Filters
Technology
Platform
Homo sapiens
29 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Mononuclear phagocytes (MPs), including monocytes and macrophages, play complex roles in the pathogenesis of age-related macular degeneration (AMD). We aimed to perform global transcriptome analysis on monocytes from AMD patients to obtain additional insight to the role of MPs in AMD. Peripheral blood was taken from treatment-nave neovascular AMD (nvAMD) patients (n=14), and age-matched controls (n=15). Peripheral blood mononuclear cells (PBMCs) were separated and monocytes were isolated via negative selection. Gene expression was evaluated with Affymetrix Gene1.0 ST microarrays. Statistical/bioinformatics analysis was performed using open sourceware programs.
Publication Title
Transcriptome Analysis on Monocytes from Patients with Neovascular Age-Related Macular Degeneration.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples
SRP082964- Homo sapiens
- 5 Downloadable Samples
Illumina HiSeq 2500
Description
Osteosarcoma (OS) is one of the most aggressive bone malignancy. Sub-optimal therapy has irretrievably compromised chances of survival of OS patients for years. Also lack of extensive research on this rare disease has hindered its therapeutic development. Cisplatin (CDDP) is an integral part of current treatment regime for OS. However, despite the proven benefits of CDDP, acquisition of resistance impedes therapy. Also, the molecular effects post CDDP insult in OS cells is poorly understood. Hence, we characterized molecular alterations associated with CDDP-exposure and resistance in OS cells. Resistance to CDDP in OS cells was developed and deep sequencing of mRNA was performed. It depicted an altered transcriptomic signature of resistant cells with enrichment of pathways regulating proliferation. Overall, a significant up-regulation of coding-RNAs and down-regulation of non-coding-RNAs were obtained. Further, analysis of immediate effect of CDDP-shock showed an increase in autophagy and JNK signaling, acting as a pro-survival strategy. Regulatory connections between MAPK signaling and autophagy favoring survival under CDDP-shock was elucidated. Taken together, this is the first study portraying not only global transcriptomic alterations in resistant OS cells but also showing key molecular changes associated with CDDP-insult in OS cells. Our results can be better utilized for future therapeutic benefit. Overall design: We analyzed 5 samples, each being the representative of stages in the acquisition of chemoresistance. Control was the parental HOS cell line with which other comparisons are/will be made in future.
Publication Title
Transcriptomic analysis associated with reversal of cisplatin sensitivity in drug resistant osteosarcoma cells after a drug holiday.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 21 Downloadable Samples
- Affymetrix Clariom S Human array (clariomshuman)
Description
About 40% IBD patients treated with anti-TNF antibodies do not respond to therapy. Baseline biomarkers of response are therefore of interest. By combining computational deconvolution of gene expression and meta-analysis approaches we identified cellular biomarkers in tissue (validated in 2 cohorts by IHC of biopsies), and investigated associated gene biomarkers in blood. This dataset provides data from the validation cohort III (blood).
Publication Title
Cell-centred meta-analysis reveals baseline predictors of anti-TNFα non-response in biopsy and blood of patients with IBD.
Sample Metadata Fields
Disease, Disease stage, Treatment, Subject, Time
View Samples- Drosophila melanogaster
- 16 Downloadable Samples
- Illumina HiSeq 2000
Description
Goal: Identify genes that are differentially expressed in hyper-aggressive Bully line. We used wildtype Canton-S flies as control. We also explored the effect of developmental temperature on gene expression. Overall design: Total RNA were extracted from 6-day-old adult heads from Canton-S or Bully lines that were raised at 19C or 25C. A total of 4 samples were obtained. For each sample, 2 independent biological replicates were included.
Publication Title
Putative transmembrane transporter modulates higher-level aggression in <i>Drosophila</i>.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Homo sapiens
- 18 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip (gene symbol), Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Sorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Sorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Sorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Internal tandem duplication (ITD) of the fms-related tyrosine kinase-3 (FLT3) gene occurs in 30% acute myeloid leukemias (AML) and confers a poor prognosis. Thirteen relapsed or chemo-refractory FLT3-ITD+ AML patients were treated with sorafenib (200-400 mg twice daily). Twelve patients showed clearance or near clearance of bone marrow (BM) myeloblasts after 27 (range 2184) days with evidence of differentiation of leukemia cells. The sorafenib response was lost in most patients after 72 (range 54287) days but the FLT3 and downstream effectors remained suppressed. Four pairs patients (before sorafenib treatment and after sorafenib relapse), total eight samples from four patients at the two time-points were subjected to microarray analysis. Gene expression profiling showed that leukemia cells which have become sorafenib resistant expressed a number of genes including ALDH1A1, JAK3 and MMP15, whose functions were unknown in AML. NOD/SCID mice transplanted with leukemia cells from patients before and during sorafenib resistance recapitulated the clinical results. Both ITD and tyrosine kinase domain (TKD) mutations at D835 were identified in leukemia initiating cells (LIC) from samples before sorafenib treatment. LIC bearing the D835 mutant have expanded during sorafenib treatment and dominated during the subsequent clinical resistance. These results suggested that sorafenib have selected more aggressive sorafenib-resistant subclones carrying both FLT3-ITD and D835 mutations and might provide important leads to further improvement of treatment outcome with FLT3 inhibitors.
Publication Title
Sorafenib treatment of FLT3-ITD(+) acute myeloid leukemia: favorable initial outcome and mechanisms of subsequent nonresponsiveness associated with the emergence of a D835 mutation.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 49 Downloadable Samples
- Illumina HiSeq 2500
Description
We analyzed the genome-wide expression by RNA-seq of a yeast strain that expresses Cas9d and a guideRNA targeted to the GAL10 locus (called +116), which inhibits GAL10 ncRNA expression from the antisense strand. We compared this strain to a strain expressing a scrambled guideRNA. The goal was to examine the effects of ncRNA inhibition and to examine if CRISPR inhibition of gene expression has off-target effects. We find that CRISPR-mediated inhibtion of GAL10 ncRNA only significantly changes expression of transcripts at the GAL1-10 locus, showing that CRISPR is highly specific, and that GAL10 ncRNA only control genes at the GAL locus. Overall design: RNA-seq of 2 strains with CRISPR scrambled and 2 strains with CRISPR +116, the latter of which inhibits GAL10 ncRNA
Publication Title
Single-Molecule Imaging Reveals a Switch between Spurious and Functional ncRNA Transcription.
Sample Metadata Fields
Cell line, Subject
View Samples