Sarcoidosis + Follow-up 6 month after
Functional genomics and prognosis in sarcoidosis--the critical role of antigen presentation.
No sample metadata fields
View SamplesThis SuperSeries is composed of the subseries listed below.
Analysis of independent microarray datasets of renal biopsies identifies a robust transcript signature of acute allograft rejection.
Sex, Age, Subject
View SamplesSpecific early diagnosis of renal allograft rejection is gaining importance in the current trend to minimize and individualize immunosuppression. Gene expression analyses could contribute significantly by defining molecular Banff signatures. Several previous studies have applied transcriptomics to distinguish different classes of kidney biopsies. However, the heterogeneity of microarray platforms, clinical samples and data analysis methods complicates the identification of robust signatures for the different types and grades of rejection. To address these issues, a comparative meta-analysis was performed across five different microarray datasets of heterogeneous sample collections from two published clinical datasets and three own datasets including biopsies for clinical indications, protocol biopsies, as well as comparative samples from non-human primates (NHP). This work identified conserved gene expression signatures that can differentiate groups with different histopathological findings in both human and NHP, regardless of the technical platform used. The marker panels comprise genes that clearly support the biological changes known to be involved in allograft rejection. A characteristic dynamic expression change of genes associated with immune and kidney functions was observed across samples with different grades of CAN. In addition, differences between human and NHP rejection were essentially limited to genes reflecting interstitial fibrosis progression. This data set comprises all renal allograft biopsies for clinical indications from patients at Hpital Tenon, Paris (February 2003 until September 2004) and few respective patients from Hpital Bictre, Paris, Hpital Pellegrin, Bordeaux, and Hpital Dupuytren, Limoges, plus control normal kidney samples from Hpital Tenon, Paris, France (first batch).
Analysis of independent microarray datasets of renal biopsies identifies a robust transcript signature of acute allograft rejection.
Subject
View SamplesSpecific early diagnosis of renal allograft rejection is gaining importance in the current trend to minimize and individualize immunosuppression. Gene expression analyses could contribute significantly by defining molecular Banff signatures. Several previous studies have applied transcriptomics to distinguish different classes of kidney biopsies. However, the heterogeneity of microarray platforms, clinical samples and data analysis methods complicates the identification of robust signatures for the different types and grades of rejection. To address these issues, a comparative meta-analysis was performed across five different microarray datasets of heterogeneous sample collections from two published clinical datasets and three own datasets including biopsies for clinical indications, protocol biopsies, as well as comparative samples from non-human primates (NHP). This work identified conserved gene expression signatures that can differentiate groups with different histopathological findings in both human and NHP, regardless of the technical platform used. The marker panels comprise genes that clearly support the biological changes known to be involved in allograft rejection. A characteristic dynamic expression change of genes associated with immune and kidney functions was observed across samples with different grades of CAN. In addition, differences between human and NHP rejection were essentially limited to genes reflecting interstitial fibrosis progression. This data set comprises all renal allograft biopsies for clinical indications from patients at Hpital Tenon, Paris (February 2003 until September 2004) and few respective patients from Hpital Bictre, Paris, Hpital Pellegrin, Bordeaux, and Hpital Dupuytren, Limoges, plus control normal kidney samples from Hpital Tenon, Paris, France (first batch).
Analysis of independent microarray datasets of renal biopsies identifies a robust transcript signature of acute allograft rejection.
Sex, Age, Subject
View SamplesTopical corticosteroids and calcineurin inhibitors are well known treatments of atopic dermatitis (AD), but differ in their efficacy and side effects. A study in AD patients has demonstrated that betamethasone valerate (BM) though clinically more efficient impaired skin barrier repair in contrast to pimecrolimus. Objective: The present study elucidates the mode of action of topical BM and pimecrolimus cream in AD.
Gene expression is differently affected by pimecrolimus and betamethasone in lesional skin of atopic dermatitis.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies.
Cell line, Treatment
View SamplesThe polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types1. However, loss-of-function mutations in PRC2 components occur in a subset of haematopoietic malignancies, sug- gesting that this complex plays a dichotomous and poorly understood role in cancer2,3. Here we provide genomic, cellular, and mouse mod- elling data demonstrating that the polycomb group gene SUZ12 func- tions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mutations in NF1. NF1 encodes a Ras GTPase-activating protein (RasGAP) and its loss drives cancer by activating Ras4. We show that SUZ12 loss potentiates the effects of NF1 mutations by amplifying Ras-driven transcription through effects on chromatin. Importantly, however, SUZ12 inactivation also triggers an epigenetic switch that sensitizes these cancers to bromodomain inhib- itors. Collectively, these studies not only reveal an unexpected con- nection between the PRC2 complex, NF1 and Ras, but also identify a promising epigenetic-based therapeutic strategy that may be exploited for a variety of cancers.
PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies.
Cell line, Treatment
View SamplesIdentification of genetic/cytogenetic alterations and differentially expressed cellular genes in HPV16 E6, E7 and E6/E7 positive human foreskin keratinocytes
Complementation of non-tumorigenicity of HPV18-positive cervical carcinoma cells involves differential mRNA expression of cellular genes including potential tumor suppressor genes on chromosome 11q13.
No sample metadata fields
View SamplesIdentification of genes differentially expressed in tumorigenic compared to non-tumorigenic, HPV18 positive cells
Complementation of non-tumorigenicity of HPV18-positive cervical carcinoma cells involves differential mRNA expression of cellular genes including potential tumor suppressor genes on chromosome 11q13.
No sample metadata fields
View SamplesCoilin iCLIP data revealed 42 novel human snoRNAs of intronic origin. To validate their expression and estimate abundance of novel and annotated snoRNAs, we performed RNA-seq on polyA- and rRNA-depleted RNA isolated from HeLa cells. Results show that expression of novel snoRNAs is comparable to the previously annotated snoRNAs. Overall design: 1 replicate of RNA depleted of polyA and ribosomal RNA.
The coilin interactome identifies hundreds of small noncoding RNAs that traffic through Cajal bodies.
No sample metadata fields
View Samples