Identification of a Potential Ovarian Cancer Stem Cell Gene Expression Profile from Advanced Stage Papillary Serous Ovarian Cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Michael Birrer
PROVIDER: E-GEOD-33874 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To identify the potential ovarian cancer stem cell gene expression profile from isolated side population of fresh ascites obtained from women with high-grade advanced stage papillary serous ovarian adenocarcinoma Microarrays were used to interrogate the differentially expressed genes between side population (SP) and main population (MP) isolated from fresh ascites obtained from women with high-grade advanced stage papillary serous ovarian adenocarcinoma, and the results were analyzed by paired T-test using BRB-ArrayTools
2011-11-23 | GSE33874 | GEO
Project description:To identify the gene signature accounting for the distinct clinical outcomes in ovarian clear cell cancer patients Clear cell ovarian cancer is an epithelial ovarian cancer histotype that is less responsive to chemotherapy and carries poorer prognosis than serous and endometrioid histotypes. Despite this, patients with these tumors are treated in a similar fashion as all other ovarian cancers. Previous genomic analysis has suggested that clear cell cancers represent a unique tumor subtype. Here we generated the first whole genomic expression profiling using epithelial component of clear cell ovarian cancers and normal ovarian surface specimens isolated by laser capture microdissection. Arrays analyzed using BRB ArrayTools and PathwayStudio software was used to identify the signaling pathways. Gene expression profiling was completed for 10 clear cell ovarian cancer specimens and 10 normal ovarian surface epithelium using the Affymetrix human U133 Plus 2.0 Arrays
2011-05-24 | E-GEOD-29450 | biostudies-arrayexpress
Project description:Ovarian cancer is a major cause of cancer mortality among women largely due to late diagnosis of advanced stage metastatic disease. More extensive molecular analysis of metastatic ovarian cancer is needed to identify post-translational modifications of proteins particularly associated with metastatic disease so that we can better understand the metastatic process and identify potential therapeutic targets. Proteins are the target of many recently developed cancer treatments, but an often neglected aspect of biomarker discovery is protein glycosylation, especially those involving tumor-associated carbohydrate antigens (TACAs) such as sialyl-Lewis(x) (SLe(x) and sialyl-Lewis(a) (SLe(a), which have been identified in various cancers. Although it is already known that considerable changes in protein glycosylation are major contributors to the initiation, progression and metastasis of tumors, specifics about glycosylation changes particularly important to the metastatic process are still lacking. In this report we describe the results of a combined glycomic and proteomic study of metastatic ovarian cancer (OC) ascites fluids. Glycoproteins in ascites fluid were enriched by affinity binding to lectins (ConA or WGA) and other affinity matrices. Separate glycomic and proteomic analyses were performed as well as glycopeptide analyses. Relative abundances of different N-glycan groups and proteins were identified from original ascites fluids and corresponding lectin bound samples. Levels of biomarkers CA125, MUC1 and fibronectin were also monitored in these samples by Western blot analysis. N-glycan analysis of ascites fluids showed the presence of large, highly fucosylated and sialylated, complex and hybrid glycans, some of which were not observed in normal serum. Proteins in OC ascites that were more abundant or not present in the serum control, were haptoglobin, fibronectin, lumican, fibulin, hemopexin, ceruloplasmin, alpha-1-antitrypsin and alpha-1-antichymotrypsin. Glycopeptide analysis identified N- and O-glycans in clusterin, hemopexin, and fibulin that were present in OC ascites.
2016-08-15 | PXD003794 | Pride
Project description:Primary cells from high grade serous ovarian carcinoma patients, derived from ascites and omentum were sequenced to study signaling networks.
2021-11-01 | E-MTAB-10611 | biostudies-arrayexpress
Project description:Background: Malignant ascites is often present at diagnostic in women with advanced ovarian cancer (OC) and its presence is associated with a worse outcome. Human peritoneal mesothelial cells (HPMCs) are key components of malignant ascites. Although the interplay between HPMCs and OC cells is believed to be critical for tumor progression, it has not been well characterized. The purpose of this study was to assess the effect of ascites on HPMCs and clarify the role of HPMCs in OC progression. Methods: Human OC ascites and benign peritoneal fluids were assessed for their ability to stimulate HPMC proliferation. Conditioned medium from ascites- and benign fluid-stimulated HPMCs were compared for their ability to attenuate apoptosis induced by TNF-related apoptosis-inducing ligand (TRAIL). We conducted a comparative analysis of global expression changes in ascites-stimulated HPMCs using Agilent oligonucleotide microarrays. Results: As compared to benign peritoneal fluids, malignant ascites stimulated the proliferation of HPMCs. TRAIL-induced apoptosis was attenuated in OC cells exposed to conditioned medium from ascites-stimulated HPMCs as compared to OC cells exposed to conditioned medium from benign fluid-stimulated HPMCs. A total of 649 genes were differentially expressed in ascites-stimulated HPMCs. Based on a ratio of more than 1.5-fold and a P < 0.05, 484 genes were up-regulated and 165 genes were down-regulated in ascites-exposed HPMCs. Stimulation of HPMCs with OC ascites resulted in differential expression of genes mainly associated with the regulation of cell growth and proliferation, cell death, cell cycle and cell assembly and organization, compared to benign peritoneal fluids. Top networks up-regulated by OC ascites included Akt and NF-M-NM-:B survival pathways whereas vascular endothelial growth factor (VEGF) pathway was down-regulated. Conclusions: The results of this study not only provide evidence supporting the importance of the interplay between cancer cells and HPMCs but also define the role that the tumor environment plays in these interactions. The expression profiles from human peritoneal mesothelial cells (HPMC) cultures exposed to peritoneal fluids and ovarian cancer ascites were compared using the Agilent Whole Human Genome Oligonucleotide microarrays, containing 44,000 genes. Microarrays were performed on HPMCs exposed to 3 malignant ascites from women with advanced (stage III/IV) serous OC and two benign peritoneal fluids. First, we generated lists of significantly up-regulated and down-regulated genes that were differentially expressed between OC ascites (OVC346, OVC508 and OVC509) and control OV370 peritoneal fluid. Then, the set of genes that were commonly expressed between control peritoneal fluids (OV370 and OV401) were subtracted from the first list of genes to generate a dataset of differentially expressed genes between malignant ascites and benign peritoneal fluids.
2014-04-14 | E-GEOD-55065 | biostudies-arrayexpress
Project description:Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumour progression. Mouse ovarian cancer ascites (MASE2) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of MASE2 into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumour burden. Microarray analysis performed on cells derived from mouse ovarian cancer ascites (MASE2) treated with and without E2 indicated that E2 treatment caused the upregulation and downregulation of genes involved in cell differentiation, proliferation and migration. In particular, Greb1 that has been also identified as a hormone-responsive gene in breast cances, was upregulated in mouse tumour cells treated with E2. Three biological replicates (MASE2 tumours grown in SCID mice, see growth protocol) were analyzed for both conditions of addition of E2 or placebo.
2014-01-20 | E-GEOD-45271 | biostudies-arrayexpress
Project description:The secretomes of tumor cells, and macrophages from high grade serous ovarian carcinoma from the ascites of patients undergoing primary surgery were analysed after 24h culture (ex vivo) via obitrap.
2017-11-17 | PXD008047 | Pride
Project description:Tumor associated macrophages from high grade serous ovarian cancer ascites were treated with 1 μM of the Prostacyclin analoga MRE and DMSO (as solvent control). The aim of this experiment is to see which effect the Prostacyclin analoga has on RNA expression (activation of signaling pathways). Background: Prostacyclin receptor expression is elevated in TAMs. Prostacyclinsynthase expression was detected mainly in CAFs.
2023-08-31 | E-MTAB-12441 | biostudies-arrayexpress
Project description:Ovarian cancer is characterized by transcoelomic metastasis into the peritoneal cavity. The peritoneal malignant ascites is enriched with ovarian cancer cells and a small amount of tumor-associated immune cells which create a unique microenvironment actively contributing to progression of the disease. However, it is remain unclear how cancer cells communicate to its local environment under the influence of chemotherapy. To address this issue, we performed LC-MS/MS analyses of ovarian cancer ascites from the same patients before and after chemotherapy. We found that neoadjuvant chemotherapy causes a significant changes in the composition of ascites, and these changes are similar in samples obtained from all patients (n=10). Functional annotation of upregulated proteins with the use of KEGG and GO databases revealed that malignant ascites after chemotherapy were enriched with the cluster of spliceosomal proteins. These splicing factors were linked to induction of epithelial-to-mesenchymal transition leading to a more aggressive phenotype of cancer cells.
2024-05-29 | PXD019327 | Pride
Project description:We present evidence for an autocrine cytokine network in human ovarian cancer that has paracrine actions on the tumour microenvironment. In experiments using bioinformatics analysis of large gene expression array datasets and ovarian cancer biopsies, we found that the inflammatory cytokines TNF-α and IL-6, the chemokine receptor CXCR4 and its ligand CXCL12, are co-regulated in malignant cells. We named this co-regulation the TNF network. We had access to a unique set of ascites cell samples from patients with advanced ovarian cancer treated with the therapeutic anti-human TNF-α antibody infliximab. Serial samples pre and during treatment were obtained during paracentesis (drainage of ascites fluid for symptomatic relief). In nine of these patients there was sufficient mRNA available for gene expression profile analysis before treatment. The Affymetrix GeneChip Human Genome U133Plus 2.0 arrays were used to define gene expression profiles in each of the ascites cell samples.
2009-12-31 | E-GEOD-18681 | biostudies-arrayexpress