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Activation of S1P2 is protective against cisplatin-induced peripheral neuropathy

ABSTRACT: Activation of S1P2 is protective against cisplatin-induced peripheral neuropathy

PROVIDER: PRJNA987890 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25033559_1.fastq.gz	Fastqsanger.gz
	SRR25033559_2.fastq.gz	Fastqsanger.gz
	SRR25033560_1.fastq.gz	Fastqsanger.gz
	SRR25033560_2.fastq.gz	Fastqsanger.gz
	SRR25033561_1.fastq.gz	Fastqsanger.gz

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Activation of S1P2 is protective against cisplatin-induced peripheral neuropathy

Project description:To elucidate the molecular mechanisms underlying the neuroprotective role of S1P2, we conduct RNASeq on dorsal root ganglions (DRGs) collected from a cisplatin-induced peripheral neuropathy (CIPN) rat model.

2024-07-01 | GSE235877 | GEO

The Possible Protective Role of Ketotifen Against Oxaliplatin Induced Peripheral Neuropathy

Project description: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.

| 488 | ecrin-mdr-crc

Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney_Tumor]

Project description:Cisplatin is a potent chemotherapeutic drug, widely used in the treatment of various solid cancers. However, its clinical effectiveness is strongly limited by frequent severe adverse effects, such as nephrotoxicity and chemotherapy-induced peripheral neuropathy. Therefore, there is an urgent medical need to identify novel strategies that would limit cisplatin-induced toxicity. In the present study, we provide evidence that the FDA-approved adenosine A2A receptor antagonist istradefylline (KW6002) significantly protects from cisplatin-induced nephrotoxicity and neuropathic pain in experimental models of acute and sub-chronic cisplatin intoxication. Importantly, we also demonstrate that the anti-tumoral properties of cisplatin were not altered by istradefylline in tumor-bearing mice and even potentiated at the molecular level. Altogether, the present results support the use of istradefylline as a new valuable preventive approach for the clinical management of patients undergoing cisplatin treatment.

2022-09-12 | GSE179246 | GEO

Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney]

2022-09-12 | GSE179245 | GEO

Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects

Project description:Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects

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The Possible Protective Role of Omeprazole Against Oxaliplatin Induced Neuropathy in Cancer Patients

Project description:Oxaliplatin(OXA) chemotherapy protocols are used in treatment of cancers like colorectal (CRC) and pancreatic cancer. OXA causes peripheral neuropathy which is considered treatment limiting factor. In recent studies, it shows that omeprazole(OME) has antioxidant effect and can inhibit organic cation transporter 2 (OCT2) in kidney. So OME can protect against peripheral neuropathy induced by OXA through oxidative stress . Also OME activates extracellular-signal-regulated kinase(ERK) / mitogen activated protein kinase ( MAPK) pathway, so improves demyelinating symptoms.

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Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney]

Project description:Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney]

| PRJNA742909 | ENA

Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney_Tumor]

Project description:Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney_Tumor]

| PRJNA742910 | ENA

Expression Data for Cisplatin Treated Dorsal Root Ganglia from A/J and C57BL/6J Mice

Project description:Peripheral sensory neuropathy is a common complication to cisplatin treatment in cancer patients. Multiple signaling pathways are likely to be implicated in the pathophysiology, there are no explicit treatments and little is known about predictive factors associated with the onset or progression of cisplatin induced peripheral neuropathy. The transcriptional profiles of differentially senesitive strains of dorsal root ganglion across two inbreed strain of mice will promote better understanding of progression and risk factors assocciated with cisplatin induced peripheral neuropathy. Peripheral neuropathy was induced with a bi-weekly treatment of 4mg/kg cisplatin. We used microarrays to detail the transciptional profile underlying cisplatin induced peirperal neuropathy in two differentailly sensitve inbreed strains of mice: A/J and C57BL/6J

2019-07-01 | GSE64174 | GEO

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

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