Comparative genomic hybridization reveals DNA copy number gains to frequently occur in human prostate cancer

The Prostate ◽  
1999 ◽  
Vol 39 (2) ◽  
pp. 79-86 ◽  
Author(s):  
Hans-Peter Sattler ◽  
Volker Rohde ◽  
Helmut Bonkhoff ◽  
Thomas Zwergel ◽  
Bernd Wullich
Keyword(s):  
Prostate Cancer ◽  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Human Prostate ◽  
Comparative Genomic ◽  
Human Prostate Cancer ◽  
Genomic Hybridization ◽  
Dna Copy Number

scholarly journals Recurrent DNA copy number changes revealed by comparative genomic hybridization in primary Merkel cell carcinomas

2004 ◽  
Vol 17 (5) ◽  
pp. 561-567 ◽  
Author(s):  
Marcelo L Larramendy ◽  
Virve Koljonen ◽  
Tom Böhling ◽  
Erkki Tukiainen ◽  
Sakari Knuutila
Keyword(s):  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Comparative Genomic ◽  
Merkel Cell ◽  
Genomic Hybridization ◽  
Dna Copy Number ◽  
Copy Number Changes

Comparative genomic hybridization reveals changes in DNA-copy number in poor-risk neuroblastoma

2001 ◽  
Vol 125 (2) ◽  
pp. 125-130 ◽  
Author(s):  
Kim Vettenranta ◽  
Yan Aalto ◽  
Sakari Wikström ◽  
Sakari Knuutila ◽  
Ulla Saarinen-Pihkala
Keyword(s):  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Comparative Genomic ◽  
Genomic Hybridization ◽  
Dna Copy Number ◽  
Poor Risk

Comparative genomic hybridization analysis of craniopharyngiomas

2003 ◽  
Vol 98 (1) ◽  
pp. 162-164 ◽  
Author(s):  
Shlomit Rienstein ◽  
Eric F. Adams ◽  
David Pilzer ◽  
Ayala Aviram Goldring ◽  
Boleslaw Goldman ◽  
...  
Keyword(s):  
Comparative Genomic Hybridization ◽  
Copy Number ◽  
Molecular Mechanisms ◽  
Genetic Alterations ◽  
Genomic Alteration ◽  
Comparative Genomic ◽  
Genomic Hybridization ◽  
Dna Copy Number ◽  
Content Type ◽  
Fine Print

Object. Craniopharyngioma is the most common childhood brain tumor and is thought to arise from embryonic remnants of the Rathke pouch. Some craniopharyngiomas are monoclonal in origin and hence presumably harbor somatic genetic alterations, although the precise molecular mechanisms involved in craniopharyngioma development are unknown. The goal of this study was to identify genetic alterations in craniopharyngiomas. Methods. To gain insight into the molecular mechanisms involved in development of these tumors, the authors analyzed nine adamantinomatous craniopharyngiomas by using comparative genomic hybridization. Six tumors (67%) displayed at least one genomic alteration, and three had six or more alterations. Only two tumors displayed a decrease in DNA copy number, and in all others an increase in DNA copy number was noted. Conclusions. The authors conclude that a subset of craniopharyngiomas consists of monoclonal tumors arising from activation of oncogenes located at specific chromosomal loci.

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