ACGH profiling of prostate tumors
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE29227 | GEO | 2011/12/19
SECONDARY ACCESSION(S): PRJNA142937
REPOSITORIES: GEO
Similar Datasets
Project description:This experiment was an aCGH study on 86 prostate tumors samples. The samples were profiled on Agilent Human Genome 44karrays to identify recurrent regions of deletion and amplification, thus revealing potential new tumor suppressor genes and/or oncogenes involved in prostate cancer. The CGH profile on the 44k arrays revealed a deletion at 5q21 in 17% of samples. CGH analysis of 86 prostate tumor samples.
2011-12-19 | E-GEOD-29227 | biostudies-arrayexpress
Project description:Advanced prostate cancer is a highly heterogenous disease with few in vitro models. We report generation of seven novel 3D organoid lines of patient-derived prostate cancer. We determine the copy number alterations of these lines using array CGH. They contain may classic alterations of prostate cancer such as lost of the short arm of chromosome 8 and gain of the long arm of chromosome 8. In addition, we found homozygous deleteion of tumor suppressor PTEN and CHD1 as well as the TMPRSS2-ERG interstitial deletion. Prostate cancer organoid lines, ~2 months after in vitro propagation, were used for profiling on Agilent 1M aCGH arrays per manufacturer's instructions. A pooled reference normal DNA was used as the reference.
2014-09-09 | E-GEOD-60612 | biostudies-arrayexpress
Project description:Title: Array-based gene expression, CGH and tissue data define a 12q24 gain in neuroblastic tumors with prognostic implication. Background: Neuroblastoma has successfully served as a model system for the identification of neuroectoderm-derived oncogenes. However, in spite of various efforts, only a few clinically useful prognostic markers have been found. Here, we present a framework, which integrates DNA, RNA and tissue data to identify and prioritize genetic events that represent clinically relevant new therapeutic targets and prognostic biomarkers for neuroblastoma. Methods: A single-gene resolution aCGH profiling was integrated with microarray-based gene expression profiling data to distinguish genetic copy number alterations that were strongly associated with transcriptional changes in two neuroblastoma cell lines. FISH analysis using a hotspot tumour tissue microarray of 37 paraffin-embedded neuroblastoma samples and in silico data mining for gene expression information obtained from previously published studies including up to 445 healthy nervous system samples and 123 neuroblastoma samples were used to evaluate the clinical significance and transcriptional consequences of the detected alterations and to identify subsequently activated gene(s). Results: In addition to the anticipated high-level amplification and subsequent overexpression of MYCN, MEIS1, CDK4 and MDM2 oncogenes, the aCGH analysis revealed numerous other genetic alterations, including microamplifications at 2p and 12q24.11. Most interestingly, we identified and investigated the clinical relevance of a previously poorly characterized amplicon at 12q24.31. FISH analysis showed low-level gain of 12q24.31 in 14 of 33 (42%) neuroblastomas. Patients with the low-level gain had an intermediate prognosis in comparison to patients with MYCN amplification (poor prognosis) and to those with no MYCN amplification or 12q24.31 gain (good prognosis) (P = 0.001). Using the in silico data mining approach, we identified elevated expression of five genes located at the 12q24.31 amplicon in neuroblastoma (DIABLO, ZCCHC8, RSRC2, KNTC1 and MPHOSPH9). Among these, DIABLO showed the strongest activation suggesting a putative role in neuroblastoma progression. Conclusions: The presented systematic and rapid framework, which integrates aCGH, gene expression and tissue data to obtain novel targets and biomarkers for cancer, identified a low-level gain of the 12q24.31 as a potential new biomarker for neuroblastoma progression. Furthermore, results of in silico data mining suggest a new neuroblastoma target gene, DIABLO, within this region, whose functional and therapeutic role remains to be elucidated in follow-up studies.
2010-05-05 | GSE18143 | GEO
Project description:67 tumor samples were aCGH profiled in order to obtain frequencies of recurrent copy number alterations intended to posterior correlations with clinical data. 16 cell lines were characterized as well.
2011-08-01 | GSE20355 | GEO
Project description:This set includes individuals from 10 different primate species whose genomic DNA was used in an array-based comparative genomic hybridization (aCGH)using human cDNA microarrays to detect gene copy number variation across 10 primate species. An organism part comparison experiment design type compares tissues, regions, organs within or between organisms. Keywords: organism_part_comparison_design, array CGH
2012-02-24 | GSE9028 | GEO
Project description:A custom high-density oligonucleotide array CGH (HD aCGH) was designed to facilitate the accurate mapping of the boundaries of the recurrent breakpoint at 3q13.31in 8 osteosarcoma tumors and cell lines Keywords: Genetic analysis by HD aCGH
2016-01-01 | GSE12788 | GEO
Project description:Oligonucleotide aCGH profiles from 37 neuroblastoma tumor samples were generated using 44K or 105K microarrays.
2014-06-01 | GSE56109 | GEO
Project description:Title: Array-based gene expression, CGH and tissue data define a 12q24 gain in neuroblastic tumors with prognostic implication. Background: Neuroblastoma has successfully served as a model system for the identification of neuroectoderm-derived oncogenes. However, in spite of various efforts, only a few clinically useful prognostic markers have been found. Here, we present a framework, which integrates DNA, RNA and tissue data to identify and prioritize genetic events that represent clinically relevant new therapeutic targets and prognostic biomarkers for neuroblastoma. Methods: A single-gene resolution aCGH profiling was integrated with microarray-based gene expression profiling data to distinguish genetic copy number alterations that were strongly associated with transcriptional changes in two neuroblastoma cell lines. FISH analysis using a hotspot tumour tissue microarray of 37 paraffin-embedded neuroblastoma samples and in silico data mining for gene expression information obtained from previously published studies including up to 445 healthy nervous system samples and 123 neuroblastoma samples were used to evaluate the clinical significance and transcriptional consequences of the detected alterations and to identify subsequently activated gene(s). Results: In addition to the anticipated high-level amplification and subsequent overexpression of MYCN, MEIS1, CDK4 and MDM2 oncogenes, the aCGH analysis revealed numerous other genetic alterations, including microamplifications at 2p and 12q24.11. Most interestingly, we identified and investigated the clinical relevance of a previously poorly characterized amplicon at 12q24.31. FISH analysis showed low-level gain of 12q24.31 in 14 of 33 (42%) neuroblastomas. Patients with the low-level gain had an intermediate prognosis in comparison to patients with MYCN amplification (poor prognosis) and to those with no MYCN amplification or 12q24.31 gain (good prognosis) (P = 0.001). Using the in silico data mining approach, we identified elevated expression of five genes located at the 12q24.31 amplicon in neuroblastoma (DIABLO, ZCCHC8, RSRC2, KNTC1 and MPHOSPH9). Among these, DIABLO showed the strongest activation suggesting a putative role in neuroblastoma progression. Conclusions: The presented systematic and rapid framework, which integrates aCGH, gene expression and tissue data to obtain novel targets and biomarkers for cancer, identified a low-level gain of the 12q24.31 as a potential new biomarker for neuroblastoma progression. Furthermore, results of in silico data mining suggest a new neuroblastoma target gene, DIABLO, within this region, whose functional and therapeutic role remains to be elucidated in follow-up studies. High-resolution aCGH was utilized to identify novel genetic alterations in two neuroblastoma cell lines, NGP and IMR-32. Through the integration of gene copy number and gene expression data, the impact of copy number changes on expression levels was determined. Fluorescence in situ hybridization (FISH) on a tissue microarray (TMA) format was used to assess the clinical significance of the identified copy number increase at 12q24.31 in neuroblastoma patients. Finally, we used in silico data mining of publicly available transcriptomics data, to evaluate the transcriptional consequences of the detected 12q24.31 alteration and to identify subsequently activated gene(s). Here, aCGH of the NGP and IMR-32 cell lines was performed. Male genomic DNA was used as reference.
2010-05-05 | E-GEOD-18143 | biostudies-arrayexpress
Project description:Parallel aSNP and aCGH analyses were performed on 22 samples from MDS patients with a normal karyotype. 55 overlapping alterations, most of these corresponding to CNVs were identified with both methods. Putative tumour specific imbalances were found with both methods in three cases, a deletion of TET2, a larger deletion containing DNMT3A and one complex molecular karyotype. In two cases putative tumour specific imbalances were only seen with aCGH: a 16p deletion in a low number of cells and a small homozygous deletion in WWOX. Telomeric UPDs were only detected with aSNP in two cases: one affecting chromosome 3q and in the other, two UPD regions were present on 4q and 5p. In total, putative relevant tumour specific genomic alterations were found in seven cases (32%). Three small aberrations only detected by aCGH were present in T-cells, suggestive of germ line alterations which may confer a risk for MDS development. This part contains the aCGH analyses, for aSNP see GSE49004.
2017-01-01 | GSE50897 | GEO
Project description:Advanced prostate cancer is a highly heterogenous disease with few in vitro models. We report generation of seven novel 3D organoid lines of patient-derived prostate cancer. We determine the copy number alterations of these lines using array CGH. They contain may classic alterations of prostate cancer such as lost of the short arm of chromosome 8 and gain of the long arm of chromosome 8. In addition, we found homozygous deleteion of tumor suppressor PTEN and CHD1 as well as the TMPRSS2-ERG interstitial deletion.
2014-09-09 | GSE60612 | GEO