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To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1749-0774.2005.00003.x Byline: Hisashi TANAKA (1,2), Donald A BERGSTROM (3), Meng-Chao YAO (1,4), Stephen J TAPSCOTT (2) Keywords: DNA palindrome; GAPF; gene amplification; genome instability Abstract: Abstract Breakage-fusion-bridge cycles contribute to chromosome aberrations and generate large DNA palindromes that facilitate oncogene amplification in cancer cells. At the molecular level, large DNA palindrome formation is initiated by chromosome breaks, and genomic architecture such as short inverted repeat sequences facilitates this process in mammalian cells. However, the prevalence of DNA palindromes in cancer cells is currently unknown. To determine the prevalence of DNA palindromes in human cancer cells, we have developed a new microarray-based approach called Genome-wide Analysis of Palindrome Formation (GAPF, Tanaka et al., Nat Genet 2005; 37: 320-7). This approach is based on a relatively simple and efficient method to purify "snap-back DNA" from large DNA palindromes by intramolecular base-pairing, followed by elimination of single-stranded DNA by nuclease S1. Comparison of Genome-wide Analysis of Palindrome Formation profiles between cancer and normal cells using microarray can identify genome-wide distributions of somatic palindromes. Using a human cDNA microarray, we have shown that DNA palindromes occur frequently in human cancer cell lines and primary medulloblastomas. Significant overlap of the loci containing DNA palindromes between Colo320DM and MCF7 cancer cell lines suggests regions in the genome susceptible to chromosome breaks and palindrome formation. A subset of loci containing palindromes is associated with gene amplification in Colo320DM, indicating that the location of palindromes in the cancer genome serves as a structural platform that supports subsequent gene amplification. Author Affiliation: (1)Division of Basic Sciences and (2)Division of Human Biology, Fred Hutchinson Cancer Research Center, and (3)Department of Laboratory Medicine, University of Washington, Seattle, USA and (4)Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan Article History: Received 1 October 2005; accepted 11 October 2005. Article note: Correspondence: Dr Hisashi Tanaka, Fred Hutchinson Cancer Research Center, Mailstop A2-168, 1100 Fairview Avenue North, Seattle, WA 98109-1024. Email: htanaka@fhcrc.org