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SRP132285
Homo sapiens
16 Downloadable Samples
Ion Torrent Proton
Description
Pulmonary sarcomatoid carcinomas (PSCs) are rare and aggressive histological types of non-small cell lung cancer (NSCLC) with a median overall survival of about 9-12 months. In detail, PSCs comprise five different histological subtypes: pleomorphic carcinoma (PLC), giant cell carcinoma (GCC), spindle cell carcinoma (SCC), carcinosarcoma (CS) and pulmonary blastoma (PB). Preoperative pathological diagnosis may fail to identify these tumors and therapeutic options are still limited. PSCs have been scarcely characterized from a molecular point of view because of their rarity, and to date no specific markers have been found for PSCs in comparison with other NSCLC types. In this study a highly sensitive amplicon based whole transcriptome quantification analysis was performed, using the Ion AmpliSeq Transcriptome Human Gene Expression Kit (Life Technologies) on a selected series of 14 PSCs (1 PB, 4 CS, 2 SCC, 2 GCC, 5 PLC) and 3 samples of normal lung parenchyma. PSCs expression data were then compared with transcriptome data of lung adenocarcinoma and squamous cell carcinoma available on The Cancer Genome Atlas database. Thirty-eight genes specifically deregulated in PSC samples were identified. Among these, IGJ and SLMAP were validated by immunohistochemistry on an independent cohort (30 PSCs, 31 lung adenocarcinoma and 31 squamous cell carcinoma cases). Furthermore, a pathway enrichment analysis, performed on differentially expressed genes, revealed that FOXO signalling and Fanconi Anemia pathways, playing a pivotal role in cancer development and progression, are enriched in PSC tumors. The description of peculiar molecular profiles besides increasing our knowledge on PSCs biology may suggest new diagnostic and therapeutic strategies. Overall design: Whole transcriptome targeted gene quantification analysis was perfomed on a selected series of 14 pulmonary sarcomatoid carcinomas (1 pulmonary blastoma, 4 carcinosarcomas, 2 spindle cell carcinomas, 2 giant cell carcinomas, 5 pleomorphic carcinomas) and 3 samples of normal lung parenchyma, using the Ion AmpliSeq Transcriptome Human Gene Expression Kit ( Life Technologies).
Publication Title
Whole transcriptome targeted gene quantification provides new insights on pulmonary sarcomatoid carcinomas.
Sample Metadata Fields
Sex, Age, Specimen part, Subject
View Samples- Homo sapiens
- 11 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
Inflammatory mediators play a role in the pathogenesis/progression of chronic heart failure (CHF). The aim of the present study was to identify diagnostic/prognostic markers and gene expression profiles of CHF vs control.
Publication Title
Gene expression profiles in peripheral blood mononuclear cells of chronic heart failure patients.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus, Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Cancer exosomes perform cell-independent microRNA biogenesis and promote tumorigenesis.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 54 Downloadable Samples
- Illumina HiSeq 2500
Description
Human lymphoid tissues harbor, in addition to CD56bright and CD56dim natural killer (NK) cells, a third NK cell population: CD69+CXCR6+ lymphoid tissue (lt)NK cells. The function and development of ltNK cells remain poorly understood. In this study we performed RNA sequencing on the CD56bright and CD56dim NK cells (from bone marrow and blood), and the ltNK cells (from bone marrow). In addition, the blood derived CD56dim, and bone marrow derived ltNK cells were further subdivided into a NKG2A+ and NKG2A- fraction. Paired blood and bone marrow samples of 4 healthy donors were included. When comparing the NKG2A fractions, only 3 genes (of 9382 genes included) had a significantly differential expression. Therefore, we pooled the expression data proportionally from the NKG2A+ and NKG2A- fractions in subsequent analyses. In ltNK cells, 1353 genes were differentially expressed compared to circulating NK cells. Several molecules involved in migration were downregulated in ltNK cells: S1PR1, SELPLG and CD62L. By flow cytometry we confirmed that the expression profile of adhesion molecules (CD49e-, CD29low, CD81high, CD62L-, CD11c-) and transcription factors (Eomeshigh, Tbetlow) of ltNK cells differed from their circulating counterparts. LtNK cells were characterized by enhanced expression of inhibitory receptors TIGIT and CD96 and low expression of DNAM1 and cytolytic molecules (GZMB, GZMH, GNLY). Their proliferative capacity was reduced compared to the circulating NK cells. By performing gene set enrichment analysis we identified DUSP6 and EGR2 as potential regulators of the ltNK cell transcriptome. Remarkably, comparison of the ltNK cell transcriptome to the published human spleen-resident memory CD8+ T (Trm) cell transcriptome revealed an overlapping gene signature. Moreover, the phenotypic profile of ltNK cells resembled that of CD8+ Trm cells in bone marrow. Together, we provide a comprehensive molecular framework of the conventional CD56bright and CD56dim NK cells as well as the tissue-resident ltNK cells and provide a core gene signature which might be involved in promoting tissue-residency. Overall design: mRNA sequencing of NK cell populations isolated from blood: CD56bright, NKG2A+ CD56dim and NKG2A- CD56dim, and bone marrow: CD56bright, CD56dim, NKG2A+ ltNK, and NKG2A- ltNK. Each sample has 4 biological replicates.
Publication Title
Human Bone Marrow-Resident Natural Killer Cells Have a Unique Transcriptional Profile and Resemble Resident Memory CD8<sup>+</sup> T Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 29 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Effect of the overexpression of the oncogenic form of the Vav2 protein in the NIH3T3 cell line under serum deprivation conditions. oncovav2-transformed NIH3T3 cells grown in serum-deprived medium (Vav2SD) are compared to the parental NIH3T3 controls under the same growth conditions (ContSD). Vav2SD cells are also compared to the oncovav2-transformed NIH3T3 cells growing exponentially and the NIH3T3 growing exponentially.
Publication Title
Microarray analysis of gene expression with age in individual nematodes.
Sample Metadata Fields
Cell line
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Drosophila males double transcription of their single X chromosome to equalize X-linked gene expression with females, which carry two X chromosomes. Increased transcription requires the Male-Specific Lethal (MSL) complex. One of the primary functions of the MSL complex is thought to be enrichment of H4Ac16 on the male X chromosome, a modification linked to elevated transcription. The roX1 and roX2 RNAs are essential but redundant components of the MSL complex. Simultaneous removal of both roX RNAs reduces MSL X-localization and leads to ectopic binding of these proteins at autosomal sites and to the chromocenter. Some H4Ac16 accumulates at these ectopic sites in roX1- roX2- males, suggesting the possibility of increased expression. The global effect of roX mutations on gene expression was measured by microarray analysis. We found that expression of the X chromosome was decreased by 26% in roX1- roX2- male larvae, supporting the involvement of roX RNAs in the up-regulation of X-linked genes. This finding is broadly comparable to reports of reduced X chromosome expression following msl2 RNAi knockdown in S2 cells. In spite of strong MSL binding and H4Ac16 accumulation at autosomal sites in roX1- roX2- males, enhanced gene expression could not be detected at these sites by microarray analysis or reverse northern blotting. Thus, failure to compensate X-linked genes, rather than inappropriate up-regulation of autosomal genes at ectopic sites of MSL binding, appears to cause male lethality upon loss of roX RNAs.
Publication Title
roX RNAs are required for increased expression of X-linked genes in Drosophila melanogaster males.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
let-7c and miR-294 were transfected into Dgcr8 -/- miRNA deficient ES cells and RNA was harvested after 12 hours
Publication Title
Opposing microRNA families regulate self-renewal in mouse embryonic stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Dicer, which is required for the processing of both microRNAs (miRNAs) and small interfering RNAs (siRNAs), is essential for oocyte maturation. Oocytes express both miRNAs and endogenous siRNAs (endo-siRNAs). To determine whether the abnormalities in Dicer knockout oocytes during meiotic maturation are secondary to the loss of endo-siRNAs and/or miRNAs, we deleted Dgcr8, which encodes a RNA binding protein specifically required for miRNA processing. In striking contrast to Dicer, Dgcr8 deficient oocytes matured normally and, when fertilized with wild-type sperm, produced healthy appearing offspring, even though miRNA levels were reduced to similar levels as Dicer deficient oocytes. Furthermore, the deletion of both maternal and zygotic Dgcr8 alleles did not impair preimplantation development including the determination of the inner cell mass (ICM) and trophectoderm. Most surprisingly, the mRNA profiles of wild-type and Dgcr8 null oocytes were essentially identical while Dicer null oocytes showed hundreds of misregulated transcripts. These findings show that miRNA function is globally suppressed during oocyte maturation and preimplantation development and that endo-siRNAs, rather than miRNAs, underlie the Dicer knockout phenotype in oocytes.
Publication Title
Opposing microRNA families regulate self-renewal in mouse embryonic stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Activation of oncogenic ras pathway accounts for up to 90% low-grade superficial urothelial carcinomas of bladder, and p53 deficiency is very common in high-grade muscle invasive carcinomas. These two pathways in bladder urothelial tumorigenesis used to be considered divergent and their potential collaboration has not been illustrated.
Publication Title
Oncogenic HRAS Activates Epithelial-to-Mesenchymal Transition and Confers Stemness to p53-Deficient Urothelial Cells to Drive Muscle Invasion of Basal Subtype Carcinomas.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
5-hydroxymethylcytosine (5hmC) occurs at maximal levels in postmitotic neurons where its accumulation is cell specific and correlated with gene expression. Here we demonstrate that the distribution of 5hmC in CG and non-CG dinucleotides is distinct, and that it reflects the binding specificity and genome occupancy of methylcytosine binding protein 2 (MeCP2). In expressed gene bodies, accumulation of 5hmCG acts in opposition to 5mCG resulting in “functional” demethylation and diminished MeCP2 binding, thus facilitating transcription. Non-CG hydroxymethylation occurs predominantly in CA dinucleotides (5hmCA) and it accumulates in regions flanking active enhancers. In these domains, oxidation of 5mCA to 5hmCA does not alter MeCP2 binding or expression of adjacent genes. We conclude that the role of 5-hydroxymethylcytosine in postmitotic neurons is to functionally demethylate expressed gene bodies while retaining the role of MeCP2 in chromatin organization. Overall design: Examination of genome wide cytosine methylation and hydroxymethylation per context in cerebellar granule cells and their function in MeCP2 binding. Nuclear RNA-Seq dataset.
Publication Title
5-hydroxymethylcytosine accumulation in postmitotic neurons results in functional demethylation of expressed genes.
Sample Metadata Fields
Cell line, Subject
View Samples