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• W2012150332 abstract "Abstract Oncogene amplification is a critical step leading to tumorigenesis, but the underlying mechanisms are still poorly understood. Despite data suggesting that DNA replication is a major source of genomic instability, little is known about replication origin usage and replication fork progression in rearranged regions. Using a single DNA molecule approach, we provide here the first study of replication kinetics on a previously characterized MYC /papillomavirus ( HPV18 ) amplicon in a cervical cancer. Using this amplicon as a model, we investigated the role DNA replication control plays in generating amplifications in human cancers. The data reveal severely perturbed DNA replication kinetics in the amplified region when compared with other regions of the same genome. It was found that DNA replication is initiated from both genomic and viral sequences, resulting in a higher median frequency of origin firings. In addition, it was found that the higher initiation frequency was associated with an equivalent increase in the number of stalled replication forks. These observations raise the intriguing possibility that unscheduled replication origin activation at inserted HPV ‐18 viral DNA sequences triggers DNA amplification in this cancer cell line and the subsequent overexpression of the MYC oncogene. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045‐2257/suppmat . © 2007 Wiley‐Liss, Inc." @default.
• W2012150332 created "2016-06-24" @default.
• W2012150332 creator A5006159649 @default.
• W2012150332 creator A5026944483 @default.
• W2012150332 creator A5045319866 @default.
• W2012150332 date "2007-04-19" @default.
• W2012150332 modified "2023-09-30" @default.
• W2012150332 title "Unscheduled DNA replication origin activation at inserted<i>HPV</i>18 sequences in a<i>HPV</i>-18/<i>MYC</i>amplicon" @default.
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• W2012150332 doi "https://doi.org/10.1002/gcc.20448" @default.
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