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 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

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

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

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.

Molecular Characterization of Distinct Hot Spot Regions on Chromosome 7q in Myeloid Leukemias.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2349-2349 ◽  
Author(s):  
Konstanze Dohner ◽  
Marianne Habdank ◽  
Frank G. Rucker ◽  
Simone Miller ◽  
Stefan Frohling ◽  
...  
Keyword(s):  
Human Genome ◽  
Molecular Characterization ◽  
Array Cgh ◽  
Hot Spot ◽  
Chromosome 7 ◽  
Myeloid Leukemias ◽  
Translocation Breakpoints ◽  
Chromosome 7Q ◽  
Chromosomal Bands

Abstract In recent years several groups initiated the molecular characterization of deletion and translocation breakpoints affecting the long arm of chromosome 7 (7q−) to identify genes that are involved in the pathogenesis of myeloid leukemias. Based on these studies a commonly deleted segment (CDS) of approximately 2 Mb in size was identified in chromosomal band 7q22 flanked by the microsatellite markers D7S1503 and D7S1841. Recently, the MLL5 gene (mixed lineage leukemia 5) has been cloned and mapped to the CDS as an interesting candidate gene for chromosome 7q associated leukemias. However, the pathogenic role of MLL5 in myeloid leukemias has not been demonstrated yet. In addition, for the less frequent deletion/translocation breakpoints affecting the distal part of chromosome 7q a 4 to 5 Mb sized CDS was defined encompassing chromosomal bands 7q35 to q36. The heterogeneity of deletion/translocation breakpoints on 7q suggests the existence of more than one disease-related gene. We aimed to identify and characterize translocation and deletion breakpoints in a large series of myeloid leukemias with chromosome 7q aberrations using fluorescence in situ hybridisation (FISH) and array-based comparative genomic hybridization (array CGH). Once, novel hot spot regions were identified, transcriptional map(s) were constructed allowing the identification of candidate genes, expressed sequences or miR-sites. FISH with a physical map of well defined YAC/BAC/PAC clones covering the long arm of chromosome 7 was performed on a series of 105 myeloid leukemias [acute myeloid leukaemia, (AML); myelodysplastic syndrome (MDS); myeloproliferative disorders, (MPD)] exhibiting chromosome 7q aberrations on banding analysis. Selected patients were analysed by array CGH and results were confirmed by hybridisation of the corresponding DNA clones. Transcriptional map(s) were constructed using public databases. While most of the deletions were large encompassing the previously published CDS, we identified a distinct 2 Mb sized CDS in the proximal part of 7q22 that was defined by five patients all exhibiting small deletions. This segment contains several candidate genes including the putative tumor-suppressor genes CUTL1, RASA4, EPO and FBXL13. Interestingly, this CDS is located close to multiple miR-sites, which usually indicate common fragile sites in the human genome. In chromosomal bands 7q35–q36 we localized the breakpoint of an unbalanced translocation from a patient with secondary AML between the markers D7S1925 and D7S1395. This region was recently characterized as a common fragile site in the human genome, named FRA7I. Furthermore, the translocation breakpoint t(3;7)(p13;q35) of a second patient with therapy-related AML was cloned into a 100 kb sized genomic segment located centromeric the CNTNAP2-gene close to the proximal border of the CDS. Our data further indicate the remarkable heterogeneity of deletion and translocation breakpoints on 7q supporting the hypothesis of multiple genes involved in 7q-associated myeloid leukemias. Using techniques such as FISH and array CGH known CDS as well as novel hot spot regions were identified. Transcriptional maps from those regions may serve as important starting points for the identification of pathogenetically relevant genes.

High-resolution array CGH of intermediate-risk prostate cancer genomes

2008 ◽  
Vol 26 (15_suppl) ◽  
pp. 5158-5158
Author(s):  
A. Ishkanian ◽  
C. Malloff ◽  
J. Ho ◽  
T. van der Kwast ◽  
A. Meng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Resolution ◽  
Array Cgh ◽  
Intermediate Risk ◽  
Cancer Genomes ◽  
Risk Prostate Cancer

scholarly journals A Genome-Wide High-Resolution Array-CGH Analysis of Cutaneous Melanoma and Comparison of Array-CGH to FISH in Diagnostic Evaluation

2013 ◽  
Vol 15 (5) ◽  
pp. 581-591 ◽  
Author(s):  
Lu Wang ◽  
Mamta Rao ◽  
Yuqiang Fang ◽  
Meera Hameed ◽  
Agnes Viale ◽  
...  
Keyword(s):  
High Resolution ◽  
Cutaneous Melanoma ◽  
Array Cgh ◽  
Diagnostic Evaluation ◽  
Genome Wide ◽  
A Genome
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