Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13723434.fastq.gz | Fastqsanger.gz | |||
| SRR13723435.fastq.gz | Fastqsanger.gz |
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Project description:Huntsman Cancer Institute (HCI)-001 patient-derived organoids (PDOs) and HCI-002 PDOs obtained from Huntsman Cancer Institute, University of Utah (Nat Med. 2011 Oct 23;17(11):1514-20). Purpose: The goals of this study is to identify molecular pathways and genes that are involved in the treatment responsiveness of breast cancer PDOs. Methods: mRNA profiles of HCI-001 and HCI-002 PDOs were generated by Illumina NovaSeq 6000 platform for paired-end sequencing, 150-bp read length, for about 20 million raw reads per sample. RNA sequencing FASTQ files were processed with HISAT2 aligner in default mode with the Ensembl human transcriptome annotation (Build version GRCh38 and transcript annotation GRCh38.89). Differential gene expression analysis was performed using DESeq2 software. Enrichment analysis was performed using ClusterProfiler software. Results: We mapped about 20 million sequence reads per sample to the human genome (build HG38) in the RNAs of HCI-001 and HCI-002 PDOs treated with paclitaxel or vehicle. We used a minimum expression cut-off of 1 FPKM in order to exclude low-levels genes and the RNA-seq data confirmed the difference expression of 67 known apoptosis-regulatory genes in treatment-sensitive PDOs (HCI-002) compare to treatment-resistant PDOs (HCI-001). Conclusions: This study identified apoptosis-regulatory genes that are differentially induced or represeed in treatment-sensitive PDOs (HCI-002) or treatment-resistant PDOs (HCI-001).
2021-09-09 | GSE183477 | GEO
Project description:We examined the effects of ICG-001 on gene expression in Mel202 uveal melanoma (UM) cells. ICG-001 exerted strong antiproliferative activity against UM cells, leading to cell cycle arrest, apoptosis, and inhibition of migration. Global gene expression profiling revealed strong suppression of genes associated with cell cycle proliferation, DNA replication, and G1/S transition. Gene set enrichment analysis revealed that ICG-001 suppressed Wnt, mTOR, and MAPK signaling. Strikingly, ICG-001 suppressed the expression of genes associated with UM aggressiveness, including CDH1, CITED1, EMP1, EMP3, SDCBP, and SPARC. Notably, the transcriptomic footprint of ICG-001, when applied to a UM patient dataset, was associated with better clinical outcome. Lastly, ICG-001 exerted anticancer activity against a UM tumor xenograft in mice.
2020-04-28 | GSE149417 | GEO
Project description:By screening a target-focused Wnt-sgnaling small compound library we identified the Wnt-modulator ICG-001 as inihibitory for activating the mitochondrial fission protein Drp1. To explore how ICG-001 might act we undertook gene expression profiling in iCG-001 treated primary macrophages.
2018-01-12 | GSE102117 | GEO
Project description:To inhibitors for ADAR1 and a strong rationale for the development of ADAR1 p150 inhibitors for cancer immunotherapy Here, we describe AVA-ADR-001, a potential first-in-class small molecule inhibitor of ADAR1 p150 targeting the Z alpha domain. AVA-ADR-001 binds specifically to the Z alpha domain of ADAR1 p150 as confirmed by fluorescence spectroscopy and showed significant interferon induction in THP1 macrophages, which have high ADAR1 p150 expression compared with monocytes. Proteomics and transcriptomics analysis revealed significant upregulation of interferon signaling upon treatment with AVA-ADR -001. Interestingly, activation of interferon signaling resulted in AVA-ADR-001 induced cell killing in ADAR1-independent cell lines. In addition, treatment with AVA-ADR -001 resulted in significant activation of PKR, which may explain the decreased cell proliferation. Finally, AVA-ADR-001 showed superior anti-tumor efficacy compared to anti-PD1 in an in vivo tumor efficacy study and has a moderately synergistic effect when combined. Overall, this study reveals that ADAR1 p150 inhibition by AVA-ADR-001 exerts a multipronged impact on anti-tumor efficacy mediated by immune cells, accumulation of interferons and activation of PKR, resulting in protein translation inhibition and cell proliferation arrest.
2023-04-17 | GSE229503 | GEO
Project description:RRx-001 (also known as ABDNAZ, 1-bromoacetyl-3,3-dinitroazetidine) is a novel aerospace-derived compound currently under investigation in several ongoing Phase II studies. In a Phase I trial, it demonstrated anti-cancer activity and evidence of resensitization to formerly effective therapies in heavily pre-treated patients with relapsed/refractory solid tumors. With a pharmacologically unprecedented dinitroazetidine scaffold, RRx-001 generates reactive oxygen and nitrogen species (ROS and RNS) and nitric oxide (NO), elicits changes in intracellular redox status, modulates tumor blood flow, hypoxia and vascular function and triggers apoptosis in cancer cells. Here, the effect of RRx-001 on the epigenome of SCC VII cancer cells was investigated. RRx-001 at 0.5 and 2 μM significantly decreased global DNA methylation, i.e., 5-methylcytosine levels, in SCC VII cells determined by analysis with an enzyme-linked immunosorbent assay (ELISA). Consistently, 0.5-5 μM RRx-001 significantly decreased Dnmt1 and Dnmt3a protein expression determined using Western blot in a dose- and time-dependent manner. In addition, global methylation profiling identified differentially methylated genes in SCC VII cells treated with 0.5, 2, and 5 μM RRx-001 compared to control cells. Twenty-three target sites were hypomethylated and 22 hypermethylated by >10% in the presence of at least two different concentrations of RRx-001. Moreover, RRx-001 at 2 μM significantly increased global acetylated histone H3 and H4 levels in SCC VII cells after 24 hour treatment determined by a fluorometric assay, suggesting that RRx-001 regulates global acetylation in cancer cells. These results demonstrate that, in contrast to the traditional “one drug one target” paradigm, RRx-001 has multi(epi)target features, which contribute to its anti-cancer activity and may rationalize the resensitization to previously effective therapies observed in clinical trials and serve as a unifying mechanism for its anticancer activity.
2016-12-31 | GSE74797 | GEO
Project description:BACKGROUND: Preclinical studies have demonstrated that pharmacological mobilization and recruitment of endogenous bone marrow stem cells and immunoregulatory cells by a combination of plerixafor and low-dose tacrolimus (MRG-001) improves wound healing, promotes tissue regeneration and prevents allograft rejection. This first‐in‐human phase I dose‐escalation study evaluates the safety, tolerability, pharmacokinetics and pharmacodynamics of MRG-001, a novel fixed-dose combination drug. METHODS: In this Phase 1, double‐blind, randomized, placebo-controlled study, multiple ascending dose (MAD) cohorts are randomized to receive MRG-001 containing up to 0.02 mL/kg (plerixafor 24 mg/mL and tacrolimus 0.5 mg/mL) or saline placebo, subcutaneously every other day (SC, QAD) for 5 days (ClinicalTrials.gov: NCT04646603)The primary outcome is safety and tolerability. Safety and functional assessments are performed throughout the study. Blood samples are collected to evaluate systemic exposure. Fluorescence-activated cell sorting analysis and RNA expression of peripheral blood mononuclear cells (PBMCs) are used to evaluate the pharmacodynamics. RESULTS: Fourteen subjects received MRG-001 and 7 received a placebo. MRG-001 is safe and well-tolerated over the selected dose range. No deaths or severe adverse events are reported. There are no clinically significant laboratory changes after MRG-001 administration, apart from the predicted generalized leukocytosis. The intermediate dose group (0.01 mL/kg) showed the most significant white blood cell mobilization over time and increased by 2-4 fold from baseline and returned to baseline levels prior to the next injection. Circulating immune cells including FOXP3+ regulatory T cells and hematopoietic stem cells (CD45IntCD34+) increased significantly after MRG-001 injection. PBMC RNA sequencing and gene set enrichment analysis revealeds 31 down-regulated pathways in the intermediate dose MRG-001 group compared to no changes in the placebo group. CONCLUSION: MRG-001 is safe and well-tolerated across the full dose ranges tested. MRG-001 may be a clinically useful therapy for immunoregulation and tissue regeneration. A Phase II trial to treat severely and critically ill COVID-19 patients with MRG-001 has been initiated (NCT04646603) and a second phase II trial will explore the potential of MRG-001 to accelerate wound healing (NCT05844527),
2023-07-24 | GSE237965 | GEO
Project description:In pediatric glioma cell lines, treatment with ICG-001 had no inhibitory effect on canonical Wnt-target genes but induced significant up regulation of various known β-catenin target genes in both cell lines and top 20 GO-annotations of down-regulated genes by ICG-001 were associated with biosynthetic and metabolic processes and cell cycle division processes. Pediatric cell lines were treated with ICG-001 or DMSO for 48h
2016-06-14 | E-GEOD-83266 | biostudies-arrayexpress
Project description:SWATH data for mouse, sample 001-004 is control, sample 005-008 is model (LPS-induced peritonitis), and sample 009-012 is maple syrup extract-treated (LPS induction plus maple syrup extract administration). For more detailed information, please contact Dr.Chang Liu (hichang813@uri.edu)
2023-06-24 | MSV000092259 | MassIVE
Project description:SWATH data for mouse, sample 001-004 is control, sample 005-008 is model (LPS-induced peritonitis), and sample 009-012 is maple syrup extract-treated (LPS induction plus maple syrup extract administration). For more detailed information, please contact Dr.Chang Liu (hichang813@uri.edu)
2023-06-13 | MSV000092153 | MassIVE