Expression data from retinoblastoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE5222 | GEO | 2007/01/29
SECONDARY ACCESSION(S): PRJNA96519
REPOSITORIES: GEO
Similar Datasets
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) 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.
2009-04-24 | E-GEOD-5222 | biostudies-arrayexpress
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
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.
2014-08-25 | GSE60720 | GEO
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
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
2016-03-31 | GSE77094 | GEO
Project description:Breast cancers can be classified using whole genome expression into distinct subtypes that show differences in patient prognosis. One of these groups, the basal-like carcinomas, are poorly differentiated, highly metastatic, and genomically unstable. These tumors also contain specific genetic alterations with one example being frequent p53 mutations. The loss of the tumor suppressor gene encoded by the retinoblastoma (RB1) locus is a well-characterized occurrence in many tumor types, however, its role in breast cancer is less clear with many reports demonstrating a Loss of Heterozygosity (LOH) that does not correlate with loss of RB1 protein expression. Here we report that LOH of the RB1 locus was observed at a high frequency in basal-like and luminal B tumors. These tumors also concurrently have low expression of RB1 mRNA as assessed by DNA microarray. As in previous reports, we also did not see a significant correlation between RB1 LOH and protein expression as measured by immunohistochemistry (IHC). p16INK4a, however, was highly expressed both by microarray and IHC, in basal-like tumors only presumably due to a previously reported feedback loop caused by RB1 loss. These results suggest that the functional loss of RB1 is a common event in the progression of basal-like and luminal B breast tumors, which may play a key role in dictating therapeutic responses Keywords: reference x sample Comparison of reference samples against treatment
2010-06-25 | E-GEOD-10884 | biostudies-arrayexpress
Project description:Background Retinoblastoma is a pediatric eye cancer associated with RB1 loss or MYCN amplification (RB1+/+MYCNA). There are controversies concerning the existence of molecular subtypes within RB1-/- retinoblastoma. To test whether these molecular subtypes exist, we performed molecular profiling. Methods Genome-wide mRNA expression profiling was performed on 76 primary human retinoblastomas. Expression profiling was complemented by genome-wide DNA profiling and clinical, histopathological, and ex vivo drug sensitivity data. Findings RNA and DNA profiling identified major variability between retinoblastomas. While gene expression differences between RB1+/+MYCNA and RB1-/- tumors seemed more dichotomous, differences within the RB1-/- tumors were gradual. Tumors with high expression of a photoreceptor gene signature were highly differentiated, smaller in volume and diagnosed at younger age compared to tumors with low photoreceptor signature expression. Tumors with lower photoreceptor expression showed increased expression of genes involved in M-phase and mRNA and ribosome synthesis and increased frequencies of somatic copy number alterations. Interpretation Molecular, clinical and histopathological differences between RB1-/- tumors are best explained by tumor progression, reflected by a gradual loss of differentiation and photoreceptor expression signature. Since copy number alterations were more frequent in tumors with less photoreceptorness, genomic alterations might be drivers of tumor progression. Fresh frozen material from 76 primary human retinoblastoma samples were profiled with Affymetrix human genome u133 plus 2.0 PM microarray
2015-07-01 | E-GEOD-59983 | biostudies-arrayexpress
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
Project description:Breast cancers can be classified using whole genome expression into distinct subtypes that show differences in patient prognosis. One of these groups, the basal-like carcinomas, are poorly differentiated, highly metastatic, and genomically unstable. These tumors also contain specific genetic alterations with one example being frequent p53 mutations. The loss of the tumor suppressor gene encoded by the retinoblastoma (RB1) locus is a well-characterized occurrence in many tumor types, however, its role in breast cancer is less clear with many reports demonstrating a Loss of Heterozygosity (LOH) that does not correlate with loss of RB1 protein expression. Here we report that LOH of the RB1 locus was observed at a high frequency in basal-like and luminal B tumors. These tumors also concurrently have low expression of RB1 mRNA as assessed by DNA microarray. As in previous reports, we also did not see a significant correlation between RB1 LOH and protein expression as measured by immunohistochemistry (IHC). p16INK4a, however, was highly expressed both by microarray and IHC, in basal-like tumors only presumably due to a previously reported feedback loop caused by RB1 loss. These results suggest that the functional loss of RB1 is a common event in the progression of basal-like and luminal B breast tumors, which may play a key role in dictating therapeutic responses Keywords: reference x sample
2008-09-18 | GSE10884 | GEO
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