We profiled human DLBCL tumor samples (FF and FFPE matched pairs) to identify the transcripts which are less prone to degradation in FFPE
CD40 pathway activation status predicts response to CD40 therapy in diffuse large B cell lymphoma.
Specimen part
View SamplesWe profiled human DLBCL patient samples to discover predictive biomarkers
CD40 pathway activation status predicts response to CD40 therapy in diffuse large B cell lymphoma.
No sample metadata fields
View SamplesGene expression patterns were assessed in normal human bronchial epithelial (NHBE) cells exposed to cigarette smoke from a reference cigarette (2R4F, University of Kentucky) and a typical American brand of "light" cigarettes ("Lights") in order to develop a better understanding of the genomic impact of tobacco exposure, which can ultimately define biomarkers that discriminate tobacco-related effects and outcomes in a clinical setting. NHBE cells were treated with whole cigarette smoke for 15 minutes and alterations to the transcriptome assessed at 2, 4, 8 and 24 hours post-exposure using high-density oligonucleotide microarrays.
Cigarette smoke induces endoplasmic reticulum stress and the unfolded protein response in normal and malignant human lung cells.
No sample metadata fields
View SamplesGene expression patterns were assessed in normal human bronchial epithelial (NHBE) cells exposed to cigarette smoke (CS) from a typical "full flavor" American brand of cigarettes in order to develop a better understanding of the genomic impact of tobacco exposure, which can ultimately define biomarkers that discriminate tobacco-related effects and outcomes in a clinical setting. NHBE cells were treated with CS for 15 minutes and alterations to the transcriptome assessed at 1,2,4 and 24 hours post-CS-exposure using high-density oligonucleotide microarrays.
Cigarette smoke induces endoplasmic reticulum stress and the unfolded protein response in normal and malignant human lung cells.
No sample metadata fields
View SamplesCerebral malaria is a severe multifactorial condition associated with the interaction of high numbers of infected erythrocytes to human brain endothelium without invasion into the brain. The result is coma and seizures with death in more than 20% of cases. Because the brain endothelium is at the interface of these processes, we investigated the global gene responses of human brain endothelium after the interaction with Plasmodium falciparuminfected erythrocytes with either high- or low-binding phenotypes. The most significantly up-regulated transcripts were found in gene ontology groups comprising the immune response, apoptosis and antiapoptosis, inflammatory response, cell-cell signaling, and signal transduction and nuclear factor B (NF-B) activation cascade. The proinflammatory NF-B pathway was central to the regulation of the P falciparummodulated endothelium transcriptome. The proinflammatory molecules, for example, CCL20, CXCL1, CXCL2, IL-6, and IL-8, were increased more than 100-fold, suggesting an important role of blood-brain barrier (BBB) endothelium in the innate defense during P falciparuminfected erythrocyte (Pf-IRBC) sequestration. However, some of these diffusible molecules could have reversible effects on brain tissue and thus on neurologic function. The inflammatory pathways were validated by direct measurement of proteins in brain endothelial supernatants. This study delineates the strong inflammatory component of human brain endothelium contributing to cerebral malaria.
Plasmodium falciparum-infected erythrocytes induce NF-kappaB regulated inflammatory pathways in human cerebral endothelium.
No sample metadata fields
View SamplesmRNA cancer cell line profiles
TRPS1 targeting by miR-221/222 promotes the epithelial-to-mesenchymal transition in breast cancer.
No sample metadata fields
View SamplesAnalysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222
TRPS1 targeting by miR-221/222 promotes the epithelial-to-mesenchymal transition in breast cancer.
Cell line, Treatment
View SamplesTo establish effective multitargeted KRAS pathway therapy, we analyzed mediators of acquired resistance to chronic momelotinib and MEK inhibitor exposure in A549 cells. Since inhibitor resistance was completely reversible after drug withdrawal for several passages, suggesting epigenetic reprogramming, we investigated whole mRNA expression profiles in A549, momelotinib and selumetinib resistant (MSR)-A549 cells and MSR-A549 cells following drug withdrawal for 10 days. In parallel, we also examined mRNA expression profiles of MSR-A549 cells treated with the BET inhibitor JQ1, to identify specific targets regulated by H3K27 acetylation. Overall design: mRNA profile of MSR-A549 cells with or without JQ1 treatment.
Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS.
Subject
View SamplesWe assessed genome-wide expression of available pretreatment specimens from CLL patients enrolled in REACH, a study of fludarabine and cyclophosphamide FC or R-FC (addition of rituximab to FC) in relapsed CLL, to understand the disease heterogeneity and explore genes that may be prognostic or predictive of benefit from R-FC treatment. REACH (NCT00090051) was registered at www.clinicaltrials.gov.
PTK2 expression and immunochemotherapy outcome in chronic lymphocytic leukemia.
Specimen part, Disease stage, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The mutation spectrum revealed by paired genome sequences from a lung cancer patient.
Specimen part
View Samples