerational effects of lead exposure-induced neurotoxicity are lacking. To address this, Drosophila, a powerful developmental animal model, was exposed to lead acetate. We found that Pb exposure during the developmental stage affected the neurodevelopment of F0 fruit flies, resulting in a loss of the correlation between the motor terminal area and muscle fiber area and the increased frequency of β-lobe midline crossing phenotype in Mushroom bodies. We also found that Pb exposure led to an increase in BRP expression, suggesting an increase in synaptic vesicle release sites and a decrease in synaptic vesicle protein SYN expression in F0 generation. This explained the results of our electrophysiological data that Pb exposure led to an increase in the amplitude of evoked excitatory junctional potential (EJP) and an increase in the frequency of spontaneous excitatory junctional potential (mEJP). Our results further confirmed that the developmental neurotoxicity of parental Pb exposure has a transgenerational effect. Neurodevelopmental defects, abnormalities in synaptic function, and repetitive behavior also were observed in the F3 offspring of F0 exposed to lead. Our Medip-seq analysis showed that Pb exposure altered the DNA methylation levels of many neurodevelopmentally associated genes (eg, hppy, nrg, baz, and spn) in the F3 offspring of the F0 generation with Pb exposure. Our findings suggest that epigenetic mechanisms may underlie the transgenerational inheritance of acquired phenotypic traits resulting from exposure to environmental factors.

2023-12-09 | GSE249281 | GEO

Preventive effect of Goshajinkigan on peripheral neurotoxicity of FOLFOX therapy: A placebo-controlled double blind randomized Phase II study (The GONE Study)

Project description:Interventions: FOLFOX4(L-OHP85mg/m2, l-LV100mg/m2x2, 5FU400mg/m2(bolus)x2, 5FU600mg/m2x2(civ)) or mFOLFOX6(L-OHP85mg/m2, l-LV200mg/m2, 5FU400mg/m2(bolus), 5FU240mg/m2(civ)).Cycles of chemotherapy are given every 2 weeks until PD or unacceptable toxicity occurred. Goshajinkigan(GJG) is given orally at a dose of 2.5 g three times a day for 26 weeks starting on the day of L-OHP infusion. FOLFOX4(L-OHP85mg/m2, l-LV100mg/m2x2, 5FU400mg/m2(bolus)x2, 5FU600mg/m2x2(civ)) or mFOLFOX6(L-OHP85mg/m2, l-LV200mg/m2, 5FU400mg/m2(bolus), 5FU240mg/m2(civ)).Cycles of chemotherapy are given every 2 weeks until PD or unacceptable toxicity occurred. Placebo is given orally at a dose of 2.5 g three times a day for 26 weeks starting on the day of L-OHP infusion. Primary outcome(s): The incidence of peripheral neurotoxicity ≥grade 2 after eight cycles of chemotherapy. Study Design: Parallel Randomized

| 2617692 | ecrin-mdr-crc

Acrylamide acute neurotoxicity in adult zebrafish

Project description:Acute exposure to acrylamide (ACR), a type-2 alkene, may lead to a ataxia, skeletal muscles weakness and numbness of the extremities in exposed human and laboratory animals. Recently, a zebrafish model for ACR neurotoxicity mimicking most of the pathophysiological processes described in mammalian models, was generated in 8 days post-fertilization larvae. In order to better understand the predictive value of the zebrafish larvae model of acute ACR neurotoxicity, in the present manuscript the ACR acute neurotoxicity has been characterized in the brain of adult zebrafish, and the results compared with those obtained with the whole-larvae. Although qualitative and quantitative analysis of the data shows important differences in the ACR effects between the adult brain and the whole-larvae, the overall effects of ACR in adult zebrafish, including a significant decrease in locomotor activity, altered expression of transcriptional markers of proteins involved in synaptic vesicle cycle, presence of ACR-adducts on cysteine residues of some synaptic proteins, and changes in the profile of some neurotransmitter systems, are similar to those described in the larvae. Thus, these results support the suitability of the zebrafish ACR acute neurotoxicity recently developed in larvae for screening of molecules with therapeutic value to treat this toxic neuropathy.

2018-10-19 | PXD008993 | Pride

Chemotherapy neurotoxicity is codependent on cancer

Project description:Chemotherapy neurotoxicity is codependent on cancer

| PRJNA523238 | ENA

Peripheral Neuropathy in Colorectal Cancer Patients Under Adjuvant Chemotherapy With FOLFOX, FLOX or XELOX Regime

Project description:Oxaliplatin is a cytotoxic platinum compound and is one of the chemotherapeutic agent used in advanced colorectal cancer. It is used combined with Fluorouracil (5 FU) and Leucovorin. The main and most suffering side effect of oxaliplatin is polyneuropathy. Oxaliplatin-induced polyneuropathy (OIPN) can be acute and/or chronic neurotoxicity. The early detection of the neurotoxicity and changing the medication dose and/or schedule can prevent its development. It has been used different neurotoxicity scales in grading OIPN. In this study the investigators try to investigate whether the evaluation of the vibrotactile perception VTP, by using a multi frequency tactilometry in a patients hand and foot is a good indicator and superior to the standard of care to detect the underlying OIPN in patients undergoing adjuvant chemotherapy treatment with FOLFOX, FLOX or XELOX regime.

| 2274232 | ecrin-mdr-crc

Gene Expression Analysis of Carbonyl Sulfide Neurotoxicity

Project description:To gain insight into the pathogenesis of carbonyl sulfide induced neurotoxicity, we examined the gene expression profile of exposed rats before the onset of morphological changes (days 1 and 2) using the most consistently affected brain region, the posterior colliculus.

2009-07-07 | GSE12018 | GEO

Defective mitochondrial dynamics underlie manganese-induced neurotoxicity

Project description:Defective mitochondrial dynamics underlie manganese-induced neurotoxicity

| PRJNA641207 | ENA

Modeling acrylamide acute neurotoxicity in zebrafish larvae

Project description:Background: Acrylamide (ACR) is a broadly spread neurotoxic chemical of public health concern, as occupational or environmental exposure of humans to ACR may lead to a synaptopathy characterized by ataxia, skeletal muscles weakness and numbness of the extremities. Currently, only the mildly affected patients undergo complete recovery, and identification of new molecules with therapeutic bioactivity against ACR acute neurotoxicity is urgently needed. Objectives: We aimed to develop a zebrafish model for human ACR neurotoxicity. Methods: Adverse effects have been assessed at different levels, including analysis of the motor function (basal locomotor activity, visual motor response, kinematic of the touch-evoked escape response), histopathological evaluation (toluidine blue and whole-mount immunofluorescence), analysis of neural transcriptional markers (qPCR), proteomic analysis (μLC-MS-MS) and neurotransmitters profile (LC-MS/MS). Results: Our results show that zebrafish mimics most of the pathophysiological processes described in humans and mammalian models. Motor function was altered, including the response to sudden changes in light intensity. Specific effects were found on the presynaptic nerve terminals at the neuromuscular junction level, but not on the axonal tracts or myelin sheath integrity. Transcriptional markers of proteins involved in synaptic vesicle cycle were selectively altered, and the proteomic analysis showed that ACR-adducts were formed on cysteine residues of some synaptic proteins. Finally, analysis of neurotransmitters profile showed a significant effect found on cholinergic and dopaminergic systems. Conclusions: Thus, the zebrafish model for ACR acute neurotoxicity is suitable to be used larvae for in vivo high-throughput screening of small molecule libraries for identifying new drugs against this synaptopathy.

2018-10-24 | PXD007169 | Pride

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