Drivers of gene expression in cervical cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE27469 | GEO | 2013/01/31
SECONDARY ACCESSION(S): PRJNA138439
REPOSITORIES: GEO
Similar Datasets
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:Cervical cancer is the one of the most common cancer type among women worldwide, with Human Papillomavirus (HPV) playing a causal role in this disease. We applied a novel integrative approach to understand the disease process and find its major drivers. We performed a meta-analysis of gene expression and chromosomal aberration studies comprising data on over 500 patients for the reconstruction of a regulatory meta-network. We found that two sub-networks representing cell cycle and antiviral response (largely involving interferon pathways) were driven by chromosomal amplifications of key regulator genes. In the majority of patients, the two types of drivers were located in the same regions of chromosomal aberrations on 3q, 1q and 1p suggesting that a synergistic effect of both processes is necessary for cervical oncogenesis. In addition, our results revealed a cause of antiviral response in the tumor supporting a model of cervical carcinogenesis in which the loss of episomal HPV mediated by immune response promotes the expression of integrated viral oncogenes and tumor progression. This series is a part of meta-analysis on gene expression in cervical cancer Forty cervical cancer biopsies and twenty normal adjacent tissue samples were obtained from patients with cervical squamous cell carcinomas. Twelve tumor samples were hybridized as pools of two samples, due to RNA quantity limitations. So, in total, there are 34 cervical cancer and 20 normal sample arrays. We used an internal reference design, where the reference RNA sample consisted of a pool of amplified RNAs from cervical cancer biopsies.
2011-12-29 | E-GEOD-26342 | biostudies-arrayexpress
Project description:Cervical cancer is the one of the most common cancer type among women worldwide, with Human Papillomavirus (HPV) playing a causal role in this disease. We applied a novel integrative approach to understand the disease process and find its major drivers. We performed a meta-analysis of gene expression and chromosomal aberration studies comprising data on over 500 patients for the reconstruction of a regulatory meta-network. We found that two sub-networks representing cell cycle and antiviral response (largely involving interferon pathways) were driven by chromosomal amplifications of key regulator genes. In the majority of patients, the two types of drivers were located in the same regions of chromosomal aberrations on 3q, 1q and 1p suggesting that a synergistic effect of both processes is necessary for cervical oncogenesis. In addition, our results revealed a cause of antiviral response in the tumor supporting a model of cervical carcinogenesis in which the loss of episomal HPV mediated by immune response promotes the expression of integrated viral oncogenes and tumor progression. This series is a part of meta-analysis on gene expression in cervical cancer
2011-12-29 | GSE26342 | GEO
Project description:Comparable plasma lipid changes in patients with high-grade cervical intraepithelial neoplasia and patients with cervical cancer
2020-10-22 | MSV000086351 | GNPS
Project description:We developed a discovery-validation mass-spectrometry based pipeline to identify a set of proteins that are regulated in serum of patients with cervical intraepithelial neoplasia (CIN) and squamous cell cervical cancer using isobaric Tags for Relative and Absolute Quantitation (iTRAQ®), label-free shotgun and targeted mass-spectrometric quantification. At the discovery stage we used a “pooling” strategy for the comparative analysis of immunodepleted serum from patients with early-(CES) and late-stage (CLS) cervical cancer versus healthy controls that revealed 15 up- and 26 down-regulated proteins. The analysis of non-depleted serum samples from patients with CIN, CES, CLS, and healthy controls showed significant changes in abundance of alpha-1-acid glycoprotein 1, alpha-1-antitrypsin, serotransferrin, haptoglobin, alpha-2-HS-glycoprotein and vitamin D-binding protein. To further validate our findings we developed a fast UPLC/MRM method for the simultaneous targeted quantification of these proteins in an independent set of serum from patients with cervical cancer or CIN and healthy controls as well as serum samples from patients with ovarian cancer. The panel of six proteins showed 72 % sensitivity and 82 % specificity for discrimination of patients with CIN from healthy controls, a stage of the disease where current protein-based biomarkers, e.g. squamous cell carcinoma antigen fail to show any discrimination.
2014-10-06 | PXD001055 | Pride
Project description:This study is aimed in identification of gene expression profiles in cervical cancer and the role of specific genes in cervical carcinogenesis. Keywords: Gene expression in cervical cancer
2008-06-04 | GSE9750 | GEO
Project description:Cervical cancer results from the accumulation of (epi)genetic aberrations following persistent infection with high-risk human papillomavirus (HPV). In order to define genetic aberrations associated with cervical carcinogenesis, chromosomal profiles of high-grade cervical intraepithelial neoplasia (CIN) were generated. Common aberrations usually encompass large genomic regions and contain numerous genes, hampering identification of actual driver genes. Consequently, direct evidence of chromosomal alterations actively contributing to cervical carcinogenesis has been lacking so far. By analyzing 60 high-grade CIN with high resolution arrayCGH we identified focal chromosomal aberrations that each harbour only one or a few genes. In total 74 focal aberrations were identified encoding 305 genes. Analysis of genes located within these focal aberrations, using two independent expression microarray datasets, revealed concurrent altered expression in high-grade CIN and/or cervical carcinomas compared to normal cervical samples for 8 genes: ATP13A3, HES1, OPA1, HRASLS, EYA2, ZMYND8, APOBEC2 and NCR2. Gene silencing of EYA2, located within a focal gain at 20q13, significantly reduced viability and migratory capacity of HPV16-transformed keratinocytes. Interestingly, for hsa-miR-375, located within the most frequently identified focal loss at 2q35, a direct correlation between a (focal) loss and significantly reduced expression was found. Down-regulation of hsa-miR-375 expression during cervical carcinogenesis was confirmed in a second independent series of cervical tissues. Moreover, ectopic expression of hsa-miR-375 in 2 cervical carcinoma cell lines reduced cellular viability. In conclusion, our data provide a proof of concept that chromosomal aberrations are actively contributing to HPV-induced carcinogenesis and identify EYA2 and hsa-mir-375 as oncogene and tumor suppressor gene, respectively. DNA from microdissected tissues: 60 samples total. 11 high-grade CIN, <5yr preceding hrHPV infection, 43 high-grade CIN >5yr preceding hrHPV infection, 6 CIN3 adjacent to SCC
2012-12-31 | E-GEOD-34575 | biostudies-arrayexpress
Project description:Cervical cancer results from the accumulation of (epi)genetic aberrations following persistent infection with high-risk human papillomavirus (HPV). In order to define genetic aberrations associated with cervical carcinogenesis, chromosomal profiles of high-grade cervical intraepithelial neoplasia (CIN) were generated. Common aberrations usually encompass large genomic regions and contain numerous genes, hampering identification of actual driver genes. Consequently, direct evidence of chromosomal alterations actively contributing to cervical carcinogenesis has been lacking so far. By analyzing 60 high-grade CIN with high resolution arrayCGH we identified focal chromosomal aberrations that each harbour only one or a few genes. In total 74 focal aberrations were identified encoding 305 genes. Analysis of genes located within these focal aberrations, using two independent expression microarray datasets, revealed concurrent altered expression in high-grade CIN and/or cervical carcinomas compared to normal cervical samples for 8 genes: ATP13A3, HES1, OPA1, HRASLS, EYA2, ZMYND8, APOBEC2 and NCR2. Gene silencing of EYA2, located within a focal gain at 20q13, significantly reduced viability and migratory capacity of HPV16-transformed keratinocytes. Interestingly, for hsa-miR-375, located within the most frequently identified focal loss at 2q35, a direct correlation between a (focal) loss and significantly reduced expression was found. Down-regulation of hsa-miR-375 expression during cervical carcinogenesis was confirmed in a second independent series of cervical tissues. Moreover, ectopic expression of hsa-miR-375 in 2 cervical carcinoma cell lines reduced cellular viability. In conclusion, our data provide a proof of concept that chromosomal aberrations are actively contributing to HPV-induced carcinogenesis and identify EYA2 and hsa-mir-375 as oncogene and tumor suppressor gene, respectively.
2012-12-31 | GSE34575 | GEO
Project description:We developed a discovery-validation mass-spectrometry based pipeline to identify a set of proteins that are regulated in serum of patients with cervical intraepithelial neoplasia (CIN) and squamous cell cervical cancer using isobaric Tags for Relative and Absolute Quantitation (iTRAQ®), label-free shotgun and targeted mass-spectrometric quantification. At the discovery stage we used a “pooling” strategy for the comparative analysis of immunodepleted serum from patients with early-(CES) and late-stage (CLS) cervical cancer versus healthy controls that revealed 15 up- and 26 down-regulated proteins. The analysis of a new of non-depleted serum samples from patients with CIN, CES, CLS, and healthy controls showed significant changes in abundance of alpha-1-acid glycoprotein 1, alpha-1-antitrypsin, serotransferrin, haptoglobin, alpha-2-HS-glycoprotein and vitamin D-binding protein. To further validate our findings we developed a fast UPLC/MRM method for the simultaneous targeted quantification of these proteins in a new set of 48 CIN, 50 CES, 34 CLS and 48 healthy controls as well as 49 serum samples from patients with ovarian cancer. The panel of six proteins showed 62% sensitivity and 82 % specificity for discrimination of patients with CIN grade 2 or worse from healthy controls, a stage of the disease where current protein-based biomarkers fail to show any discrimination.
2014-10-06 | PXD001034 | Pride
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 Keywords: parallel sample
2005-04-13 | GSE1715 | GEO