Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Phase Ib/IIa Study of CR6086 in Combination With Balstilimab in pMMR-MSS Metastatic Colorectal Cancer Patients

ABSTRACT: This Phase Ib/IIa study has been designed according to a 3+3 dose escalation/dose expansion design. A dose expansion will be conducted at both the intermediate and high dose levels, if tolerated, with the purpose of generating additional and more robust safety and preliminary efficacy data. No control arm was included, as the target patient population of this study consists of patients in whom the overall survival is less than 6 months and treatment options are very limited and often poorly tolerated, making unlikely that the study results can be significantly biased.

DISEASE(S): Solid Tumor,Refractory Metastatic Colorectal Cancer,Colorectal Neoplasms,Mismatch Repair Protein Proficient,Metastatic Microsatellite-stable Colorectal Cancer

PROVIDER: 2402028 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Proteomics Reveals the Potential Mechanism of Tanshinone IIA Promoting the Ex Vivo Expansion of Human Bone Marrow Mesenchymal Stem Cells.

Project description:Bone marrow mesenchymal stem cells (BMSCs) is a promising cell type for tissue engineering, however, the application of BMSCs are largely hampered for the limited number harvested from bone marrow cells. The methods or strategies that focused on promoting the capacity of BMSCs expansion ex vivo become more and more important. Tanshinone IIA (Tan IIA), the main active components of Danshen, has been found to promote BMSCs proliferation, but the underlying mechanism is still unclear. This present work employed biological techniques combined with quantitative proteome analysis to explore the effect and underlying mechanism of Tan IIA on the ex vivo expansion capacity of BMSCs from human. The results showed that a total of 84 differentially expressed proteins were annotated and among them 51 upregulated proteins and 33 downregulated proteins were identified. Besides, Tan IIA could promote hBMSCs proliferation by regulating the progression of S phase via increasing the release of fibroblast growth factor 2 (FGF2), FGF-mediated PI3K/AKT signaling pathways may play an important role in Tan IIA’s effect on hBMSCs expansion. The results of this study may provide further evidence about the potential of Tan IIA to be used for the research of hBMSCs therapies.

2022-11-28 | PXD036093 | Pride

Transcriptomic analysis of myosin IIa-deficient B cells

Project description:Myosin IIa-deficient follicular B cells have a hyperactivated phenotype. To identify what pathways are regulated by myosin IIa, we performed RNA-seq of coding RNA on flow cytometry sorted follicular B cells from CD23Cre+Myh9fl/fl and CD23Cre+Myh9wt/fl mice.

2018-04-14 | GSE113114 | GEO

Expression data from five human leukemia cell lines treated with DMSO or tanshinone IIA

Project description:Tanshinone IIA (Tan IIA) is a diterpene quinone extracted from the root of Salvia miltiorrhiza, a Chinese traditional herb. Although previous studies have reported the anti-tumor effects of Tan IIA on various human cancer cells, the underlying mechanisms are not clear. We used microarrays to detail the global programme of gene expression underlying Tan IIA's apoptotic effects on leukemia cells and identified significantly differentially expressed genes (SDEGs). Five human leukemia cell lines were selected for RNA extraction and hybridization on Affymetrix microarrays.To identify genes that are related to Tan IIA sensitivities, we carried out expression profiling on five cell lines.The sample named HL60, MEG01, MOLT,THP1 and U937_control were treated with DMSO. U937 cell line was selected with Tan IIA treatment for 12 h and 24 h, respectively.

2011-11-03 | E-GEOD-33358 | biostudies-arrayexpress

Lacticaseibacillus paracasei strain:IIA

Project description:Lacticaseibacillus paracasei strain:IIA Genome sequencing

| PRJNA790635 | ENA

The interaction of secreted phospholipase A2-IIA with the microbiota alters its lipidome and promotes inflammation

Project description:Secreted phospholipase A2-IIA (sPLA2-IIA) hydrolyzes phospholipids to liberate lysophospholipids and fatty acids. Given its poor activity toward eukaryotic cell membranes, its role in the generation of proinflammatory lipid mediators is unclear. Conversely, sPLA2-IIA efficiently hydrolyzes bacterial membranes. Here, we show that sPLA2-IIA impacts on the immune system by acting on the intestinal microbial flora. Using mice overexpressing transgene-driven human sPLA2-IIA, we found that the intestinal microbiota was critical for both induction of an immune phenotype and promotion of inflammatory arthritis. The expression of sPLA2-IIA led to alterations of the intestinal microbiota composition, but housing in a more stringent pathogen-free facility revealed that its expression could affect the immune system in the absence of changes to the composition of this flora. In contrast, untargeted lipidomic analysis focusing on bacteria-derived lipid mediators revealed that sPLA2-IIA could profoundly alter the fecal lipidome. The data suggest that a singular protein, sPLA2-IIA, produces systemic effects on the immune system through its activity on the microbiota and its lipidome.

2021-11-25 | GSE189441 | GEO

Effect of group IIA phospholipase A2 deletion on gene expression in the small intestine

Project description:Besides promoting inflammation by mobilizing lipid mediators, secreted phospholipase A2 group IIA (sPLA2-IIA) prevents bacterial infection by degrading bacterial membranes. Here we show that despite the restricted intestinal expression of sPLA2-IIA in BALB/c mice, its genetic deletion leads to amelioration of cancer and exacerbation of psoriasis in distal skin. Intestinal expression of sPLA2-IIA is reduced after antibiotics treatment or under germ-free conditions, suggesting its upregulation by gut microbiota. Metagenome, transcriptome and metabolome analyses have revealed that sPLA2-IIA deficiency alters the gut microbiota, accompanied by notable changes in the intestinal expression of genes related to immunity and metabolism as well as the levels of various blood metabolites and fecal bacterial lipids, suggesting that sPLA2-IIA contributes to shaping of the gut microbiota. The skin phenotypes in Pla2g2a–/– mice are lost when they are co-housed with littermate wild-type mice, resulting in mixing of the microbiota between the genotypes, or when they are housed in a more stringent pathogen-free facility, where Pla2g2a expression in wild-type mice is low and the gut microbial compositions in both genotypes are nearly identical. Thus, our results highlight a new aspect of sPLA2-IIA as a modulator of gut microbiota, perturbation of which affects distal skin responses.

2022-01-01 | GSE182283 | GEO

Expression data from five human leukemia cell lines treated with DMSO or tanshinone IIA

2011-11-03 | GSE33358 | GEO

Selective Class IIa HDAC inhibitor alters gene expression in NRVMs

Project description:Expression profiling of neonatl rat ventricular cardiomyocytes (NRVMs) upon the treatement of Class IIa HDAC inhibitor

2019-04-23 | GSE130150 | GEO

Genome-wide Analysis of Class IIa Histone Deacetylase Regulation of Hepatic Gluconeogenesis

Project description:Analysis of Class II Histone Deacetylase (HDAC) regulation of hepatic gluconeogenesis at the gene expression level. We show that in liver, Class IIa HDACs (HDAC4, 5, and 7) are all phosphorylated and excluded from the nucleus by AMPK family kinases. In response to the fasting hormone glucagon, Class IIa HDACs rapidly translocate to the nucleus where they directly bind to the promoters of gluconeogenic enzymes such as G6Pase. In turn, HDAC4/5 mediate the acute transcriptional induction of these genes via deacetylation and activation of Foxo family transcription factors. Loss of Class IIa HDACs in the murine liver results in inhibition of FOXO target genes and lowers blood glucose, resulting in increased glycogen storage. Total RNA obtained from primary hepatocytes infected with shGFP or shHDAC4 & 5 subjected to 2 or 4 hours treatment with DMSO or forskolin.

2011-09-08 | E-GEOD-20979 | biostudies-arrayexpress

Genome-wide Analysis of Class IIa Histone Deacetylase Regulation of Hepatic Gluconeogenesis

2011-09-09 | GSE20979 | GEO