Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

13 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Whole genome scanning of lung tumors and mucosal biopsies on Affymetrix NspI-250K platform

ABSTRACT: Matched normal lymph node, tumors and corresponding mucosal biopsies from 4 lung cancer patients were scrutinized on Affymetrix 250K-NspI array platform. Frequently deleted regions genes were identified based on the LOH call as per manufacturer's guidelines and normalization. Frequently deleted genes in the tumors and mucosa were identified though this approach Affymetrix 250K-NspI- SNP arrays were performed according to the manufacturer's directions on DNA extracted from lung cancer and corresponding mucosal biopsy specimens. LOH analysis was done to identify genes that are frequently deleted.

ORGANISM(S): Homo sapiens

SUBMITTER: Santanu Dasgupta

PROVIDER: E-GEOD-29365 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

SH3GL2 is frequently deleted in non-small cell lung cancer and downregulates tumor growth by modulating EGFR signaling.

Dasgupta Santanu S Jang Jin Sung JS Shao Chunbo C Mukhopadhyay Nitai D ND Sokhi Upneet K UK Das Swadesh K SK Brait Mariana M Talbot Conover C Yung Rex C RC Begum Shahnaz S Westra William H WH Hoque Mohammad Obaidul MO Yang Ping P Yi Joanne E JE Lam Stephan S Gazdar Adi F AF Fisher Paul B PB Jen Jin J Sidransky David D

Journal of molecular medicine (Berlin, Germany) 20120912 3

The purpose of this study was to identify key genetic pathways involved in non-small cell lung cancer (NSCLC) and understand their role in tumor progression. We performed a genome wide scanning using paired tumors and corresponding 16 mucosal biopsies from four follow-up lung cancer patients on Affymetrix 250K-NSpI array platform. We found that a single gene SH3GL2 located on human chromosome 9p22 was most frequently deleted in all the tumors and corresponding mucosal biopsies. We further valida ...[more]

PMID: 22968441

Similar Datasets

SNP array analysis on Maffucci tumours

Project description:Here we have used four enchondromas and two chondrosarcomas of Maffucci patients. We also had one normal sample available for paired analysis in one of the chondrosarcoma II. We did not find any LOH or coomon copy number variation in all Maffucci enchondromas while chondrosarcomas are genetically unstable. Affymetrix SNP 6.0 array was performed using 4 EC and 2CS of Maffucci patients. Illumina expression v3 array was possible to perform using only 1 EC and 2 CS due to rarity of the disease. For SNP array, we used 29 control samples submitted previously (GSE22965) to creat baseline.

2011-07-18 | E-GEOD-26674 | biostudies-arrayexpress

Affymetrix SNP6.0 on Ollier disease-related tumors

Project description:Mutations in the PTH1R gene were reported but these mutations are limited to a small subgroup of patients. The etiology of Ollier disease is unknown. We therefore undertook genome-wide copy number and loss of heterozygosity (LOH) analysis using Affymetrix SNP 6.0 arrays on 37 tumors of 28 Ollier patients in combination with expression array using Illumina Beadarray v3.0 for 7 tumors of 6 patients. We used Affymetrix SNP 6.0 to find out LOH and copy number alterations in Ollier tumors. To understand the genetic mechanism behind the development of enchondroma, we mainly focus on enchondromas and found alterations were validated. We used 14 enchondromas and 23 chondrosarcomas of 28 Ollier patients. We also used 30 controls (blood, saliva or frozen tissue). As controls, normal DNA derived from fresh frozen muscle tissue (n=3), peripheral blood lymphocytes (n=4) or saliva (n=4) was available for 11 Ollier patients and 3 patients with unrelated bone diseases. We used blood lymphocyte DNA from 12 healthy controls and 1 HapMap sample. We also isolated DNA from saliva for 3 of these controls to validate the use of saliva DNA in this study.

2011-08-26 | E-GEOD-22984 | biostudies-arrayexpress

250K SNP array data for 40 high-grade myogenic cancers

Project description:Many common human mesenchymal tumors, including gastrointestinal stromal tumor (GIST), rhabdomyosarcoma (RMS), and leiomyosarcoma (LMS), feature myogenic differentiation. Here we report that intragenic deletion of the dystrophin-encoding and muscular dystrophy-associated DMD gene is a frequent mechanism by which myogenic tumors progress to high-grade, lethal sarcomas. Dystrophin is expressed in nonneoplastic and benign counterparts for GIST, RMS and LMS, and the DMD deletions inactivate larger dystrophin isoforms, including 427kDa dystrophin, while preserving expression of an essential 71kDa isoform. Dystrophin inhibits myogenic sarcoma cell migration, invasion, anchorage independence, and invadopodia formation, and dystrophin inactivation was found in 96%, 100%, and 62% of metastatic GIST, embryonal RMS, and LMS, respectively. These findings validate dystrophin as a tumor suppressor and likely anti-metastatic factor, suggesting that therapies in development for muscular dystrophies may also have relevance in treatment of cancer. High molecular weight genomic DNA was isolated from 40 high-grade myogenic cancers (including 7 normal tissue/tumor pairs and 33 additional tumors) using QIAamp DNA Mini Kit (QIAGEN) and analyzed by Affymetrix 250K SNP array.

2014-05-02 | E-GEOD-53021 | biostudies-arrayexpress

INTEGRATIVE ONCOGENOMIC AND HIGH-THROUGHPUT SEQUENCING ANALYSES OF THE COMMONLY DELETED REGION IN CHROMOSOME 7q32 IN SPLENIC MARGINAL ZONE LYMPHOMA (SNP data)

Project description:Using high-resolution genomic microarray analysis, a distinct genomic profile was defined in 114 samples from patients with splenic marginal zone lymphoma (SMZL). Notably, deletion or uniparental disomy of chromosome 7q were detected in 39% of SMZLs but in only 9 of 170 (5%) mature B-cell lymphomas (p<10-6). The presence of unmutated IgVH genes, genomic complexity, 17p13-P53 deletion and 8q gain including MYC gene, but not 7q deletion, were correlated with shorter overall survival. Extensive mapping analyses narrowed down the commonly deleted region to 2.7 Mb. in 7q32.1-q32.2 from SND1 to COPG2 genes. High-throughput sequencing analysis of the 7q32 deleted segment in SMZL cells did not identify bi-allelic deletions, insertions or clear pathogenic mutations, but detected six single nucleotide changes in IRF5 (n=2), TMEM209 (n=2), CALU (n=1) and ZC3HC1 (n=1). Comparative expression analysis found that IRF5, TMEM209 and CALU genes had down-regulated expression in lymphomas with 7q32 deletion vs. non-deleted tumors. Ectopic expression of IRF5 in marginal-zone lymphoma cells decreased cell proliferation and induced apoptosis. These results indicate that small deletions, insertions and/or point mutations inactivating genes within 7q32 are not common events in SMZL. Further studies are required to evaluate the putative role of IRF5 in SMZL pathogenesis. Affymetrix GeneChip 50k-XbaI and/or 250-NspI/StyI SNP microarrays were performed for 59 SMZL samples and 4 Marginal Zone cell lines according to the manufacturer's directions.

2012-07-31 | E-GEOD-35329 | biostudies-arrayexpress

Maffucci tumours

Project description:This SuperSeries is composed of the following subset Series: GSE26667: Expression array using Maffucci tumours GSE26674: SNP array analysis on Maffucci tumours Refer to individual Series

2011-07-18 | E-GEOD-26675 | biostudies-arrayexpress

Oncogene-like induction of cellular invasion from centrosome amplification

Project description:Centrosome amplification has long been recognized as a feature of human tumors, however its role in tumorigenesis remains unclear. Centrosome amplification is poorly tolerated by non-transformed cells, and, in the absence of selection, extra centrosomes are spontaneously lost. Thus, the high frequency of centrosome amplification, particularly in more aggressive tumors, raises the possibility that extra centrosomes could, in some contexts, confer advantageous characteristics that promote tumor progression. Using a three-dimensional model system and other approaches to culture human mammary epithelial cells, we find that centrosome amplification triggers cell invasion. This invasive behavior is similar to that induced by overexpression of the breast cancer oncogene ErbB2 and indeed enhances invasiveness triggered by ErbB2. We show that, through increased centrosomal microtubule nucleation, centrosome amplification increases Rac1 activity, which disrupts normal cell-cell adhesion and promotes invasion. These findings demonstrate that centrosome amplification, a structural alteration of the cytoskeleton, can promote features of malignant transformation. genome-wide human SNP 6.0 arrays from Affymetrix was used to determine the copy number changes of MCF10A cells with extra centrosomes or depleted of MCAK after grown 4 days in 3-D cultures

2014-03-01 | E-GEOD-55042 | biostudies-arrayexpress

The reversed evolution from multicellularity to unicellularity during carcinogenesis

Project description:Using xenograft-based experimental evolution, we characterize the full life history from initiation to metastasis of a tumor at the genomic and transcriptomic levels. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from cell lines or xenograft tumor samples.

2014-11-27 | E-GEOD-63630 | biostudies-arrayexpress

DNA copy number changes in malignant mesothelioma

Project description:Malignant mesothelioma (MM) is an asbestos-related malignancy. Discrimination between MM and reactive mesothelial hyperplasia (RM) is often difficult. MM cells have a broad histological spectrum, and consist mainly of epithelioid, sarcomatoid, and biphasic cell types. The prognosis of MM is generally poor, but better prognosis has been reported with the epithelioid type of MM than the non-epithelioid type. We applied a genome-wide analysis to the identification of new markers that may aid in differentiating the epithelioid type of MM from other histological types and from RM cells. Array-based comparative genomic hybridization analysis was performed on malignant mesothelioma (MM) primary cell cultures, reactive mesothelial hyperplasia (RM) primary cell cultures; early passage of in vitro primary cell cultures to minimize acquisition of additional genomic changes. If available, matched peripheral blood was applied to analysis.

2014-11-22 | E-GEOD-52788 | biostudies-arrayexpress

CNV and LOH analysis of patient sample PN11-0204

Project description:We saw a patient who presented with respiratory distress from birth due to interstitial lung disease. Before the age of three months a diagnosis of nephrotic syndrome was made. Lung biopsy revealed pulmonary interstitial glycogenosis. Despite extensive investigations, no known genetic or infectious cause was found for the congenital nephrotic syndrome. The patient died at the age of 8 months due to respiratory failure. A 20 Mb homozygous region was identified on chromosome 17 in the patientM-bM-^@M-^Ys DNA, revealing a novel homozygous missense variant in ITGA3 gene. Genomic DNA was obtained from peripheral blood samples of the patient with interstitial lung fibrosis and nephrotic syndrome. Copy number variation (CNV) screening by means of microarray analyses was carried out on the Affymetrix GeneChip 250k (NspI) SNP array platform (Affymetrix, Inc., Santa Clara, CA, USA), which contains 25-mer oligonucleotides representing a total of 262,264 SNPs. Hybridizations were performed according to the manufacturerM-bM-^@M-^Ys protocols. Copy numbers and M-bM-^@M-^\long contiguous stretches of homozygosityM-bM-^@M-^] (LCSH/LOH) were determined using the 2.0 version of the CNAG (Copy Number Analyzer for Affymetrix GeneChip mapping) software package (Nannya Y, Sanada M, et al (2005) "A robust algorithm for copy number detection using high-density oligonucleotide single nucleotide polymorphism genotyping arrays." Cancer Res; 65: 6071M-bM-^@M-^S6079.). The average resolution of this array platform, described by McMullan et al is 150M-bM-^@M-^S200 kb (Mc McMullan DJ, Bonin M et al. (2009), M-bM-^@M-^\Molecular karyotyping of patients with unexplained mental retardation by SNP arrays: a multicenter studyM-bM-^@M-^] Hum Mutat. Jul;30(7):1082-92).

2012-08-28 | E-GEOD-40405 | biostudies-arrayexpress

Non-allelic homologous recombination between retrotransposable elements is a major driver of de novo unbalanced translocations.

Project description:Large scale analysis of balanced chromosomal translocation breakpoints has shown nonhomologous end joining and microhomology-mediated repair to be the main drivers of interchromosomal structural aberrations. Breakpoint sequences of de novo unbalanced translocations have not yet been investigated systematically. We analyzed 12 de novo translocations and mapped the breakpoints in 9. Surprisingly, in contrast to balanced translocations, we identify non-allelic homologous recombination (NAHR) between (retro)transposable elements and especially long interspersed elements (LINEs) as the main mutational mechanism. This finding implicates (retro)transposons to be a major driver of genomic rearrangements and exposes a profoundly different mutational mechanism compared to balanced chromosomal translocations. Furthermore, we show the existence of compound maternal/paternal derivative chromosomes, reinforcing the hypothesis that human cleavage stage embryogenesis is a cradle of chromosomal rearrangements. In total 36 non-amplified genomic DNA samples (12 patients plus parents) extracted from blood or amniocytes were analyzed by 250K Nsp I SNP arrays (GEO accession number GPL3718).

2012-07-12 | E-GEOD-39303 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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