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GSE57658
Homo sapiens
12 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
REtr causes genomic instability in U937 cells. Activated forms of c-KIT, like c-KIT(N822K), rescues the Retr induced genomic instability by increasing the rate of DNA repair by homologous recombination
Publication Title
Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This work is part of the paper: Generation of a murine hepatic angiosarcoma cell line and reproducible mouse tumor model, Rothweiler S et al, Laboratory Investigation, 2014
Publication Title
Generation of a murine hepatic angiosarcoma cell line and reproducible mouse tumor model.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 124 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Hepatocellular carcinoma (HCC) is a heterogeneous disease, and despite considerable research efforts, no molecular classification of HCC has been introduced in clinical practice. The existing molecular classification systems were established using resected tumors, which introduces a selection bias towards patients without liver cirrhosis and with early stage HCCs. So far, these classification systems have not been validated in liver biopsy specimens from tumors diagnosed at intermediate and late stages. We generated and analyzed expression profiles from 60 HCC biopsies from an unselected patient population with all tumor stages. Unbiased clustering identified 3 HCC classes. Class membership correlated with survival, tumor size, and with Edmondson and BCLC stage. Most biopsy specimens could be assigned to the classes of published classification systems, demonstrating that gene expression profiles obtained from patients with early stage disease are preserved in all stages of HCC. When a reference set of healthy liver samples was integrated in the analysis, we observed that the differentially regulated genes up- or down-regulated in a given class relative to other classes were actually dysregulated in the same direction in all HCCs, with quantitative rather than qualitative differences between the molecular subclasses. With the exception of a subset of samples with a definitive -catenin gene signature, biological pathway analysis could not identify class specific pathways reflecting the activation of distinct oncogenic programs. Our results suggest that gene expression profiling of HCC biopsies has limited potential to direct therapies that target specific driver pathways, but can identify subgroups of patients with different prognosis.
Publication Title
Gene expression analysis of biopsy samples reveals critical limitations of transcriptome-based molecular classifications of hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 24 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Squamous cell carcinoma (SCC) is the second most common cancer worldwide and accounts for approximately 30% of all keratinocyte cancers. The vast majority of cutaneous SCCs of the head and neck (cSCCHN) are readily curable with surgery and/or radiotherapy unless high-risk features are present. Perineural invasion (PNI) is recognized as one of these high-risk features. The molecular changes during clinical PNI in cSCCHN have not been previously investigated. In this study, we assessed the global gene expression differences between cSCCHN with or without incidental or clinical PNI. The results of the analysis showed signatures of gene expression representative of activation of p53 in tumors with PNI compared to tumors without, amongst other alterations. Immunohistochemical staining of p53 showed cSCCHN with clinical PNI to be more likely to exhibit a diffuse over-expression pattern, with no tumors showing normal p53 staining. DNA sequencing of cSCCHN samples with clinical PNI showed no difference in mutation number or position with samples without PNI, however a significant difference was observed in regulators of p53 degradation, stability and activity. Our results therefore suggest that cSCCHN with clinical PNI may be more likely to contain alterations in the p53 pathway, compared to cSCCHN without PNI.
Publication Title
Expression profiling of cutaneous squamous cell carcinoma with perineural invasion implicates the p53 pathway in the process.
Sample Metadata Fields
Disease, Disease stage
View Samples- Homo sapiens
- 19 Downloadable Samples
IlluminaHiSeq2000
Description
Mucosal-associated invariant T (MAIT) cells are abundant in humans and recognize conserved bacterial antigens derived from riboflavin precursors, presented by the non-polymorphic MHC class I-like molecule MR1. Here, we show via transcriptomic analysis that human MAIT cells are remarkably oligoclonal in both blood and liver, display high inter-individual homology, and exhibit a restricted length CDR3ß domain of the TCRVß chain. We extend this analysis to a second sub-population of MAIT cells expressing a semi-invariant TCR conserved between individuals. Overall design: Study of CDR3 regions of TCRalpha and beta sequences
Publication Title
Parallel T-cell cloning and deep sequencing of human MAIT cells reveal stable oligoclonal TCRβ repertoire.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 40 Downloadable Samples
- Affymetrix Human Genome U133B Array (hgu133b), Affymetrix Human Genome U133A Array (hgu133a)
Description
Gene expression profiles in blasts from three APL patients expressing PML/RAR were assessed before and after treatment with 1 uM retinoic acid (RA) in vitro for four hours. We then studied a U937 clone conditionally expressing PML/RAR (U937-PR), (Grignani et al. 1993) (Alcalay et al. 2003), and compared the gene expression profile prior to and after 4 hours of treatment with 1 uM RA, to that obtained from a cell line bearing an empty vector (U937-MT). For each sample, biotinylated cRNA targets were synthesized starting from 5ug of total RNA, and hybridized to the complete set of HG-U133 Affymetrix oligonucleotide chips, which explores the expression of approximately 45,000 human transcripts. Results were analyzed using MASv5 and further elaborated with the GenePicker software. GeneChip probe sets regulated by RA in each sample were clustered into non-redundant regulated genes according to UniGene release Hs.166.
Publication Title
Molecular signature of retinoic acid treatment in acute promyelocytic leukemia.
Sample Metadata Fields
Specimen part, Disease, Cell line, Subject, Compound
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina mouse-6 v1.1 expression beadchip
Description
The transcription factor STAT3 is constitutively activated in tumors of different origin but the molecular bases for STAT3 addiction of tumor cells have not yet been clearly identified. We generated knock/in mice carrying the constitutively active Stat3 allele, Stat3C, and showed that Stat3C could enhance Neu oncogenic power, triggering the production of earlier onset, more invasive mammary tumors. Tumor-derived cell lines displayed higher migration and invasion and disrupted distribution of cell-cell junction markers. The tensin family member Cten (C-Terminal Tensin-like), known to mediate EGF-induced migration and highly expressed in inflammatory breast cancer, was up-regulated in both Neu;Stat3C cells and tumors. Both Cten expression and enhanced migration were strictly dependent on Stat3, and Cten silencing normalized cell migration and rescued cell-cell contact defects. Importantly, the pro-inflammatory cytokine IL-6 could mediate Cten induction in MCF10 cells, in an exquisitely Stat3-dependent way. This model allowed us to shed some light on the oncogenic role of Stat3 in the breast, suggesting moreover a mechanism through which inflammatory signals can cooperate with EGF receptors in inflammatory breast cancer.
Publication Title
Constitutively active Stat3 enhances neu-mediated migration and metastasis in mammary tumors via upregulation of Cten.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 28 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Tumor tissue heterogeneity is a well known feature of several solid tumors. Neuroblastic Tumors (NTs) is a group of paediatric cancers with a great tissue heterogeneity. Most of NTs are composed of undifferentiated, poorly differentiated or differentiating neuroblastic (Nb) cells with very few or absent Schwannian stromal (SS) cells: these tumors are grouped as Neuroblastoma (Schwannian stroma-poor). The remaining NTs are composed of abundant SS cells and classified as Ganglioneuroblastoma (Schwannian stroma-rich) intermixed or nodular and Ganglioneuroma. The importance to understand Nb and SS gene signatures in NTs, is to clarify the complex network mechanism of tumor growth and progression. In order to identify the Nb and SS cells gene signatures, we analyzed the gene expression profiling of 19 cases of neuroblastic tumors: 10 stroma poor (NTs-SP) and 9 stroma rich (NTs-SR), by high density oligonucleotide microarrays. Moreover, the analysis was performed in parallel on both whole and laser microdissected tumor samples: from 4 of 19 cases, was isolated different areas all composed of pure cellular populations.
Publication Title
Identification of low intratumoral gene expression heterogeneity in neuroblastic tumors by genome-wide expression analysis and game theory.
Sample Metadata Fields
No sample metadata fields
View Samples- 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
- 77 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Approximately one third of acute myeloid leukemias (AMLs) are characterized by aberrant cytoplasmic localization of Nucleophosmin (NPMc+ AML), consequent to mutations in the NPM putative nucleolar localization signal. These events are mutually exclusive with the major AML-associated chromosomal rearrangements, and are frequently associated with normal karyotype, Fms-like tyrosine kinase (FLT3) mutations and multilineage involvement. We report the gene expression profiles of 78 de novo AMLs (72 with normal karyotype; 6 with non-major chromosomal abnormalities) that were characterized for the subcellular localization and mutation status of NPM. Unsupervised clustering clearly separated NPMc+ from NPMc- AMLs, regardless of the presence of FLT3 mutations or non-major chromosomal rearrangements, supporting the concept that NPMc+ AML represents a distinct entity. The molecular signature of NPMc+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem cell phenotype, suggesting that NPMc+ AML may derive from a multipotent hematopoietic progenitor.
Publication Title
Acute myeloid leukemia bearing cytoplasmic nucleophosmin (NPMc+ AML) shows a distinct gene expression profile characterized by up-regulation of genes involved in stem-cell maintenance.
Sample Metadata Fields
Specimen part
View Samples