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Int. J. Mol. Sci. 2017, 18(7), 1339;

Oncogene-Induced Replication Stress Drives Genome Instability and Tumorigenesis

Department of Genetics, The Life Sciences Institute, The Hebrew University, 91904 Jerusalem, Israel
Author to whom correspondence should be addressed.
Received: 29 May 2017 / Revised: 15 June 2017 / Accepted: 20 June 2017 / Published: 22 June 2017
(This article belongs to the Special Issue Mechanisms Leading to Genomic Instability)
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Genomic instability plays a key role in driving cancer development. It is already found in precancerous lesions and allows the acquisition of additional cancerous features. A major source of genomic instability in early stages of tumorigenesis is DNA replication stress. Normally, origin licensing and activation, as well as replication fork progression, are tightly regulated to allow faithful duplication of the genome. Aberrant origin usage and/or perturbed replication fork progression leads to DNA damage and genomic instability. Oncogene activation is an endogenous source of replication stress, disrupting replication regulation and inducing DNA damage. Oncogene-induced replication stress and its role in cancer development have been studied comprehensively, however its molecular basis is still unclear. Here, we review the current understanding of replication regulation, its potential disruption and how oncogenes perturb the replication and induce DNA damage leading to genomic instability in cancer. View Full-Text
Keywords: oncogene; DNA replication; replication stress; genomic instability; cancer oncogene; DNA replication; replication stress; genomic instability; cancer

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Sarni, D.; Kerem, B. Oncogene-Induced Replication Stress Drives Genome Instability and Tumorigenesis. Int. J. Mol. Sci. 2017, 18, 1339.

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