A Genome-Wide Analysis of Array-Based Comparative Genomic Hybridization (CGH) Data to Detect Intra-Species Variations and Evolutionary Relationships

Comparative genomic hybridization (CGH) is an established genetic method which enables a genome‐wide survey of chromosomal imbalances. For each chromosome region, one obtains the information whether there is a loss or gain of genetic material, or whether there is no change at that place. Therefore, large amounts of data quickly accumulate which must be put into a logical order. Cluster analysis can be used to assign individual cases (samples) to different clusters of cases, which are similar and where each cluster may be related to a different tumour biology. Another approach consists in a clustering of chromosomal regions by rewriting the original data matrix, where the cases are written as rows and the chromosomal regions as columns, in a transposed form. In this paper we applied hierarchical cluster analysis as well as two implementations of self‐organizing feature maps as classical and neuronal tools for cluster analysis of CGH data from prostatic carcinomas to such transposed data sets. Self‐organizing maps are artificial neural networks with the capability to form clusters on the basis of an unsupervised learning rule. We studied a group of 48 cases of incidental carcinomas, a tumour category which has not been evaluated by CGH before. In addition we studied a group of 50 cases of pT2N0‐tumours and a group of 20 pT3N0‐carcinomas. The results show in all case groups three clusters of chromosomal regions, which are (i) normal or minimally affected by losses and gains, (ii) regions with many losses and few gains and (iii) regions with many gains and few losses. Moreover, for the pT2N0‐ and pT3N0‐groups, it could be shown that the regions 6q, 8p and 13q lay all on the same cluster (associated with losses), and that the regions 9q and 20q belonged to the same cluster (associated with gains). For the incidental cancers such clear correlations could not be demonstrated.

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Genome-wide survey for chromosomal imbalances in ganglioglioma using comparative genomic hybridization

Cancer Genetics and Cytogenetics ◽

10.1016/s0165-4608(01)00611-2 ◽

2002 ◽

Vol 134 (1) ◽

pp. 71-76 ◽

Cited By ~ 29

Author(s):

Xiao-Lu Yin ◽

Angela Bik-Yu Hui ◽

Jesse Chung-Sean Pang ◽

Wai Sang Poon ◽

Ho-Keung Ng

Keyword(s):

Comparative Genomic Hybridization ◽

Comparative Genomic ◽

Genomic Hybridization ◽

Chromosomal Imbalances ◽

Genome Wide ◽

Genome Wide Survey

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Genome-wide comparison of paired fresh frozen and formalin-fixed paraffin-embedded gliomas by custom BAC and oligonucleotide array comparative genomic hybridization: facilitating analysis of archival gliomas

Acta Neuropathologica ◽

10.1007/s00401-010-0773-z ◽

2010 ◽

Vol 121 (4) ◽

pp. 529-543 ◽

Cited By ~ 12

Author(s):

Gayatry Mohapatra ◽

David A. Engler ◽

Kristen D. Starbuck ◽

James C. Kim ◽

Derek C. Bernay ◽

...

Keyword(s):

Comparative Genomic Hybridization ◽

Array Comparative Genomic Hybridization ◽

Oligonucleotide Array ◽

Comparative Genomic ◽

Genomic Hybridization ◽

Genome Wide ◽

Formalin Fixed Paraffin ◽

Formalin Fixed Paraffin Embedded ◽

Fresh Frozen ◽

Formalin Fixed

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Novel chromosomal imbalances in mantle cell lymphoma detected by genome-wide array-based comparative genomic hybridization

Blood ◽

10.1182/blood-2004-07-2730 ◽

2005 ◽

Vol 105 (4) ◽

pp. 1686-1693 ◽

Cited By ~ 53

Author(s):

Margit Schraders ◽

Rolph Pfundt ◽

Huub M. P. Straatman ◽

Irene M. Janssen ◽

Ad Geurts van Kessel ◽

...

Keyword(s):

Mantle Cell Lymphoma ◽

Comparative Genomic Hybridization ◽

Cell Lymphoma ◽

Comparative Genomic ◽

Hotspot Detection ◽

Genomic Hybridization ◽

Positional Candidate ◽

Genome Wide ◽

Multiple Biopsies ◽

Mantle Cell

AbstractMantle cell lymphoma (MCL) is an aggressive, highly proliferative B-cell non-Hodgkin lymphoma, characterized by the specific t(11;14)(q13;q32) translocation. It is well established that this translocation alone is not sufficient to promote MCL development, but that additional genetic changes are essential for malignant transformation. We have identified such additional tumorigenic triggers in MCL tumors, by applying genome-wide array-based comparative genomic hybridization with an 800-kilobase (kb) resolution. This strategy, combined with a newly developed statistical approach, enabled us to confirm previously reported genomic alterations such as loss of 1p, 6q, 11q, 13q and gain of 3q and 8q, but it also facilitated the detection of novel recurrent genomic imbalances, such as gain of 4p12-13 and loss of 20p12.1-12.3, 20q12-13.2, 22q12.1-12.3, and 22q13.31-13.32. Genomic hotspot detection allowed for the identification of small genomic intervals that are frequently affected (57%-93%), resulting in interesting positional candidate genes such as KITLG, GPC5, and ING1. Finally, by assessing multiple biopsies from the same patient, we show that seemingly stable genomes do show subtle genomic changes over time. The follow-up of multiple biopsies of patients with MCL by high-resolution genomic profiling is expected to provide us with new clues regarding the relation between clinical outcome and in vivo cytogenetic evolution. (Blood. 2005;105:1686-1693)

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