Sequential array comparative genomic hybridization analysis identifies copy number changes during blastic transformation of chronic myeloid leukemia

2012 ◽  
Vol 36 (4) ◽  
pp. 418-421 ◽  
Author(s):  
Seung-Tae Lee ◽  
Yongick Ji ◽  
Hee-Jin Kim ◽  
Chang-Seok Ki ◽  
Chul Won Jung ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Myeloid Leukemia ◽  
Array Comparative Genomic Hybridization ◽  
Comparative Genomic ◽  
Comparative Genomic Hybridization Analysis ◽  
Genomic Hybridization ◽  
Blastic Transformation ◽  
Copy Number Changes

scholarly journals Genomic Profiling by Array Comparative Genomic Hybridization Reveals Novel DNA Copy Number Changes in Breast Phyllodes Tumours

2009 ◽  
Vol 31 (1) ◽  
pp. 31-39
Author(s):  
Arno Kuijper ◽  
Antoine M. Snijders ◽  
Els M. J. J. Berns ◽  
Vibeke Kuenen-Boumeester ◽  
Elsken van der Wall ◽  
...  
Keyword(s):  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Array Comparative Genomic Hybridization ◽  
Copy Number Change ◽  
Genetic Alterations ◽  
Comparative Genomic ◽  
Genomic Profiling ◽  
Genomic Hybridization ◽  
Dna Copy Number ◽  
Copy Number Changes

Breast phyllodes tumour (PT) is a rare fibroepithelial tumour. The genetic alterations contributing to its tumorigenesis are largely unknown. To identify genomic regions involved in pathogenesis and progression of PTs we obtained genome-wide copy number profiles by array comparative genomic hybridization (CGH).DNA was isolated from fresh-frozen tissue samples. 11 PTs and 3 fibroadenomas, a frequently occurring fibroepithelial breast tumour, were analyzed. Arrays composed of 2464 genomic clones were used, providing a resolution of ~1.4 Mb across the genome. Each clone contains at least one STS for linkage to the human genome sequence.No copy number changes were detected in fibroadenomas. On the other hand, 10 of 11 PT (91%) showed DNA copy number alterations. The mean number of chromosomal events in PT was 5.5 (range 0–16) per case. A mean of 2.0 gains (range 0–10) and 3.0 losses (range 0–9) was seen per case of PT. Three cases showed amplifications. DNA copy number change was not related to PT grade. We observed recurrent loss on chromosome 1q, 4p, 10, 13q, 15q, 16, 17p, 19 and X. Recurrent copy number gain was seen on 1q, 2p, 3q, 7p, 8q, 16q, 20.In this study we used array CGH for genomic profiling of fibroepithelial breast tumours. Whereas most PT showed chromosomal instability, fibroadenomas lacked copy number changes. Some copy number aberrations had not previously been associated with PT. Several well-known cancer related genes, such as TP53 and members of the Cadherin, reside within the recurrent regions of copy number alteration. Since copy number change was found in all benign PT, genomic instability may be an early event in PT genesis.

scholarly journals Array comparative genomic hybridization reveals genomic copy number changes associated with outcome in diffuse large B-cell lymphomas

Blood ◽  
2006 ◽  
Vol 107 (6) ◽  
pp. 2477-2485 ◽  
Author(s):  
Weiyi Chen ◽  
Jane Houldsworth ◽  
Adam B. Olshen ◽  
Gouri Nanjangud ◽  
Seeta Chaganti ◽  
...  
Keyword(s):  
B Cell ◽  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Array Comparative Genomic Hybridization ◽  
Array Cgh ◽  
B Cell Lymphoma ◽  
Comparative Genomic ◽  
Genomic Hybridization ◽  
Copy Number Changes ◽  
Large B Cell

Abstract To identify, in high-resolution regions of DNA, the copy number changes associated with outcome in patients with diffuse large B-cell lymphoma (DLBCL), a disease with an approximately 50% mortality rate, we performed array comparative genomic hybridization (array-CGH) on specimens from 64 patients with newly diagnosed DLBCL treated with anthracycline-based chemotherapy. For the entire cohort, 55 commonly gained/lost regions, ranging in size from less than 1 Mbp to entire chromosomes, were identified using 1- to 2-Mbp and 2- to 4-Mbp resolution BAC arrays. Copy number changes of 9 minimal regions significantly correlated with overall survival, of which 6 were 10 Mbp or smaller. On multivariate analysis, loss of chromosomes 2 (2.4-4.1 Mbp) and 16 (33.8-35.6 Mbp) were found to be prognostic indicators of poor survival, independent of clinical features routinely used to predict outcome. Loss of chromosome 1 (78.2-79.1 Mbp) was predictive of good outcome. For a subset of 55 specimens classified according to cell-of-origin expression signature subtype, gain of chromosome 12 (45.4-53.8 Mbp) was found to be significantly associated with the germinal center B-cell-like DLBCL subtype. Overall, array-CGH identified relatively small genomic regions associated with outcome, which, along with follow-up expression studies, may reveal target genes important in DLBCL clinical behavior. (Blood. 2006;107:2477-2485)

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