Oncogenes create a unique landscape of fragile sites

Karin Miron, Tamar Golan-Lev, Raz Dvir, Eyal Ben-David and Batsheva Kerem ()
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Karin Miron: The Life Sciences Institute, The Hebrew University
Tamar Golan-Lev: The Life Sciences Institute, The Hebrew University
Raz Dvir: The Life Sciences Institute, The Hebrew University
Eyal Ben-David: The Life Sciences Institute, The Hebrew University
Batsheva Kerem: The Life Sciences Institute, The Hebrew University

Nature Communications, 2015, vol. 6, issue 1, 1-7

Abstract: Abstract Recurrent genomic instability in cancer is attributed to positive selection and/or the sensitivity of specific genomic regions to breakage. Among these regions are fragile sites (FSs), genomic regions sensitive to replication stress conditions induced by the DNA polymerase inhibitor aphidicolin. However, the basis for the majority of cancer genomic instability hotspots remains unclear. Aberrant oncogene expression induces replication stress, leading to DNA breaks and genomic instability. Here we map the cytogenetic locations of oncogene-induced FSs and show that in the same cells, each oncogene creates a unique fragility landscape that only partially overlaps with aphidicolin-induced FSs. Oncogene-induced FSs colocalize with cancer breakpoints and large genes, similar to aphidicolin-induced FSs. The observed plasticity in the fragility landscape of the same cell type following oncogene expression highlights an additional level of complexity in the molecular basis for recurrent fragility in cancer.

Date: 2015
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DOI: 10.1038/ncomms8094

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