50K SNP Copy Number Analysis of Ovarian Carcinomas
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE13813 | GEO | 2009/02/17
SECONDARY ACCESSION(S): PRJNA110585
REPOSITORIES: GEO
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Project description:Genome-wide copy number variation was measured in primary tumours of the ovary, Fallopian tube and peritoneum. A well-defined subset of advanced-stage serous tumors was then used to relate CNV to primary resistance to treatment. Analysis is described in "Integrated Genome-wide DNA Copy Number and Expression Analysis Identifies Distinct Mechanisms of Primary Chemo-resistance in Ovarian Carcinomas", Etemadmoghadam et al. In press, Clinical Cancer Research. Experiment Overall Design: 118 needle-dissected or whole tumours (>80% tumour content) were analysed.
2009-03-01 | E-GEOD-13813 | biostudies-arrayexpress
Project description:A number of studies find that metastasis suppressor proteins, including RhoGDI2, may function in part though controlling expression of genes regulating metastasis (reviewed in Smith and Theodorescu, Nature Reviews Cancer, 2009, PMID: 19242414). To uncover systematically gene expression patterns dependent on RhoGDI2 expression, we profiled gene expression in stably transfected control (GFP empty vector) UM-UC-3 bladder carcinoma cells (which have lost endogenous expression of RhoGDI2, as occurs commonly in the progression of bladder cancer PMID: 15173088), as well as stably transfected GFP-tagged RhoGDI2 expressing UM-UC-3 cells. References: Moissoglu K, McRoberts KS, Meier JA, Theodorescu D et al. Rho GDP dissociation inhibitor 2 suppresses metastasis via unconventional regulation of RhoGTPases. Cancer Res 2009 Apr 1;69(7):2838-44. PMID: 19276387 Wu Y, Moissoglu K, Wang H, Wang X et al. Src phosphorylation of RhoGDI2 regulates its metastasis suppressor function. Proc Natl Acad Sci U S A 2009 Apr 7;106(14):5807-12. PMID: 19321744 Smith SC, Theodorescu D. Learning therapeutic lessons from metastasis suppressor proteins. Nat Rev Cancer 2009 Apr;9(4):253-64. PMID: 19242414 Theodorescu D, Sapinoso LM, Conaway MR, Oxford G et al. Reduced expression of metastasis suppressor RhoGDI2 is associated with decreased survival for patients with bladder cancer. Clin Cancer Res 2004 Jun 1;10(11):3800-6. PMID: 15173088
2012-04-15 | GSE35014 | GEO
Project description:To characterize Homologous recombination deficiency (BRCAness) in triple-negative breast cancer PDX models genomic signature was utilized. After normalization using Genotyping Console we obtained absolute copy number profiles using the GAP software (Popova et al, Genome Biol, 2009). The number of Large-scale State Transitions (LSTs) was used to annotate PDX as BRCAness or not (Popova et al, Cancer Res 2012).
2020-01-01 | E-MTAB-8654 | biostudies-arrayexpress
Project description:To characterize Homologous recombination deficiency (BRCAness) in triple-negative breast cancer PDX models genomic signature was utilized. After normalization using ChAS we obtained absolute copy number profiles using the GAP software (Popova et al, Genome Biol, 2009). The number of Large-scale State Transitions (LSTs) was used to annotate PDX as BRCAness or not (Popova et al, Cancer Res 2012).
2020-01-01 | E-MTAB-8653 | biostudies-arrayexpress
Project description:Integration of several ovarian cancer datasets to identify a reproducible predictors of survival Four microarray datasets from different institutions were reprocessed in a uniform manner, into a single training dataset. Survival analysis was performed and a validation cohort (61 patients from 3 institutions) was profiled using a custom array to confirm the prognostic value of the predictors. The four datasets were obtained from the following reports: Spentzos D, Levine DA, Ramoni MF, et al. Gene expression signature with independent prognostic significance in epithelial ovarian cancer. J Clin Oncol 2004;22:4700-10 Bild AH, Yao G, Chang JT, et al. Oncogenic pathway signatures in human cancers as a guide to targeted therapies. Nature 2006;439:353-7 Marquez RT, Baggerly KA, Patterson AP, et al. Patterns of gene expression in different histotypes of epithelial ovarian cancer correlate with those in normal fallopian tube, endometrium, and colon. Clin Cancer Res 2005;11:6116-26 Zhang L, Volinia S, Bonome T, et al. Genomic and epigenetic alterations deregulate microRNA expression in human epithelial ovarian cancer. Proc Natl Acad Sci U S A 2008;105:7004-9 61 samples
2011-06-15 | E-GEOD-19161 | biostudies-arrayexpress
Project description:A number of studies find that metastasis suppressor proteins, including RhoGDI2, may function in part though controlling expression of genes regulating metastasis (reviewed in Smith and Theodorescu, Nature Reviews Cancer, 2009, PMID: 19242414). To uncover systematically gene expression patterns dependent on RhoGDI2 expression, we profiled gene expression in stably transfected control (GFP empty vector) UM-UC-3 bladder carcinoma cells (which have lost endogenous expression of RhoGDI2, as occurs commonly in the progression of bladder cancer PMID: 15173088), as well as stably transfected GFP-tagged RhoGDI2 expressing UM-UC-3 cells. References: Moissoglu K, McRoberts KS, Meier JA, Theodorescu D et al. Rho GDP dissociation inhibitor 2 suppresses metastasis via unconventional regulation of RhoGTPases. Cancer Res 2009 Apr 1;69(7):2838-44. PMID: 19276387 Wu Y, Moissoglu K, Wang H, Wang X et al. Src phosphorylation of RhoGDI2 regulates its metastasis suppressor function. Proc Natl Acad Sci U S A 2009 Apr 7;106(14):5807-12. PMID: 19321744 Smith SC, Theodorescu D. Learning therapeutic lessons from metastasis suppressor proteins. Nat Rev Cancer 2009 Apr;9(4):253-64. PMID: 19242414 Theodorescu D, Sapinoso LM, Conaway MR, Oxford G et al. Reduced expression of metastasis suppressor RhoGDI2 is associated with decreased survival for patients with bladder cancer. Clin Cancer Res 2004 Jun 1;10(11):3800-6. PMID: 15173088 Two paired biological replicates of GFP (control) and GFP-RhoGDI2 (experimental) UM-UC-3 cells were prepared at different times, isolated during log phase growth, and subjected to gene expression profiling using the Affymetrix HG-U133 Plus 2.0 oligonucleotide microarray platform.
2012-04-14 | E-GEOD-35014 | biostudies-arrayexpress
Project description:Integration of several ovarian cancer datasets to identify a reproducible predictors of survival Four microarray datasets from different institutions were reprocessed in a uniform manner, into a single training dataset. Survival analysis was performed and a validation cohort (61 patients from 3 institutions) was profiled using a custom array to confirm the prognostic value of the predictors. The four datasets were obtained from the following reports: Spentzos D, Levine DA, Ramoni MF, et al. Gene expression signature with independent prognostic significance in epithelial ovarian cancer. J Clin Oncol 2004;22:4700-10 Bild AH, Yao G, Chang JT, et al. Oncogenic pathway signatures in human cancers as a guide to targeted therapies. Nature 2006;439:353-7 Marquez RT, Baggerly KA, Patterson AP, et al. Patterns of gene expression in different histotypes of epithelial ovarian cancer correlate with those in normal fallopian tube, endometrium, and colon. Clin Cancer Res 2005;11:6116-26 Zhang L, Volinia S, Bonome T, et al. Genomic and epigenetic alterations deregulate microRNA expression in human epithelial ovarian cancer. Proc Natl Acad Sci U S A 2008;105:7004-9
2011-06-15 | GSE19161 | GEO
Project description:Our study presents the first genetic models of de novo high-grade serous carcinomas (HGSC) that originate in fallopian tube secretory epithelial cells and recapitulate the key genetic alterations and precursor lesions characteristic of human invasive ovarian cancer. Genomic copy number analysis, using array CGH, was performed on murine tumors in order to compare the overlap of copy number alterations between HGSC models and TCGA data. Array CGH was performed on genomic DNA isolated from murine HGSC tumors. Genomic DNA from three normal mouse fallopian tubes was pooled and used as the reference.
2013-12-17 | E-GEOD-49827 | biostudies-arrayexpress
Project description:The cell of origin of serious ovarian cancer is unknown. To create a mouse model for this lethal cancer and identify early cancer biomarkers, we conditionally deleted both Dicer (essential for microRNA biosynthesis) and Pten (a negative regulator of the PI3K pathway) in the female reproductive tract. Beginning at ~3-5 months, these Dicer/Pten mutant mice develop high-grade serious carcinomas that initiate in the stroma of the fallopian tube through a mesenchymal-to-epithelial transition (MET), subsequently envelop the ovary, and then metastasize throughout the peritoneum, resulting in ascites and 100% lethality by 13 months. The fallopian tube cancers demonstrate upregulation of genes encoding known and novel secreted proteins that are potential biomarkers. This study uncovers a new paradigm for the initiation of high-grade serous ovarian cancer. RNA was isolated from the fallopian tube cancers of independent DKO mice and normal fallopian tubes of control mice and subjected to mRNA expression analysis using an Illumina platform (MouseWG-6 v2 Expression BeadChip).
2012-02-16 | E-GEOD-28720 | biostudies-arrayexpress
Project description:We performed whole exome sequencing and copy number analysis for 15 triplets, each comprising normal colorectal tissue, primary colorectal carcinoma, and its synchronous matched liver metastasis. We analyzed the similarities and differences between primary colorectal carcinoma and matched liver metastases in regards to somatic mutations and somatic copy number alterationss (SCNAs). The genomic profiling demonstrated mutations in APC(73%), KRAS (33%), ARID1A and PIK3CA (6.7%) genes between primary colorectal and metastatic liver tumors. TP53 mutation was observed in 47% of the primary samples and 67% in liver metastatic samples. The grouped pairs, in hierarchical clustering showed similar SCNA patterns, in contrast to the ungrouped pairs. Many mutations (including those of known key cancer driver genes) were shared in the grouped pairs. The ungrouped pairs exhibited distinct mutation patterns with no shared mutations in key driver genes. Four ungrouped liver metastasis samples had mutations in DNA mismatch repair genes along with hypermutations and a substantial number of copy number of alterations. Genomically, colorectal and metastatic liver tumors were very similar. However, in a subgroup of patients, there were genetic variations in liver metastases in the loss of DNA mismatch repair genes.
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