Array comparative genomic hybridization (CGH) analysis of ameloblastoma tumor
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE132473 | GEO | 2019/06/11
REPOSITORIES: GEO
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Project description:Array comparative genomic hybridization (CGH) analysis of ameloblastoma tumor
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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
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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: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
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