Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Safety of the oxaliplatin readministration by the desensitization for metastatic colorectal cancer patients having oxaliplatin allergy

ABSTRACT: Interventions: desensitization Primary outcome(s): the rate of oxaliplatin readministration without allergy Study Design: Single arm Non-randomized

DISEASE(S): Colorectal Carcinoma

PROVIDER: 2625519 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Differentially expressed genes between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples [Clinical samples-RNA-seq]

Project description:To identify key drivers of oxaliplatin resistance, we collected and analyzed the DEGs between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples

2023-02-28 | GSE206501 | GEO

Identification of molecular pathways involved in oxaliplatin-associated sinusoidal dilatation

Project description:Oxaliplatin-based chemotherapy for colorectal liver metastases (CRLM) can result in vascular liver lesions such as sinusoidal dilatations. Physiopathology remains unclear and variability between patients suggests that there is individual susceptibility. A better understanding of the molecular mechanisms of oxaliplatin liver toxicity may allow to identification of biomarkers and adaptation of chemotherapy delivery. non-tumor frozen liver samples were obtained from patients operated on for CRLM after an exclusive oxaliplatin-based chemotherapy. Gene-expression profiles were first analyzed by microarray on a selected population of 20 patients; 9 patients with severe sinusoidal dilatation (SD) after a short period of chemotherapy and 10 patients without any sinusoidal dilatation after a long period of chemotherapy. These were compared with a control group of 5 patients without any chemotherapy and lesions. This dataset is part of the TransQST collection.

2012-03-01 | E-GEOD-32384 | biostudies-arrayexpress

METTL3 Confers Oxaliplatin Resistance Through the Activation of G6PD-enhanced Pentose Phosphate Pathway in Hepatocellular Carcinoma

Project description:Oxaliplatin-based therapeutics is a widely used treatment approach for hepatocellular carcinoma (HCC) patients; however, drug resistance poses a significant clinical challenge. Epigenetic modifications have been implicated in the development of drug resistance. In our study, employing siRNA library screening, we identified that silencing the m6A writer METTL3 significantly enhanced the sensitivity to oxaliplatin in both in vivo and in vitro HCC models. Further investigations through combined RNA-seq and non-targeted metabolomics analysis revealed that silencing METTL3 impeded the pentose phosphate pathway (PPP), leading to a reduction in NADPH and nucleotide precursors. This disruption induced DNA damage, decreased DNA synthesis, and ultimately resulted in cell cycle arrest. Mechanistically, METTL3 was found to modify E3 ligase TRIM21 near the 3'UTR with N6-methyladenosine, leading to reduced RNA stability upon recognition by YTHDF2. TRIM21, in turn, facilitated the degradation of the rate-limiting enzyme of PPP, G6PD, through the ubiquitination-proteasome pathway. Importantly, high expression of METTL3 was significantly associated with adverse prognosis and oxaliplatin resistance in HCC patients. Notably, treatment with the specific METTL3 inhibitor, STM2457, significantly improved the efficacy of oxaliplatin. These findings underscore the critical role of the METTL3/TRIM21/G6PD axis in driving oxaliplatin resistance and present a promising strategy to overcome chemoresistance in HCC.

2024-08-23 | GSE241802 | GEO

Response to oxaliplatin in CCD-18Co

Project description:We obtained the gene expression signature from oxaliplatin-treated fibroblasts and quantified the association of oxaliplatin-activated fibroblasts with disease progression in colorectal cancer.

2023-01-16 | GSE181020 | GEO

Differentially expressed genes between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples [Clinical samples-RNA-seq]

Project description:Differentially expressed genes between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples [Clinical samples-RNA-seq]

| PRJNA851088 | ENA

Differential ncRNAs of oxaliplatin-resistant versus parental HCT116 cells

Project description:Oxaliplatin resistance frequently leads to therapeutic failure in colorectal cancer (CRC). Increasing evidence has shown that noncoding RNAs (ncRNAs) play pivotal roles in chemoresistance of CRC. However, the roles and mechanisms of ncRNAs in oxaliplatin resistance are not well understood. In this study, to identify the ncRNAs induced by oxaliplatin, we profile the expression of ncRNAs in oxaliplatin-resistant HCT116 CRC cells (HCT116oxR) and parental HCT116 cells using next-generation sequencing technology.

2023-08-31 | GSE119603 | GEO

Difference of gene expression among DLD1, oxaliplatin resistant clones derived from DLD1, HCT116, and oxaliplatin resistant clones derived from HCT116

Project description:Gene expression between DLD1 and DLD1 derived oxaliplatin resistant clones (DLD/OHP1, DLD/OHP4, and DLD/OHP5) was assessed Gene expression between HCT116 and HCT116 derived oxaliplatin resistant clones (HCT/OHP1, HCT/OHP3, and HCT/OHP5) was assessed

2020-05-31 | GSE77932 | GEO

Oxaliplatin resistance is enhanced by saracatinib via upregulation of ABCG1 and Wnt/β-catenin signaling in hepatocellular carcinoma

Project description:Background:Oxaliplatin-resistant hepatocellular carcinoma (HCC) is associated with increased insulin-like growth factor 1 (IGF1) paracrine signaling, and the IGF1 receptor can be downregulated by inhibition of Src kinases. Therefore, we sought to determine whether Src inhibition and oxaliplatin treatment exerted synergistic effects on HCC cell lines. Methods: The antitumor effects of combined treatment with saracatinib and oxaliplatin on proliferation were evaluated in HCC cells as well as in saracatinib- and oxaliplatin-resistant HCC cell lines using cell viability assays, plate colony formation assays, and cell cycle distribution detection. RNA sequencing was used to explore the resistance mechanism, and the effects on ABCG1 and Wnt signaling in oxaliplatin resistance were confirmed. Results: Chemotherapy with oxaliplatin and saracatinib individually induced strong anti-HCC effects, while combined or sequential treatment of HCC cells with these two drugs exhibited reduced efficacy compared to treatment with the single drugs. Furthermore, treatment with saracatinib caused oxaliplatin resistance. RNA sequencing revealed 458 genes that were altered by treatment with saracatinib and oxaliplatin. Of these, the gene encoding the ATP-binding cassette transporter G1 ABCG1 and Wnt-associated genes were significantly upregulated. Upregulation of ABCG1 and oxaliplatin resistance were associated with activation of Wnt signaling. Interference with ABCG1 expression or inhibition of Wnt signaling resulted in reversal of the saracatinib-induced oxaliplatin resistance in the HCC cell lines. Conclusions: These studies demonstrated that combined or sequential chemotherapy with oxaliplatin and saracatinib reduced antitumor efficacy, and this antagonism was attributed to the upregulation of ABCG1 and activation of Wnt signaling pathway by saracatinib.

2019-03-30 | GSE129071 | GEO

SILAC-Based Quantitative Proteomics Identifies Multifactorial Mechanism of Oxaliplatin Resistance in Pancreatic Cancer Cells

Project description:Oxaliplatin is a commonly used chemotherapeutic drug for the treatment of pancreatic cancer. Understanding the cellular mechanisms of oxaliplatin resistance is important for developing new strategies to overcome drug resistance in pancreatic cancer. In this study, we performed a stable isotope labelling by amino acids in cell culture (SILAC)-based quantitative proteomics analysis of oxaliplatin-resistant and sensitive pancreatic cancer PANC-1 cells. We identified 107 proteins whose expression levels changed between oxaliplatin-resistant and sensitive cells, which were involved in multiple biological processes, including DNA repair, drug response, apoptotic signalling, and the type 1 interferon signalling pathway. Notably, myristoylated alanine-rich C-kinase substrate (MARCKS) and wntless homolog protein (WLS) were upregulated in oxaliplatin-resistant cells compared to sensitive cells, as confirmed by qRT-PCR and Western blot analysis. We further demonstrated the activation of AKT and β-catenin signalling (downstream targets of MARCKS and WLS, respectively) in oxaliplatin-resistant PANC-1 cells. Additionally, we show that the siRNA-mediated suppression of both MARCKS and WLS enhanced oxaliplatin sensitivity in oxaliplatin-resistant PANC-1 cells. Taken together, our results provide insights into multiple mechanisms of oxaliplatin resistance in pancreatic cancer cells and reveal that MARCKS and WLS might be involved in the chemotherapeutic resistance in pancreatic cancer.

2021-09-09 | PXD021251 | Pride

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data