MCGH of cervical cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE1715 | GEO | 2005/04/13
SECONDARY ACCESSION(S): PRJNA90375
REPOSITORIES: GEO
Similar Datasets
Project description:Genomic alteration of cervical cancer samples. Analysis by CGH array. Array spotted at AECOM (NY) with human ESTs. Analysis as in Bourdon et al. Cancer Res. 2002 Nov 1;62(21):6218-23
2010-06-10 | E-GEOD-1715 | biostudies-arrayexpress
Project description:Gene expression profiling of 82 patients with cervical cancer was performed. The expression data were correlated with copy number alterations of the same patients, as assessed with array CGH in a separate study, in order to identify drivers of cervical cancer carcinogenesis.
2013-01-31 | GSE27469 | GEO
Project description:BACKGROUND: Cervical carcinoma develops as a result of multiple genetic alterations. Different studies investigated genomic alterations in cervical cancer mainly by means of metaphase comparative genomic hybridization (mCGH) and microsatellite marker analysis for the detection of loss of heterozygosity (LOH). Currently, high throughput methods such as array comparative genomic hybridization (array CGH), single nucleotide polymorphism array (SNP array) and gene expression arrays are available to study genome-wide alterations. Integration of these 3 platforms allows detection of genomic alterations at high resolution and investigation of an association between copy number changes and expression. RESULTS: Genome-wide copy number and genotype analysis of 10 cervical cancer cell lines by array CGH and SNP array showed highly complex large-scale alterations. A comparison between array CGH and SNP array revealed that the overall concordance in detection of the same areas with copy number alterations (CNA) was above 90%. The use of SNP arrays demonstrated that about 75% of LOH events would not have been found by methods which screen for copy number changes, such as array CGH, since these were LOH events without CNA. Regions frequently targeted by CNA, as determined by array CGH, such as amplification of 5p and 20q, and loss of 8p were confirmed by fluorescent in situ hybridization (FISH). Genome-wide, we did not find a correlation between copy-number and gene expression. At chromosome arm 5p however, 22% of the genes were significantly upregulated in cell lines with amplifications as compared to cell lines without amplifications, as measured by gene expression arrays. For 3 genes, SKP2, ANKH and TRIO, expression differences were confirmed by quantitative real-time PCR (qRT-PCR). CONCLUSION: This study showed that copy number data retrieved from either array CGH or SNP array are comparable and that the integration of genome-wide LOH, copy number and gene expression is useful for the identification of gene specific targets that could be relevant for the development and progression in cervical cancer. Keywords: DNA copynumber RNA expression correlation
2007-07-31 | GSE8605 | GEO
Project description:Cervical intraepithelial neoplasia (CIN), also known as cervical dysplasia, is premalignant lesions of the cervical squamous cell carcinoma (CSCC) that shows abnormal growth of squamous cells in the cervix epithelium. Given the evidence suggesting that differences may exist between CIN and CSCC, we hypothesize that progression may be mediated by subpopulation selection or by acquisition of additional alterations, including gene mutations or chromosomal alterations. In this study, we analyzed cervical CIN, microinvasive carcinoma (MIC) and CSCC by whole-exome sequencing and array-comparative genomic hybridization (array-CGH) and found that CIN genomes harbored fewer mutations (especially fewer driver mutations) and copy number alterations (CNAs), suggesting that additional genomic alterations might burst onto the CIN genome at the final stage of CIN progression to CSCC or an early stage of CSCC.
2014-12-31 | GSE60067 | GEO
Project description:Arrays analyses of CEM non infected and CEM infected by HIV wtNDK or HIV m7NDK (mutant). The arrays used were done at AECOM (ET arrays) and by affymetrix. They were hybridized with RNA of the cell lines infected or not. The analyses done as in bourdon et al. Cancer Res. 2002 Nov 1;62(21):6218-23, and with genesis. Keywords: parallel sample
2005-04-13 | GSE1716 | GEO
Project description:Array CGH data were used to depict the prognostic 3p region and its candidate target genes in cervical cancer
2013-03-08 | E-MTAB-1161 | biostudies-arrayexpress
Project description:Gene expression profiling of 82 patients with cervical cancer was performed. The expression data were correlated with copy number alterations of the same patients, as assessed with array CGH in a separate study, in order to identify drivers of cervical cancer carcinogenesis. In total, 82 patients with cervical cancer, stage 1b bulky through 4a, were included. Pretreatment biopsies were taken from the tumors and analyzed with Illumina gene expression BeadArrays (Human WG-6 v3).
2013-01-31 | E-GEOD-27469 | biostudies-arrayexpress
Project description:BACKGROUND: Cervical carcinoma develops as a result of multiple genetic alterations. Different studies investigated genomic alterations in cervical cancer mainly by means of metaphase comparative genomic hybridization (mCGH) and microsatellite marker analysis for the detection of loss of heterozygosity (LOH). Currently, high throughput methods such as array comparative genomic hybridization (array CGH), single nucleotide polymorphism array (SNP array) and gene expression arrays are available to study genome-wide alterations. Integration of these 3 platforms allows detection of genomic alterations at high resolution and investigation of an association between copy number changes and expression. RESULTS: Genome-wide copy number and genotype analysis of 10 cervical cancer cell lines by array CGH and SNP array showed highly complex large-scale alterations. A comparison between array CGH and SNP array revealed that the overall concordance in detection of the same areas with copy number alterations (CNA) was above 90%. The use of SNP arrays demonstrated that about 75% of LOH events would not have been found by methods which screen for copy number changes, such as array CGH, since these were LOH events without CNA. Regions frequently targeted by CNA, as determined by array CGH, such as amplification of 5p and 20q, and loss of 8p were confirmed by fluorescent in situ hybridization (FISH). Genome-wide, we did not find a correlation between copy-number and gene expression. At chromosome arm 5p however, 22% of the genes were significantly upregulated in cell lines with amplifications as compared to cell lines without amplifications, as measured by gene expression arrays. For 3 genes, SKP2, ANKH and TRIO, expression differences were confirmed by quantitative real-time PCR (qRT-PCR). CONCLUSION: This study showed that copy number data retrieved from either array CGH or SNP array are comparable and that the integration of genome-wide LOH, copy number and gene expression is useful for the identification of gene specific targets that could be relevant for the development and progression in cervical cancer. Keywords: DNA copynumber RNA expression correlation Cervival cancer cell lines were hybridized to Affymetrix Focus arrays in duplicate. Correlations were made with copynumber profiles from arrayCGH and SNP arrays.
2010-06-05 | E-GEOD-8605 | biostudies-arrayexpress
Project description:Arrays analyses of CEM non infected and CEM infected by HIV wtNDK or HIV m7NDK (mutant). The arrays used were done at AECOM (ET arrays) and by affymetrix. They were hybridized with RNA of the cell lines infected or not. The analyses done as in bourdon et al. Cancer Res. 2002 Nov 1;62(21):6218-23, and with genesis. Keywords: parallel sample
2010-06-10 | E-GEOD-1716 | biostudies-arrayexpress
Project description:Cervical cancer is the second most common malignancy in women worldwide, with high risk subtypes of human papillomavirus (HPV) constituting the major etiological agent. However, only a small percentage of women infected by the virus develop disease suggesting that additional host genetic alterations are necessary for disease progression. In this study we examined the genomes of a panel of commonly used model cervical cancer cell lines using a recently developed whole genome tiling path array for CGH analysis. Detailed analysis of genomic profiles enabled the detection of many novel aberrations which may have been missed by conventional cytogenetic methods. In total, 27 minimal regions of recurrent copy number alteration were identified that are potentially involved in tumorigenesis. Interestingly, fine mapping of the 3q gain, which is associated with the progression of precursor lesions to invasive cervical cancer, identified a minimal region of alteration harboring genes distinct from previous candidates. Novel regions of gene amplification, including the co-amplification of both the Birc and MMP gene clusters on 11q22, were also evident. Lastly, characterization of genomic structure at sites of HPV integration identified the copy number gain of host cellular sequences between the viral-host genomic boundaries in both SiHa and SW756, suggesting a direct role for HPV integration in the development of genetic abnormalities that initiate cervical cancer. This work represents the highest resolution look at a cervical cancer genome to date and offers definitive characterization of the alteration status of these cancer genomes. Keywords: array CGH, copy number, cervical cancer, genetic alterations, HPV integration, 3q
2007-06-12 | GSE5049 | GEO