Introduction: Mechanisms that contribute to the pathogenesis of liver damage caused by hepatitis C virus (HCV) are not fully understood. Our previous work on liver biopsies from chronic HCV patients has shown modulation of the expression of certain cell cycle proteins indicating HCV-induced modifications of cell cycle events. We therefore hypothesize that HCV infection disrupts normal regulation of cell cycle that contributes to disease progression. Objective: To identify molecular disruptions during the course of HCV-associated disease progression, using liver biopsy specimens of chronic hepatitis C patients. Methods: Liver biopsy samples classified on histological basis as early (fibrosis stage 0-1) or advanced (fibrosis stage 3-4) disease stage were studied using oligonucleotide array ( HG U133 Plus 2.0, Affymetrix GeneChip System). For comparison, liver specimens from patients with non-viral hepatitis were also analyzed by microarray. Expression data was analyzed using Genespring (GX 7.2) and Ingenuity Pathway analysis (3.0). The differential expression of selected cell cycle genes (cyclin D2, KPNA2, HERC5 and Bcl-2) identified after microarray analysis was confirmed by quantitative real-time RT-PCR. Results: Microarray analysis revealed two-fold or greater transcriptional change in 792 genes of the total 38,500 known human genes in HCV-advance disease stage (HCV-A) as compared to HCV-early disease stage (HCV-E). Most of the genes have a defined role in immune response, extracellular matrix and cell cycle and apoptosis.
Gene profiling of early and advanced liver disease in chronic hepatitis C patients.
Specimen part, Disease, Disease stageView Samples
We have performed gene expression microarray analysis to profile transcriptomic signatures affected by EtOH in human dental pulp stem cells
Genome-wide transcriptomic alterations induced by ethanol treatment in human dental pulp stem cells (DPSCs).
Specimen partView Samples
We have performed gene expression microarry analysis to profile molecular alterations in normal human oral keratinocytes that are induced by EtOH and/or nicotine. Our goal is to examine molecular signatures that are dysregulated by EtOH or nicotine and define the effects of co-use of alcohol and nicotine on normal oral epithelial cells and potentially on carcinogenesis.
Gene expression signatures affected by ethanol and/or nicotine in normal human normal oral keratinocytes (NHOKs).
Specimen partView Samples
Comparison of gene expression signatures in undifferentiated hESCs against differentiated embryoid bodies to identify key signatures defining self-renewal of hESCs.
Discovery of consensus gene signature and intermodular connectivity defining self-renewal of human embryonic stem cells.
Specimen part, Cell lineView Samples
We studied alcohol's effect on human embryonic stem cell line, H9. Our main objective was to delineate the molecular mechanisms that are involved in changing the differentiation potential of hESCs.
Gene expression signatures affected by alcohol-induced DNA methylomic deregulation in human embryonic stem cells.
Cell lineView Samples
To investigate the role of RPRD1B in regulating gene expression in NIH3T3 cells. Overall design: Examination of mRNA expression levels in cells with control or RPRD1B knockdown NIH3T3 cells
Crosstalk between RNA Pol II C-Terminal Domain Acetylation and Phosphorylation via RPRD Proteins.
Specimen part, Cell line, Treatment, SubjectView Samples
We performed a 3' RACE of a novel HIV RNA TAR-gag in order to determine the sequence of the RNA at the 3' end. Our data had shown that TAR-gag was potentially a noncoding RNA and our hypothesis was that TAR-gag ended somewhere prior to the end of the gag region of the HIV genome. The 3' RACE experiment showed that TAR-gag actually consists of four different RNA clusters, the longest of which ends at 615 bases from the transcription start site; this is in the middle of the p17 region of the gag gene. In addition, we sequenced all host RNAs in the EVs. Overall design: RNA from J1.1 and U1 exosomes was isolated and converted to cDNA. Sequencing libraries of the cDNA were made and a 3' RACE was perforemed to determine how long TAR-gag RNA is. Please note that the clustering analysis (published in PMID 28536264) was done only on the unfragmented samples (i.e. *-U samples).
An Omics Approach to Extracellular Vesicles from HIV-1 Infected Cells.
Specimen part, SubjectView Samples
Breast cancer is a major health problem affecting millions of women worldwide. Over 200,000 new cases are diagnosed annually in the USA, with approximately 40,000 of these cases resulting in death. HER2-positive (HER2+) breast tumors, representing 20â€“30 % of early-stage breast cancer diagnoses, are characterized by the amplification of the HER2 gene. However, the critical genes and pathways that become affected by HER2 amplification in humans are yet to be specifically identified. Furthermore, it is yet to be determined if HER2 amplification also affects the expression of long intervening non-coding (linc)RNAs, which are involved in the epigenetic regulation of gene expression. We examined changes in gene expression by next generation RNA sequencing in human tumors pre- and post- HER2 inhibition by trastuzumab in vivo, and changes in gene expression in response to HER2 knock down in cell culture models. We integrated our results with gene expression analysis of HER2+ tumors vs matched normal tissue from The Cancer Genome Atlas. The integrative analyses of these datasets led to the identification of a small set of mRNAs, and the associated biological pathways that become deregulated by HER2 amplification. Furthermore, our analyses identified three lincRNAs that become deregulated in response to HER2 amplification both in vitro and in vivo. Our results should provide the foundation for functional studies of these candidate mRNAs and lincRNAs to further our understanding of how HER2 amplification results in tumorigenesis. Also, the identified lincRNAs could potentially open the door for future RNA-based biomarkers and therapeutics in HER2+ breast cancer. Overall design: We compared changes in gene expression of both mRNAs and lincRNAs in BT474 cells that are treated with HER2 siRNAs vs cells treated with negative control siRNAs by RNA-seq.
Integrative transcriptome-wide analyses reveal critical HER2-regulated mRNAs and lincRNAs in HER2+ breast cancer.
No sample metadata fieldsView Samples
To get more insight in cause and consequences of proteinuria, we studied glomerular gene expression patterns before and after the onset of increased urinary albumin excretion in a proteinuric rat strain.
Increased dynamin expression precedes proteinuria in glomerular disease.
No sample metadata fieldsView Samples