Array comparative genomic hybridization (CGH) analysis of ameloblastoma tumor
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE132473 | GEO | 2019/06/11
REPOSITORIES: GEO
Similar Datasets
Project description:Array comparative genomic hybridization (CGH) analysis of ameloblastoma tumor
| PRJNA548170 | ENA
Project description:This study investigates genomic imbalance in chronic lymphocytic leukemia (CLL) and aims to identify genomic gains and losses with prognostic significance.
2013-09-07 | GSE40834 | GEO
Project description:Array-CGH profiles of Merkel cell carcinoma tumors Experiment Overall Design: We perfromed array-CGH on 25 Merkel cell carcinoma tumor samples (2 primary/metastasis pairs) looking for recurrent gains/losses among the cohort of tumors. Experiment Overall Design: Results from the Analysis of Copy Errors (ACE) may be found in GSE13239_MccACEAnalyzedData.txt. Experiment Overall Design: The overall profiles of the primary/metastasis pairs are similar. These metastases samples, 1m and 3m, were excluded from the ACE analysis.
2009-01-14 | E-GEOD-13239 | biostudies-arrayexpress
Project description:Two commercial neuroblastoma cell lines (SIMA and SK-N-DZ) enriched their cancer stem cell (CSC) like cell population content by the use of conditioned cell culture media for neurospheres. Genomic gains and losses were analized by comparative genomic hybridization (CGH) array in CSC-like versus standard tumor cells culture.
2014-11-14 | E-MTAB-2866 | biostudies-arrayexpress
Project description:A series of studies have been published that evaluate the chromosomal copy number changes of different tumor classes using array Comparative Genomic Hybridization (array CGH), however the chromosomal aberrations that distinguish the different tumor classes have not been fully characterized. Therefore, we performed a meta-analysis of different array CGH data sets in an attempt to classify samples tested across different platforms. As opposed to RNA expression a common reference is used in dual channel CGH arrays: normal human DNA, theoretically facilitating cross-platform analysis. To this aim, cell line and primary cancer data sets from three different dual channel array CGH platforms obtained by four different institutes were integrated. The cell line data were used to develop preprocessing methods which performed noise reduction and transformed samples into a common format. The transformed array CGH profiles allowed perfect clustering by cell line, but importantly not by platform or institute. The same preprocessing procedures used for the cell line data were applied to data from 373 primary tumors profiled by array CGH, including controls. Results indicated that there is no apparent feature related to the institute or platform and that array CGH allows for unambiguous cross-platform meta-analysis. Major clusters with common tissue origin were identified. Interestingly, tumors of hematopoietic and mesenchymal origins cluster separately from tumors of epithelial origin. Therefore it can be concluded that chromosomal aberrations of tumors from hematopoietic and mesenchymal origin versus tumors of epithelial origin are distinct, and these differences can be picked up by metaanalysis of array CGH data. This suggests the possibility of prospectively using combined analysis of diverse copy number datasets for cancer subtype classification. Keywords: comparative genomic hybridization, meta-analysis, cancer
2006-08-29 | GSE5051 | GEO
Project description:Malignant melanoma is an aggressive heterogeneous disease for which new biomarkers for diagnosis and clinical outcome are needed. We investigated by array-CGH the presence of DNA gains and losses to provide better genomic profile of primary malignant melanoma and to explore the possibility to distinguish metastatic from non metastatic melanomas using this technology. High resolution array-CGH (Agilent Technologies, Palo Alto, CA), with more than 40.000 probes, has been used to analyze 20 frozen tissues of vertical growth phase primary melanoma with a minimum follow-up time of 36 months. Eight patients developed nodal metastatic disease and twelve did not. For results validation, 83 additional melanoma samples with similar clinical characteristics were analysed by FISH. DNA copy number aberrations (CNA) were observed in 19 out of 20 cases. The most frequent changes were complete or partial losses in chromosomes 9 (12 cases, 60%) and 10 (9 cases, 45%), partial gains or trisomies of chromosome 7 (10 cases, 50%); and monosomy of chromosome 19 (7 cases, 35%). Sixty-four recurrent aberrant regions (SORIs) were precisely delimited and used as variables for clustering. Unsupervised Cluster analysis allowed the segregation of samples into two genomic groups that naturally fitted with the metastatic condition of the cases. Four of these aberrant regions were chosen for their biological interest and were confirmed as aberrant using FISH technique on fixed paraffin embedded tissues. Conclusion: Supervised classification allowed obtaining aberrations useful to separate samples with different clinical outcome. Obtained results are useful to improve the knowledge about melanoma tumorigenesis but unfortunately cannot be used as a marker for metastatic progression. Experiment Overall Design: Comparative experiment: pheripheral blood pool of ten healthy female donors: CONTROL vs. 20 Primary Vertigal Growth Phase Melanoma samples.
2009-01-14 | E-GEOD-11109 | biostudies-arrayexpress
Project description:Adenoid cystic carcinoma (AAC) is a rare but distinctive tumor. Array comparative genomic hybridization (CGH) has been applied for detecting chromosomal copy number alterations in seventeen frozen salivary or pulmonary ACCs samples. There were recurrent gains at 1p36, 6p21, 16q24, 17q21, and 22q11-13, and recurrent losses at 1p35, 6q22, 8q12-13, 9p21, 12q12-13, and 17p11-13. The minimal common regions (MCRs) of these alterations contained several well-known cancer genes, including TP53, CDKN2A/CDKN2B, SKI, CDK10, and VEGF. CDK10 was the only oncogene that localized to the MCR of gain at 16q24.1-24.3. In addition, we identified LIMA1 as the sole putative tumor suppressor gene residing in the MCR of deletion at 12q12q12-13.2. Among well defined and narrow, but unique alterations, there were gains harboring MDM2, cyclin D1, and KIT, as well as one loss involving the hsa-mir-124a-2 miRNA. Using immunohistochemistry, we found abnormal protein expression in the cases with gain of cyclin D1 or MDM2. In conclusion, the majority of previously reported chromosomal copy number alterations are found using array CGH in this small cohort. The suspicion that genes such as TP53, CDKN2A/CDKN2B, and VEGF might play a role in ACC, is strengthened by our results. CDK10 and LIMA1 emerge from our analysis as candidate cancer genes
2008-04-18 | E-TABM-267 | biostudies-arrayexpress
Project description:Low grade flat ductal intraepithelial neoplasia (DIN1a, flat epithelial atypia) is one of the earliest morphologically recognizable neoplastic lesions of the breast. Frequently, it occurs in association with lobular intraepithelial neoplasia (LIN). The aim of this study was to elucidate chromosomal aberrations in these early neoplastic breast lesions using array comparative genomic hybridization (CGH) analysis. Laser capture microdissection of 12 archival formalin-fixed, paraffin-embedded specimens harbouring both foci of DIN1a as well as LIN was performed. All analyzed cases of DIN1a and LIN showed chromosomal gains and losses. The aberration encountered most often was loss on 16q in 7 DIN1a (70%) and 10 LIN (91%) cases. Regarding changes in chromosome 1, four DIN1a (40%) and 7 LIN (64%) cases showed a gain on 1q. The results of our study show concurrent chromosomal aberrations of 1q gains and 16q losses in several cases with coexisting LIN and low grade flat DIN. These aberrations are known to be common in low grade invasive ductal carcinomas as well as more advanced (conventional) types of low grade DIN (low grade ductal carcinoma in-situ). Our results raise the possibility of similar molecular-genetic pathways in most of the cases with coexisting LIN and low grade flat DIN.
2010-05-05 | GSE18187 | GEO
Project description:Additional chromosomal abnormalities are currently detected in Burkitts lymphoma. They play major roles in the progression of BL and in prognosis. The genes involved remain elusive. A whole-genome oligonucleotide array CGH analysis correlated with karyotype and FISH was performed in a set of 15 Burkitts lymphoma-derived cell lines ( in dye_swap with Human CGH 44K (G4410B) and Human CGH 244K (G4411B) ) and 12 primary tumors with Human CGH 44K (G4410B) . More than half of the 145 CNAs <2 Mb were mapped to Mendelian CNVs, including GSTT1, glutathione s-transferase T1, and BIRC6, an anti-apoptotic protein, possibly predisposing to some cancers. Somatic cell line-specific CNVs localized to the IG locus were consistently observed with the 244 K aCGH platform. Among 136 CNAs > 2 Mb, gains were found in 1q (12/27), 13q (7/27), 7q (6/27), 8q(4/27), 2p (3/27), 11q (2/27) and 15q (2/27). Losses were found in 3p (5/27), 4p (4/27), 4q (4/27), 9p (4/27), 13q (4/27), 6p (3/27), 17p (3/27), 6q (2/27),11pterp13 (2/27) and 14q12q21.3 (2/27). Twenty one minimal critical regions (MCR), (range 0.04-71.36 Mb), were delineated in tumors and cell lines. Three MCRs were localized to 1q. The proximal one was mapped to 1q21.1q25.2 with a 6.3 Mb amplicon (1q21.1q21.3) harboring BCA2 and PIAS3. In the other 2 MCRs, 1q32.1 and 1q44, MDM4 and AKT3 appeared as possible drivers of these gains respectively. The 13q31.3q32.1 <89.58-96.81> MCR contained an amplicon and ABCC4 might be the driver of this amplicon. The 40 Kb 2p16.1 <60.96-61> MCR was the smallest gained MCR and specifically encompassed the REL oncogene which is already implicated in B cell lymphomas. The most frequently deleted MCR was 3p14.1 <60.43-60.53> that removed the fifth exon of FHIT. Further investigations which combined gene expression and functional studies are essential to understand the lymphomagenesis mechanism and for the development of more effective, targeted therapeutic strategies
2009-09-18 | E-TABM-703 | biostudies-arrayexpress
Project description:In order to investigate the chromosomal alterations (gains or losses) of tumor tissuees developed in TH-MYCN mice, a neuroblastoma model, we carried out array comparative genomic hybridization. We investigated whether chromosomal alterations occured in the tumor tissues developed in the abdomen of TH-MYCN hemizygote mice.
2017-04-01 | GSE89739 | GEO