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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human retinoblastoma samples to compare the transcriptomes of retinoblastoma with LOH on 16q to tumors without alterations on 16q

ABSTRACT: Genomic losses on chromosome 16q are among the most frequent alterations found in retinoblastoma. In this study, Affymetrix GeneChip analyses along with LOH analysis of microsatellie markers was used to identify candidate tumor suppressor loci in a set of retinoblastoma. We used microarrays to identify genes differentially expressed in retinoblastoma with LOH on 16q (M19484, M22590, M22641, M22860) compared to retinoblastoma without alterations in this region (M20517, M22067, M22233, M23209, M23449, M23818, M23896, M23978) Experiment Overall Design: To compare the transcriptosomes of retinoblastoma with and without LOH on 16q, total RNA was isolated from a 30 mg block of each tumor and subjected to Affymetrix microarray analysis on HG-U133A arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Ludger Klein-Hitpass

PROVIDER: E-GEOD-5222 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Allelic loss in a minimal region on chromosome 16q24 is associated with vitreous seeding of retinoblastoma.

Gratias Sandrine S Rieder Harald H Ullmann Reinhard R Klein-Hitpass Ludger L Schneider Stephanie S Bölöni Réka R Kappler Martin M Lohmann Dietmar R DR

Cancer research 20070101 1

In addition to RB1 gene mutations, retinoblastomas frequently show gains of 1q and 6p and losses of 16q. To identify suppressor genes on 16q, we analyzed 22 short tandem repeat loci in 58 patients with known RB1 mutations. A subset of tumors was also investigated by conventional and matrix comparative genomic hybridization. In 40 of 58 (69%) tumors, we found no loss of heterozygosity (LOH) at any 16q marker. LOH was detected in 18 of 58 (31%) tumors, including five with allelic imbalance at some ...[more]

PMID: 17210724

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Expression data from retinoblastoma

Project description:Genomic losses on chromosome 16q are among the most frequent alterations found in retinoblastoma. In this study, Affymetrix GeneChip analyses along with LOH analysis of microsatellie markers was used to identify candidate tumor suppressor loci in a set of retinoblastoma. We used microarrays to identify genes differentially expressed in retinoblastoma with LOH on 16q (M19484, M22590, M22641, M22860) compared to retinoblastoma without alterations in this region (M20517, M22067, M22233, M23209, M23449, M23818, M23896, M23978) Keywords: Disease progression

2007-01-29 | GSE5222 | GEO

Gene expression profiles of retinoblastoma cell lines

Project description:In order to identify the gene targets of frequently altered chromosomal regions in retinoblastoma, a meta-analysis of genome-wide copy number alterations studies on primary retinoblastoma tissue and retinoblastoma cell lines was performed. Published studies were complemented by copy number and gene expression analysis on primary and cell line samples of retinoblastoma. This dataset includes the gene expression data of the retinoblastoma cell lines This data set contains the gene expression (Affymetrix human genome u133 plus 2.0 PM) results for 7 unique retinoblastoma cell lines. For one of the 7 unique cell lines, 3 RNA isolations were performed and were profiled on seperate arrays, adding up to 9 unique array files. Copy number data for primary retinoblastoma (tumor and blood DNA) and retinoblastoma cell lines are available (controlled-access) at the European Genomics Archive. Gene expression data of primary retinoblastoma is available under GSE59983. The GSE59983 records represent the primary tissue gene expression data and the CN data will be deposited into a controlled-access database, probably EGA.

2016-03-31 | E-GEOD-77094 | biostudies-arrayexpress

Affymetrix SNP array data for cone precursor derived retinoblastoma like samples

Project description:Retinoblastoma is a childhood retinal tumor that initiates in response to biallelic RB1 inactivation. We show that post-mitotic human cone precursors are uniquely sensitive to the oncogenic effects of Rb depletion. Rb knockdown induced cone precursor proliferation in prospectively isolated populations. SNP-array analysis of two Rb/p130-depleted cone precursor cell lines, revealing no megabase-size loss of heterozygosity (LOH) or copy number alterations (CNAs). SNP-array analysis of one Rb/p130-depleted (tumor 1) or one Rb-depleted (tumor 2) cone precursor-derived tumors, revealing no megabase-size LOH or CNAs, consistent with the lack of DNA copy number alterations in some retinoblastomas. Thus, the cone precursor tumors resembled human retinoblastomas at the molecular cytogenetic level. High resolution SNP-array DNA copy number analyses were performed using CytoScan® HD (Affymetrix, 901835) according to the manufacturer's directions. Data were analyzed using Chromosome Analysis Suite 2.0 (Affymetrix). DNA was extracted from two Rb/p130 depleted cone precursor cell lines and two cryopreserved mouse retinoblastoma samples from eyes xenograted with Rb/p130 or Rb depleted cone precursors. Affymetrix SNP analysis on retinoblastoma cell lines Y79, RB176, and WERI were used as control. Normal human genome 19 was used as reference.

2014-08-25 | E-GEOD-60720 | biostudies-arrayexpress

Gene Expression profiles in Retinoblastoma

Project description:Gene expression profiles in retinoblastoma by whole Human Genome DNA microarrays in comparison to the normal retina gave an insight into several genes and pathways that were regulated in the tumor. The upregulated and the downregulated genes were further validated by quantitative real time PCR and tissue microarray (TMA) on retinoblastoma tumors. Theoverall goal is to determine the global gene expression profile in retinoblastoma tumors which is first of its kind on a whole genome microarray. Two coloured microarray:retinoblastoma tumor (4 samples) vs. normal retina (4 samples).

2012-03-30 | E-GEOD-33048 | biostudies-arrayexpress

Gene expression profiling identifies different sub-types of retinoblastoma

Project description:Background: Mutation of the RB1 gene is necessary but not sufficient for the development of retinoblastoma. The nature of events occurring subsequent to RB1 mutation is unclear, as is the retinal cell-of-origin of this tumour. Methods: Gene expression profiling of 21 retinoblastomas was carried out to identify genetic events that contribute to tumorigenesis and to obtain information about tumour histogenesis. Results: Expression analysis showed a clear separation of retinoblastomas into two groups. Group 1 retinoblastomas express genes associated with a range of different retinal cell types, suggesting derivation from a retinal progenitor cell type. Recurrent chromosomal alterations typical of retinoblastoma, for example, chromosome 1q and 6p gain and 16q loss were also a feature of this group, and clinically they were characterised by an invasive pattern of tumour growth. In contrast, group 2 retinoblastomas were found to retain many characteristics of cone photoreceptor cells and appear to exploit the high metabolic capacity of this cell type in order to promote tumour proliferation. Conclusion: Retinoblastoma is a heterogeneous tumour with variable biology and clinical characteristics. Kapatai, G et al. Br J Cancer (2013) 109, 512-525 doi: 10.1038/bjc.2013.283

2021-04-16 | GSE172170 | GEO

Affymetrix SNP array data for cone precursor derived retinoblastoma like samples

2014-08-25 | GSE60720 | GEO

Germline Variant in Ctcf Links Mental Retardation to Wilms Tumor Predisposition

Project description:SNP arrays was combined with next generation sequencing (NGS) to identify an LOH in 16q together with an unreported CTCF missense variant in its zinc finger domain. CTCF is within 16q LOH. We found that germline heterozygous variant I446K became homozygous in the tumor due to a loss of heterozygosity rearrangement affecting the whole q arm on chromosome 16. Based on CTCF role in regulating the epigenetic architechture of the genome, our findings reveal CTCF variant I446K as a link between MRD21 and Wilms tumor predisposition.

2022-01-11 | GSE193233 | GEO

QUANTITATIVE PHOSPHOPROTEOMIC PROFILING OF PRIMARY RETINOBLASTOMA TUMORS

Project description:Retinoblastoma is a malignant tumor of the retina which most often occurs in children below 5 years of age with an incident rate of about 1 in 15,000 to 18,000 live births. Retinoblastoma is the first ever cancer that was reported to have a genetic basis. It occurs widely due to inactivating mutations in RB1 gene. Gene expression studies, copy number variation analysis, epigenetic profiling including miRNA and methylation of retinoblastoma has been carried to understand the disease mechanism and key players in the disease. Our group has earlier performed differential proteomics of retinoblastoma to identify proteins of therapeutic importance. However, there are no studies to understand the signalling mechanisms associated with retinoblastoma. Hence, global phosphoproteomics of retinoblastoma was carried out to identify signalling events associated with this cancer. Our study identified stress response proteins to be hyper phosphorylated which included H2AFX and sirtuin 1. In particular, Ser140 of H2AFX also known as gamma-H2AX was found to be hyperphosphorylated in retinoblastoma that indicated activation of DNA damage response pathways. We also observed activation of anti-apoptotic proteins in retinoblastoma compared to control. These observations showed activation of survival pathways and signalling networks activated in tumors.

2019-11-11 | PXD007228 | Pride

Proteomic profiling of retinoblastoma by high resolution mass spectrometry

Project description:We performed a high throughput comparative proteomics study to identify differentially expressed proteins that could serve as putative targets in retinoblastoma. We used iTRAQ based quantitative proteomics approach and analyzed the samples on orbitrap velos mass spectrometer. We identified and quantified a total of 3733 proteins in retinoblastoma when compared with normal adult retina. In total, we identified 987 proteins that were differentially expressed in retinoblastoma with a fold change of ≥2 of which 392 proteins were upregulated and 595 were downregulated.

2016-12-23 | PXD002774 | Pride

Gene expression profiles of retinoblastoma cell lines

2016-03-31 | GSE77094 | GEO

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