Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

35 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A framework for identification of actionable cancer genome dependencies in small cell lung cancer

ABSTRACT: We analyzed copy numbers of 60 SCLC cell lines using 6.0 SNP-arrays. For a subgroup of 36 cell lines, previously published copy number data was utilized. CEL and SEG files are included for all cell lines, for which copy number data were not publicly available. DNA was extracted from SCLC cell lines and copy number data was generated for all samples

ORGANISM(S): Homo sapiens

SUBMITTER: Felix Dietlein

PROVIDER: E-GEOD-40142 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

NFIB is a driver of SCLC initiation, progression and metastasis in mouse and marks metastatic disease in patients

Project description:Small Cell Lung Cancer (SCLC) is the most aggressive type of lung cancer with early metastatic dissemination and invariable development of resistant disease for which no effective treatment is available to date. Mouse models of SCLC based on inactivation of Rb1 and Trp53 developed earlier showed frequent amplifications of two transcription factor genes: Nfib and Mycl. Overexpression of Nfib but not Mycl in SCLC mouse results in an enhanced and altered metastatic profile, and appears to be associated with genomic instability. NFIB promotes tumor heterogeneity with the concomitant expansive growth of poorly differentiated, highly proliferative, and invasive tumor cell populations. Consistent with the mouse data, NFIB expression in high-grade human neuroendocrine carcinomas correlates with advanced stage III/IV disease warranting its further assessment as a potentially valuable progression marker in a clinical setting. Genomic DNA from mouse small cell lung tumor samples was analyzed by mate pair sequencing and low coverage sequencing. And RNA from Nfib overexpressing mouse small cell lung cancer cell lines was further analyzed for high quality RNA profiles using Illumina Hiseq2500. This series contains only RNA-seq data.

2016-07-29 | E-GEOD-82005 | biostudies-arrayexpress

A DNA Hypomethylation Signature Predicts Novel Anti-Tumor Activity of LSD1 Inhibitors in SCLC (ChIP-Seq)

Project description:Epigenetic dysregulation has emerged as an important mechanism in cancer. Alterations in epigenetic machinery have become a major focus for new targeted therapies. The current report describes the discovery and biological activity of a cyclopropylamine containing inhibitor of Lysine Demethylase 1 (LSD1), GSK2879552. This small molecule is a potent, selective, orally bioavailable, mechanism-based irreversible inhibitor of LSD1. A proliferation screen of cell lines representing a number of tumor types indicated that small cell lung carcinoma (SCLC) is sensitive to LSD1 inhibition. The subset of SCLC lines and primary samples that undergo growth inhibition in response to GSK2879552 exhibit DNA hypomethylation of a signature set of probes suggesting this may be used as a predictive biomarker of activity. The targeted mechanism coupled with a novel predictive biomarker make LSD1 inhibition an exciting potential therapy for SCLC, a highly prevalent, rarely cured, tumor type representing approximately 15% of all lung cancers. To investigate the mechanism of LSD1 efficacy in SCLC cell lines we used chromatin immunoprecipitation (ChIP) sequencing studies to examine the genomic distribution of LSD1 as well as H3K4me2 and H3K4me1 in NCI-H526 SCLC cells in the absence and presence of LSD1 inhibition.

2015-07-14 | E-GEOD-66297 | biostudies-arrayexpress

A framework for identification of actionable cancer genome dependencies in small cell lung cancer

Project description:We analyzed copy numbers of 60 SCLC cell lines using 6.0 SNP-arrays. For a subgroup of 36 cell lines, previously published copy number data was utilized. CEL and SEG files are included for all cell lines, for which copy number data were not publicly available.

2012-09-21 | GSE40142 | GEO

Genotyping of human SCLC cell line profiling on 100K arrays

Project description:Twenty three small-cell lung carcinoma (SCLC) cell lines from ATCC profiled on 100K genotyping arrays Experiment Overall Design: The cell lines were run on 100K SNP genotyping arrays to obtain copy number information

2008-06-15 | E-GEOD-7068 | biostudies-arrayexpress

Array CGH-based Characterization of Genetic Alterations in Pulmonary Neuroendocrine Tumors

Project description:The goal of this study was to characterize and classify pulmonary neuroendocrine tumors based on Array Comparative Genomic Hybridization (aCGH). Using aCGH, we performed karyotype analysis of 33 small cell lung cancer (SCLC) tumors, 13 SCLC cell lines, 19 bronchial carcinoids, and 9 gastrointestinal (GI) carcinoids. In contrast to the relatively stable karyotypes of carcinoid tumors, the karyotypes of SCLC tumors and cell lines were highly aberrant. High copy number (CN) gains were detected in SCLC tumors and cell lines in cytogenetic bands encoding JAK2, FGFR1, and MYC family members. In some of those samples, the CN of these genes exceeded 100, suggesting that they could represent driver alterations and potential drug targets in subgroups of SCLC patients. Recurrent CN alterations of a total of 203 genes, including the RB1 gene, and 59 microRNAs, most of which locate in the DLK1-DIO3 domain, were observed in SCLC tumors, bronchial carcinoids and carcinoids of GI origin; in contrast, CN alterations of the TP53 gene and the MYC family members were observed more frequently in SCLC. These findings suggest the existence of partially shared tumor-specific CN alterations in these tumors. Furthermore, we demonstrated that the aCGH profile of SCLC cell lines highly resemble that of clinical SCLC specimens. Finally, by analyzing potential drug targets, we provide a genomics based rationale for targeting the AKT-mTOR and apoptosis pathways in SCLC. Carcinoids, including 19 bronchial carcinoids and 9 carcinoid of gastrointestinal origin, and small cell lung cancer, including 33 patients' tumor samples and 13 cell line samples, were compared.

2010-04-22 | E-GEOD-21468 | biostudies-arrayexpress

Conversion of Fibroblasts into Functional Trophoblast Stem-like Cells

Project description:Here we demonstrate the generation of stable induced trophoblast stem cells (iTSCs) from fibroblasts by the transient expression of Gata3, Eomes and Tfap2c. Transcriptome and methylome analyses and functional assays such as hemorrhagic lesion formation and placenta contribution suggested a high degree of conversion. Careful examination of the reprogramming process indicated that the cells did not go through a transient pluripotent state. Detect and compare different H2A.X deposition patterns in ES cells,MEFs and iTSC and TS cells, with Illumina HiSeq 2000

2016-07-05 | E-GEOD-70234 | biostudies-arrayexpress

Array CGH-based Characterization of Genetic Alterations in Pulmonary Neuroendocrine Tumors

2010-04-22 | GSE21468 | GEO

MYC drives resistance to PI3K/mTOR targeted inhibition (Sty SNP array)

Project description:Genomic copy-number changes were measured using 250K StyI SNP arrays after selection of cells to enrich for resistance to BEZ235. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted using Qiagen DNeasy from engineered human cell-lines. Resulting alterations in copy numbers were calculated based on SNP intensities.

2011-08-30 | E-GEOD-25170 | biostudies-arrayexpress

ChIP seq for p63, H3K27ac and BRD4 in L3.6pl, BxPC-3 pancreatic cancer cell lines and ChIP-seq of H3K27ac and BRD4 in Panc-1 pancreatic cell line

Project description:We investigated the regions that are occupied by deltaNp63 in BxPC-3 and L3.6pl and identification of super enhancers in different pancreatic cancer cell lines. Thereby, we identified a group of 45 super enhancers that are associated with poorer prognosis and are highly dependent on deltaNp63.

2018-12-18 | E-MTAB-7034 | biostudies-arrayexpress

FOXO3 shares common targets with ASCL1 genome-wide and inhibits ASCL1-dependent neurogenesis

Project description:FOXO transcription factors are central regulators of longevity from worms to humans. FOXO3 – the FOXO isoform associated with exceptional human longevity – preserves adult neural stem cell pools. Here we identify FOXO3 direct targets genome-wide in primary cultures of adult neural progenitor cells (NPCs). Interestingly, FOXO3-bound sites are enriched for motifs for bHLH transcription factors and FOXO3 shares common targets with the pro-neuronal bHLH transcription factor ASCL1/MASH1 in NPCs. Analysis of the chromatin landscape reveals that FOXO3 and ASCL1 are particularly enriched at the enhancers of genes involved in neurogenic pathways. Intriguingly, FOXO3 inhibits ASCL1-dependent neurogenesis in NPCs and direct neuronal conversion in fibroblasts. FOXO3 also restrains neurogenesis in vivo. Our study identifies a genome-wide interaction between the pro-longevity transcription factor FOXO3 and the cell fate determinant ASCL1, and raises the possibility that FOXO3’s ability to restrain ASCL1-dependent neurogenesis may help preserve the neural stem cell pool. ChIP-seq profiles of two transcription factors (FOXO3 and ASCL1) and three histone marks (H3K4me1, H3K4me3 and H3K27me3) in adult mouse neural progenitor cells.

2013-08-13 | E-GEOD-48336 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data