scholarly journals Integrated Cytogenetic and High-Resolution Array CGH Analysis of Genomic Alterations Associated with MYCN Amplification

2011 ◽  
Vol 134 (1) ◽  
pp. 27-39 ◽  
Author(s):  
A. Pandita ◽  
J. Bayani ◽  
J. Paderova ◽  
P. Marrano ◽  
C. Graham ◽  
...  
Keyword(s):  
High Resolution ◽  
Array Cgh ◽  
Genomic Alterations

scholarly journals Integrated high-resolution array CGH and SKY analysis of homozygous deletions and other genomic alterations present in malignant mesothelioma cell lines

2013 ◽  
Vol 206 (5) ◽  
pp. 191-205 ◽  
Author(s):  
Geula Klorin ◽  
Ester Rozenblum ◽  
Oleg Glebov ◽  
Robert L. Walker ◽  
Yoonsoo Park ◽  
...  
Keyword(s):  
High Resolution ◽  
Cell Lines ◽  
Malignant Mesothelioma ◽  
Array Cgh ◽  
Genomic Alterations ◽  
Mesothelioma Cell ◽  
Homozygous Deletions

High-resolution genome-wide array-CGH reveals copy number variations associated with premature ovarian failure

Placenta ◽  
2011 ◽  
Vol 32 ◽  
pp. S282
Author(s):  
Paola Scaruffi ◽  
Sara Stigliani ◽  
Annamaria Jane Nicoletti ◽  
Pier Luigi Venturini ◽  
Gian Paolo Tonini ◽  
...  
Keyword(s):  
High Resolution ◽  
Premature Ovarian Failure ◽  
Copy Number ◽  
Array Cgh ◽  
Copy Number Variations ◽  
Ovarian Failure ◽  
Genome Wide

Novel amplicons on the short arm of chromosome 7 identified using high resolution array CGH contain over expressed genes in addition toEGFR in glioblastoma multiforme

2005 ◽  
Vol 44 (4) ◽  
pp. 392-404 ◽  
Author(s):  
Michael R. Rossi ◽  
Jeffrey La Duca ◽  
Sei-Ichi Matsui ◽  
Norma J. Nowak ◽  
Lesleyann Hawthorn ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
High Resolution ◽  
Array Cgh ◽  
Chromosome 7

High-resolution chromosome arm 5p array CGH analysis of small cell lung carcinoma cell lines

2005 ◽  
Vol 42 (3) ◽  
pp. 308-313 ◽  
Author(s):  
Bradley P. Coe ◽  
Laura-Jane Henderson ◽  
Cathie Garnis ◽  
Ming-Sound Tsao ◽  
Adi F. Gazdar ◽  
...  
Keyword(s):  
High Resolution ◽  
Lung Carcinoma ◽  
Array Cgh ◽  
Carcinoma Cell ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Carcinoma Cell Lines ◽  
Chromosome Arm

scholarly journals High‐resolution genomic alterations in Barrett's metaplasia of patients who progress to esophageal dysplasia and adenocarcinoma

2019 ◽  
Vol 145 (10) ◽  
pp. 2754-2766 ◽  
Author(s):  
Jorge L. Sepulveda ◽  
Elena V. Komissarova ◽  
Sarawut Kongkarnka ◽  
Richard A. Friedman ◽  
Jon M. Davison ◽  
...  
Keyword(s):  
High Resolution ◽  
Genomic Alterations ◽  
Esophageal Dysplasia ◽  
Barrett's Metaplasia ◽  
Barrett’S Metaplasia

P718Genome-wide copy number profiling of atherosclerotic plaques

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Sleptcov ◽  
M S Nazarenko ◽  
A N Kazantsev ◽  
N N Burkov ◽  
N A Skryabin ◽  
...  
Keyword(s):  
Coronary Arteries ◽  
Array Cgh ◽  
Comparative Genomic ◽  
Control Group ◽  
Atherosclerotic Plaques ◽  
Cellular Interactions ◽  
Genomic Alterations ◽  
Structural Genomic ◽  
Atherosclerotic Process ◽  
In Cells

Abstract Background Atherosclerotic plaque formation results from complex cellular interactions in the intima of arteries, which take place between resident cells of the vessel wall (smooth muscle cells (SMC) and endothelial cells) and cells of the immune system (macrophages (MF)). Less well known is the genomic alterations in cells involving in the atherosclerotic process as can be important in plaque progression and instability. Aim The main purpose of the study is to assess the spectrum of structural genomic alterations in the tissue of atherosclerotic artery wall and to evaluate of difference between structural variants (SV) in SMC and MF. Materials and methods Samples of atherosclerotic plaques of the internal carotid artery (ICA) was collected from patients during endarterectomy (n=100) and the atherosclerotic coronary arteries (ACA) was obtained by coronary artery bypass surgery (n=10, group: bpACA) and by autopsy (n=8, apACA). Specimens were stored in liquid nitrogen. White blood cells (WBC) derived from the same patients. Control group was the health persons with same age (WBC, n=100). The genomic imbalances in bpACA were assessed by array comparative genomic hybridization (array-CGH, CGH Microarray 2x400K). Identified SVs was verified by droplet-digital PCR using TaqMan-assays (reference assay is RNAse P) in bpACA and ICA groups.SMC and MF were immunostained (Anti-Human CD68 Antibody and Alpha-SMA Antibody) and collected by laser capture microdissection of fresh frozen apACA samples (30–40 cells of each per sample). Collected cells were lysed and DNA amplified by whole genome amplification technique along with WBC of the same person, then analyzed by array-CGH. Results We found 90 SV in atherosclerotic coronary arteries, 13% of them were no mentioned before in Database of Genomic Variants. We selected interested SVs that contains only one gene (ACACB, ABCC9, ERLIN1, SFMBT1, PRKRA, and SIRPB1). The loss in the 3p21.1 region (SFMBT1) was in 11.48% patients and 8.5% in control group. Among patients who had diabetes mellitus (DM2) had more frequently loss of SFMBT1 (16%) than patients without DM2 (8%). The frequency of gain 2q31.2 (PRKRA) was 6% in patients whereas in control group we identified it in only one person. The frequency of loss 20p13 (SIRPB1) was approx. 67% in both groups. Several aneuploidies were found in MF (9 trisomies and 3 monosomies) and SMCs (1 trisomy and 8 monosomies). In two patients, SMCs had a normal karyotype. The ratio of duplications and deletions in MF and SMCs was 1:0.8 and 1:7, respectively. In MF of 6 patients identified same duplication in chromosome region 9q34.13-q34.2, (arr[hg19] 9q34.13(9:134337452-135931774)x3) about 2Mb in size. Conclusion Our study indicates that genomic alterations are diverse in their structure and are widely represented in cells involved in the atherosclerotic process.

High-resolution array CGH of metanephric adenomas: lack of DNA copy number changes

2010 ◽  
Vol 56 (2) ◽  
pp. 212-216 ◽  
Author(s):  
Adrianna Szponar ◽  
Maria V Yusenko ◽  
Gyula Kovacs
Keyword(s):  
High Resolution ◽  
Copy Number ◽  
Array Cgh ◽  
Dna Copy Number ◽  
Copy Number Changes

High-resolution array CGH increases heterogeneity tolerance in the analysis of clinical samples

Genomics ◽  
2005 ◽  
Vol 85 (6) ◽  
pp. 790-793 ◽  
Author(s):  
Cathie Garnis ◽  
Bradley P. Coe ◽  
Stephen L. Lam ◽  
Calum MacAulay ◽  
Wan L. Lam
Keyword(s):  
High Resolution ◽  
Array Cgh ◽  
Clinical Samples

Identification of High-Level DNA Amplifications in AML with Complex Karyotype Using Array-CGH.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1914-1914
Author(s):  
Frank G. Rücker ◽  
Lars Bullinger ◽  
Simone Miller ◽  
Hans A. Kestler ◽  
Peter Lichter ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Resolution ◽  
Candidate Genes ◽  
Array Cgh ◽  
Screening Tools ◽  
Comparative Genomic ◽  
Complex Karyotype ◽  
General Role ◽  
Custom Made ◽  
High Level

Abstract Complex karyotype acute myeloid leukemia (AML), commonly defined as the presence of three or more chromosome abnormalities without specific fusion transcripts, is seen in approximately 10–15% of all AML cases. In this subset of cases, genomic losses and gains are much more frequent than balanced translocations, indicating other mechanisms of leukemogenesis. One possible mechanism is the activation of oncogenes through high-level DNA amplifications. To detect high-level DNA amplifications and to identify corresponding candidate genes, we applied comparative genomic hybridization to microarrays (array-CGH) in 100 cases of complex karyotype AML and correlated the findings with gene expression profiling (GEP) data. For array-CGH a custom-made 2.8k-microarray was used consisting of 2799 different BAC- or PAC-vectors with an average resolution of approximately 2 Mb. Hybridization experiments were performed in a dye-swap setting; significant aberrations were defined as mean plus/minus three times the standard deviation of a set of balanced clones for each individual experiment. In selected cases correlation with global gene expression studies was performed to further delineate candidate genes. We identified 50 high-level DNA amplifications in 20 different genomic regions. Amplifications occurring in at least two cases mapped to (candidate genes in the amplicon) 11q23.3-q24.1 (n=10; ETS, FLI1, APLP2); 11q23.3 (n=8;MLL, DDX6, LARG, SC5DL); 21q22 (n=5; ERG, ETS2); 9p24 (n=4; JAK2); 13q12 (n=4; CDX2, FLT3, PAN3); 8q24 (n=3; C8FW, MYC); 12p13 (n=2; FGF6, CCND2); 20q11 (n=2; ID1, BCL2L1); and 11q13 (n=2; STARD10, GARP, RAD30, DLG2). To better characterize the genomic architecture of the amplicons, we applied array-CGH using an 8.0k-microarray with an average resolution of approximately 1 Mb. Using this approach highly complex amplicon structures with several distinct amplicon peaks were identified for e.g. the amplified regions in 8q24, 11q23, and 13q12. In addition, parallel analysis of GEP in a subset of 43 of 100 cases displayed overexpressed candidate genes in the critical amplified regions; for some of the genes an oncogenic role has been implicated e.g. C8FW and MYC in 8q24, ETS1, FLI1 and APLP2 in 11q24.1, as well as FLT3 and CDX2 in 13q12. In conclusion, using high-resolution genome-wide screening tools such as array-CGH, a large number of high-level DNA amplifications were identified in AML with complex karyotype suggesting a more general role for protooncogene activation in this AML subset. This high-resolution technique allows the detection of complex amplicon structures with several distinct amplicon peaks pinpointing to selective candidate genes. In addition, correlation with GEP studies facilitates the delineation of overexpressed candidate genes within the amplified regions.

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