Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Possible Protective Role of Ketotifen Against Oxaliplatin Induced Peripheral Neuropathy

ABSTRACT: The aim of current study is to evaluate the possible protective role of Ketotifen against oxaliplatin-induced peripheral sensory neuropathy in patient with stage III colorectal cancer. This study will be a randomized placebo controlled parallel study.64 patients with colorectal cancer will be randomized to 2 groups: Group I (control group; n=32) which will receive 12 cycles of modified FOLFOX-6 regimen plus placebo tablets twice daily. Group II (ketotifen group; n=32) which will receive modified FOLFOX-6 regimen in addition to ketotifen 2 mg daily Blood sample collection and biochemical assessment: * Serum IL-6 as a marker of inflammation. * Serum superoxide dismutase (SOD) as a biomarker of oxidative stress. * Serum neurotensin as a biomarker for neuropathy. Assessment of oxaliplatin induced peripheral sensory neuropathy will be done through: * The implication of National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE, Version 5, 2017) for grading of neuropathy at baseline and by the end of every two oxaliplatin cycles. * The use of Neurotoxicity- 12 item questionnaire score (Ntx-12) from the validated Functional Assessment of Cancer Therapy/Gynecologic Oncology Group "FACT/GOG-Ntx-12" at baseline and by the end of every two oxaliplatin cycles. * The assessment of the severity of neuropathic pain through brief pain inventory short form "BPI-SF" worst item. Severity of neuropathic pain will be assessed at baseline and by the end of every two oxaliplatin cycles.

DISEASE(S): Peripheral Nervous System Diseases,Neuropathy;peripheral

PROVIDER: 488 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Protective Effect of Pentoxifylline Against Chemotherapy Induced Toxicities in Patients With Colorectal Cancer

Project description:This study aims to: - Evaluate the possible protective effect of pentoxifylline against oxaliplatin induced peripheral neuropathy and chemotherapy induced mucositis in patients with stage II and stage III colorectal cancer. This study will be a randomized placebo controlled parallel study.48 patients with colorectal cancer will be randomized to 2 groups: Group I (control group; n=24) which will receive 12 cycles of FOLFOX-6 regimen plus placebo tablets twice daily. Group II (Pentoxiphylline group; n=24) which will receive FOLFOX-6 regimen in addition to pentoxifylline 400 mg twice daily. Blood sample collection and biochemical assessment: * Malondialdehyde (MDA) as oxidative stress marker (colorimetry). * Tumor necrosis factor alfa (TNF-α) as pro inflammatory marker (ELISA). * Neurotensin (NT) as a potential marker for neuropathic pain (ELISA). * Citrulline as a biomarker for mucositis (ELISA). Clinical assessment of oxaliplatin induced neuropathy will be done through: The assessment of the severity of neuropathic pain through "Brief Pain Inventory-Short Form" at baseline and by the end of every two chemotherapy cycles. The implication of National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE, Version 5, 2017) for grading of neuropathy every 2 cycles. The use of Neurotoxicity- 12 item questionnaire score (Ntx-12) from the validated Functional Assessment of Cancer Therapy/Gynecologic Oncology Group at baseline and by the end of every two chemotherapy cycles). Mucositis will be assessed at baseline and by the end of every two chemotherapy cycles through the use of common terminology criteria for adverse events "CTCAE, version 5.00, 2017

| 2752184 | ecrin-mdr-crc

Microarray analyses of mouse dorsal root ganglia tissue for six different pain models

Project description:Six different mouse pain models were studied: (1) tumour-injection model for bone cancer pain; (2) partial sciatic nerve ligation (PSL) for neuropathic pain; (3) mechanical joint loading for osteoarthritis pain; (4) oxaliplatin-induced painful neuropathy for chemotherapy-induced pain; (5) hyperalgesic priming model for chronic muscle pain; and (6) complete Freund’s adjuvant (CFA)-injection for inflammatory pain. Transcriptomic microarray analyses were performed using RNA isolated from dorsal root ganglia.

2018-06-11 | E-MTAB-6864 | biostudies-arrayexpress

Oral Glutamine in the Prevention of Oxaliplatin-induced Neurotoxicity

Project description:Primary Objective: To assess the benefit of glutamine when added to calcium-magnesium on the occurrence of grade 2, 3 and 4 peripheral sensory neuropathy (PSN) related to oxaliplatin with the National Cancer Institute-Common Terminology Criteria for Adverse Event (NCI-CTCAE) scale taking into account the time from start of oxaliplatin at which the first event occurred. Secondary Objective: To determine cumulative dose of oxaliplatin and time when the first occurrence of grade 2, 3 or 4 PSN. To determine the incidence of dose-reductions, dose-delays and discontinuations of oxaliplatin due to PSN grade 3 or 4. To assess effects of glutamine when added to calcium-magnesium on patients-reported outcomes using the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity 12 items questionnaire (FACT/GOG NTX-12) subscale. To evaluate the incidence of diarrhea. To determine Progression Free Survival (PFS) in metastatic patients.

| 2086375 | ecrin-mdr-crc

Role of Xaliproden on Recovery Rate From Severe Neuropathy in Patients Who Have Completed Adjuvant Chemotherapy With Oxaliplatin Based Regimens

Project description:Primary objective: To assess the effect of xaliproden hydrochloride (xaliproden) 1 mg per oral daily on the rate of complete resolution of peripheral sensory neuropathy (PSN) at 6 months, following randomization, after the completion of oxaliplatin-based adjuvant chemotherapy for colon cancer. Secondary objective: * To assess the effect of xaliproden on patient-reported outcomes using the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity scale (FACT/GOG NTX-12 subscale). * To assess the effect of xaliproden on the rate of at least partial recovery of grade > 2 PSN at 6 months * To assess the effects of xaliproden on the time to complete recovery from PSN * To evaluate the safety profile of xaliproden

| 2049763 | ecrin-mdr-crc

Gene expression signatures of chemotherapy-induced neuropathy induced by cisplatin and oxaliplatin

Project description:Vincristine, oxaliplatin, and cisplatin are commonly prescribed chemotherapeutic agents for the treatment of several cancer types. However, a main side-effect is chemotherapy-induced peripheral neuropathy (CIPN), which may lead to decreased quality of life, changes in chemotherapeutic treatment or even treatment cessation. Although painful symptoms associated with CIPN are faithfully recapitulated by mouse models, there is limited knowledge of how these drugs affect the expression of genes in peripheral sensory neurons. The present study carried out a transcriptomic analysis of dorsal root ganglia isolated from mice treated with vincristine, oxaliplatin, and cisplatin with a view to gain insight into the comparative pathophysiological mechanisms of CIPN. RNA-Seq using 75-nucleotide single end runs revealed 368, 295 and 256 differential expressed genes (DEGs) induced by treatment with vincristine, oxaliplatin and cisplatin, respectively. Although there were many similarities in DEGs between chemotherapeutic agents, only 5 genes were dysregulated in all groups. Cell type enrichment analysis (CTEA) and gene set enrichment analysis (GSEA) showed predominant effects on genes associated with the immune system after treatment with vincristine, while oxaliplatin treatment affected mainly neuronal genes. Treatment with cisplatin resulted in a mixed inflammatory and neuropathic gene expression signature. Only ‘regulation of transport’ and ‘response to external stimuli’ were gene ontology terms shared between all treatments. These results provide insight into the recruitment of innate and adaptive immune responses to DRG tissue and indicate enhanced neuro-inflammatory processes following administration of vincristine, oxaliplatin, and cisplatin. These gene expression signatures may provide insight into novel drug targets for treatment of CIPN.

2019-06-01 | GSE125002 | GEO

Gene expression signatures of chemotherapy-induced neuropathy induced by vincristine

2019-06-01 | GSE125001 | GEO

mRNA expression of spinal dorsal horn in oxaliplatin-treated rats

Project description:Oxaliplatin-induced neuropathic pain is a common dose-limiting side effect of cancer treatment but the underlying mechanisms are largely unknown. The neuropathic pain model was established by oxaliplatin intraperitoneal administration for five consecutive days. In the present study, we performed whole genome expression microarray analysis by using spinal dorsal horn from oxaliplatin-treated and vehicle-treated rats on day 10.

2020-03-11 | GSE146739 | GEO

Comparison of Neurotoxic Potential of Abraxane versus Oxaliplatin and Paclitaxel

Project description:Interventions: Patients receiving abraxane chemotherapy for pancreatic cancer, breast cancer, colorectal cancer, non-small cell lung cancer or ovarian cancer will be recruited into the study to document the natural history of Abraxane-induced neurotoxicity through cross-sectional and prospective clinical and neurophysiological assessment. Examples of neurotoxicity seen with abraxane therapy include sensory dysasthesia including numbness and tingling in the hands and feet. Patients will be assessed monthly from the commencement of treatment until cessation, with 3-monthly follow up 6-12 months following cessation of treatment, to a maximum period of 2 years following enrolment. Primary outcome(s): To document the natural history of Abraxane-induced neurotoxicity through cross-sectional and prospective clinical and neurophysiological assessment. The severity of neuropathy will be assessed using the Total Neuropathy Score (TNS). This will be used to evaluate neuropathy in a number of different categories; sensory neuropathic symptoms, examination findings and nerve conduction results.[Assessed at monthly intervals from the commencement of treatment until cessation, with 3-monthly follow up 6-12 months following cessation of treatment.] Study Design: Purpose: Natural history;Duration: Longitudinal;Selection: Defined population;Timing: Prospective

| 2462598 | ecrin-mdr-crc

A role for fibroblast and mural cell subsets in models of neuropathic pain [bulkRNA-seq]

Project description:Neuropathic pain is a particularly intractable type of chronic pain that can result from physical nerve damage due to surgery or entrapment. Here, we present data which suggest that a particular subclass of fibroblast and mural cells may be implicated in the sensory neuron dysfunction that is characteristic of this pain state. In a mouse model of traumatic painful neuropathy, we used RNA sequencing, cell sorting and nerve tissue clearing to study mesenchymal lineage cells. We show that Pdgfrb+ fibroblasts and mural cells are increased in number for at least two months post-nerve damage and express high levels of known and putative pro-algesic mediators, which are further upregulated in neuropathy. We go on to demonstrate that a human nerve pericyte line releases a selection of these pro-algesic mediators at protein level. Moreover, conditioned media from stimulated human pericytes induces intra-cellular changes in human induced pluripotent stem cell derived sensory neurons; these changes (phosphorylation of the transcription factor STAT3) have been previously linked to sensory neuron activation. In summary, our data indicate that mesenchymal cell abnormalities should be considered when developing novel strategies to tackle neuropathic pain.

2024-12-19 | GSE283281 | GEO

A role for fibroblast and mural cell subsets in models of neuropathic pain [scRNA-seq]

2024-12-19 | GSE283177 | GEO