Analysis of transcription profile for High Grade Serous Ovarian Cancer (HGSC) cell line panel and how it relates to chromosomal instability (CIN)
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ABSTRACT:
PROVIDER: PRJNA649284 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12340858.fastq.gz | Fastqsanger.gz | |||
| SRR12340858_1.fastq.gz | Fastqsanger.gz | |||
| SRR12340858_2.fastq.gz | Fastqsanger.gz | |||
| SRR12340859.fastq.gz | Fastqsanger.gz | |||
| SRR12340859_1.fastq.gz | Fastqsanger.gz |
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Project description:Seven HGSC cancer cell lines were analysed with two immortalised Fallopian tube derived cell lines as controls. RNAseq was used to identify which genes showed transcript changes in cell lines showing particular phenotypes for chromosomal instability; enrichment of genes in particular pathways was used to identify possible mechanisms of CIN.
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Project description:Profiling of loss of heterozygosity (LOH) in HGSC, subcrouping HGSC by LOH-based clustering and comparing to the LOH profiles of triple-negative breast cancer [previously submitted; GSE19594]. Study for the correlation of LOH burdern and LOH-based subgroups to clinical response to platinum-based chemotherapy in patients suffered from HGSC. SNP data (Affymetrix GenChip 250K SNP Nsp) from 47 high grade serous ovarian cancer were generated and used for LOH and copy number analysis, LOH-based hierarchical clustering to subclassify HGSC, and comparison to the chromosomal alterations in high grade brest cancer. The associstion between LOH-based subgroups and LOH burden and clinical resposne to platinum-based chemotherapy was investigated. The results were validated in two independent public opening datasets.
2012-11-06 | E-GEOD-39130 | biostudies-arrayexpress
Project description:Profiling of loss of heterozygosity (LOH) in HGSC, subcrouping HGSC by LOH-based clustering and comparing to the LOH profiles of triple-negative breast cancer [previously submitted; GSE19594]. Study for the correlation of LOH burdern and LOH-based subgroups to clinical response to platinum-based chemotherapy in patients suffered from HGSC.
2012-11-06 | GSE39130 | GEO
Project description:Background: The aim of this study was to identify differentially expressed miRNAs in high-grade serous ovarian carcinoma (HGSC), clear cell ovarian carcinoma (CCC) and ovarian surface epithelium (OSE). Selected miRNAs were evaluated for association with clinical parameters including survival, and miRNA/mRNA interactions were mapped. Results: Differentially expressed miRNAs between HGSC, CCC and OSE were identified, of which 18 were validated (p<0.01) using RT-qPCR in an extended cohort. Compared with OSE, miR-205-5p was the most overexpressed miRNA in HGSC. miR-200 family members and miR-182-5p were the most overexpressed in HGSC and CCC compared with OSE, whereas miR-383 was the most underexpressed. miR-509-3-5p, miR-509-5p, miR-509-3p and miR-510 were among the strongest differentiators between HGSC and CCC, all being significantly overexpressed in CCC compared with HGSC. High miR-200c-3p expression was associated with poor progression-free (p=0.031) and overall (p=0.026) survival in HGSC. Interacting miRNAs and mRNA targets, including those of a TP53-related pathway presented previously, were identified in HGSC. Conclusions: Several miRNAs are overexpressed in HGSC and CCC compared with OSE, including the miR-200 family, among which miR-200c-3p is associated with survival in HGSC. A set of miRNAs differentiates CCC from HGSC, of which miR-509-3-5p and miR-509-5p are the strongest classifiers. Several interactions between miRNAs and mRNAs in HGSC were mapped. Methods: Differences in miRNA expression between HGSC, CCC and OSE scrapings were analyzed by global miRNA expression profiling (Affymetrix GeneChip miRNA 2.0 Arrays, n=30), validated by RT-qPCR (n=63), and evaluated for associations with clinical parameters. For HGSC, differentially expressed miRNAs were linked to differentially expressed mRNAs identified previously (GSE36668).
2014-02-13 | E-GEOD-47841 | biostudies-arrayexpress
Project description:Here we show that ovarian progesterone is a crucial endogenous factor inducing metastatic ovarian cancer in a mouse model of high-grade serous carcinoma (HGSC). To examine the molecular signaling pathways underlying progesterone (P4)-induced HGSC development, we performed gene-expression profiling using RNA sequencing.
2020-12-29 | GSE157960 | GEO
Project description:Background: The aim of this study was to identify differentially expressed miRNAs in high-grade serous ovarian carcinoma (HGSC), clear cell ovarian carcinoma (CCC) and ovarian surface epithelium (OSE). Selected miRNAs were evaluated for association with clinical parameters including survival, and miRNA/mRNA interactions were mapped. Results: Differentially expressed miRNAs between HGSC, CCC and OSE were identified, of which 18 were validated (p<0.01) using RT-qPCR in an extended cohort. Compared with OSE, miR-205-5p was the most overexpressed miRNA in HGSC. miR-200 family members and miR-182-5p were the most overexpressed in HGSC and CCC compared with OSE, whereas miR-383 was the most underexpressed. miR-509-3-5p, miR-509-5p, miR-509-3p and miR-510 were among the strongest differentiators between HGSC and CCC, all being significantly overexpressed in CCC compared with HGSC. High miR-200c-3p expression was associated with poor progression-free (p=0.031) and overall (p=0.026) survival in HGSC. Interacting miRNAs and mRNA targets, including those of a TP53-related pathway presented previously, were identified in HGSC. Conclusions: Several miRNAs are overexpressed in HGSC and CCC compared with OSE, including the miR-200 family, among which miR-200c-3p is associated with survival in HGSC. A set of miRNAs differentiates CCC from HGSC, of which miR-509-3-5p and miR-509-5p are the strongest classifiers. Several interactions between miRNAs and mRNAs in HGSC were mapped.
2014-02-13 | GSE47841 | GEO
Project description:Samples were taken from colorectal cancers in surgically resected specimens in 35 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes that can be used for molecular markers for CIN phynotype. Specimens from 35 consecutive stage II and stage III patients who had undergone surgical resection of CRC were studied. Patients with familial adenomatous polyposis and HNPCC were excluded from the study. Specimens from tumors and corresponding normal tissues in surgically resected specimens were snap-frozen in liquid nitrogen and stored at -80 ºC until use. Parallel tumor specimens were formalin fixed and paraffin embedded for histological examination. DNA and RNA was extracted from paired tumor and normal tissue using frozen samples. The patients provided written, informed consent to the collection of specimens, and the local Ethics Committee approved the study protocol. MSI and LOH phenotype analysis were done as follows; Using DNA, we performed the polymerase chain reaction (PCR) and determined the MSI status. In addition to five microsatellite markers recommended by the National Cancer Institute workshop, we also used TP53, D18S46, D18S363 and D18S474.9 We determined LOH status in non–MSI-high tumors, because LOH is rare in MSI-high tumors and also interpretation of LOH is difficult in MSI-high tumors. We defined LOH at each locus as a 50% reduction in the height of one of two allele peaks in tumor DNA relative to non-neoplastic control DNA. LOH was defined as present if any of the markers on the same chromosome show LOH. In order to evaluate the severity of chromosomal instability based on the actual frequency of LOH among evaluable loci, we defined the LOH Ratio (%) as: LOH Ratio (%) = Total number of chromosomes with LOH / Total number of chromosomes that could be evaluated for LOH × 100. Depending on the LOH Ratio, we classified tumors as having high levels of chromosomal instability (CIN-high) (33% < LOH Ratio < 100%) or low levels of chromosomal instability (CIN-low) (0% < LOH Ratio <33%). Furthermore, CIN-high tumors were divided into two subgroups; CIN-high (mild type) (33% < LOH Ratio < 75%) and CIN-high (severe type) (75% < LOH Ratio <100%).
2012-07-03 | E-GEOD-30540 | biostudies-arrayexpress
Project description:Samples were taken from colorectal cancers in surgically resected specimens in 33 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes that can be used for molecular markers for CIN phynotype Specimens from 33 consecutive stage II and stage III patients who had undergone surgical resection of CRC were studied. Patients with familial adenomatous polyposis and HNPCC were excluded from the study. Specimens from tumors and corresponding normal tissues in surgically resected specimens were snap-frozen in liquid nitrogen and stored at -80degreesC until use. Parallel tumor specimens were formalin fixed and paraffin embedded for histological examination. DNA and RNA was extracted from paired tumor and normal tissue using frozen samples. The patients provided written, informed consent to the collection of specimens, and the local Ethics Committee approved the study protocol. MSI and LOH phenotype analysis were done as follows; Using DNA, we performed the polymerase chain reaction (PCR) and determined the MSI status. In addition to five microsatellite markers recommended by the National Cancer Institute workshop, we also used TP53, D18S46, D18S363 and D18S474.9 We determined LOH status in non–MSI-high tumors, because LOH is rare in MSI-high tumors and also interpretation of LOH is difficult in MSI-high tumors. We defined LOH at each locus as a 50% reduction in the height of one of two allele peaks in tumor DNA relative to non-neoplastic control DNA. LOH was defined as present if any of the markers on the same chromosome show LOH. In order to evaluate the severity of chromosomal instability based on the actual frequency of LOH among evaluable loci, we defined the LOH Ratio (%) as: LOH Ratio (%) = Total number of chromosomes with LOH / Total number of chromosomes that could be evaluated for LOH × 100. Depending on the LOH Ratio, we classified tumors as having high levels of chromosomal instability (CIN-high) (33% < LOH Ratio < 100%) or low levels of chromosomal instability (CIN-low) (0% < LOH Ratio <33%). Furthermore, CIN-high tumors were divided into two subgroups; CIN-high (mild type) (33% < LOH Ratio < 75%) and CIN-high (severe type) (75% < LOH Ratio <100%).
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Project description:Samples were taken from colorectal cancers in surgically resected specimens in 35 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133 Plus 2.0 arrays. Comparison between the sample groups allow to identify a set of discriminating genes that can be used for molecular markers for CIN phynotype.
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2012-11-29 | GSE34489 | GEO