The DOI matches its Crossref record; 232 of the 232 references it cites were found in a registry or an index.
Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place
Open accessAbstract
Oncogene activation disturbs cellular processes and accommodates a complex landscape of changes in the genome that contribute to genomic instability, which accelerates mutation rates and promotes tumorigenesis. Part of this cellular turmoil involves deregulation of physiologic DNA replication, widely described as replication stress. Oncogene-induced replication stress is an early driver of genomic instability and is attributed to a plethora of factors, most notably aberrant origin firing, replication–transcription collisions, reactive oxygen species, and defective nucleotide metabolism. Significance: Replication stress is a fundamental step and an early driver of tumorigenesis and has been associated with many activated oncogenes. Deciphering the mechanisms that contribute to the replication stress response may provide new avenues for targeted cancer treatment. In this review, we discuss the latest findings on the DNA replication stress response and examine the various mechanisms through which activated oncogenes induce replication stress. Cancer Discov; 8(5); 537–55. ©2018 AACR.
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“DNA damage is also responsible for oncogene-induced senescence, which involves replication stress and subsequent DSBs as the consequence of hyper-replication associated with activated oncogenes68.”
From The central role of DNA damage in the ageing process (2021) · cites this paper as [68]
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Metadata
- Authors
- Kotsantis, P., Petermann, E., & Boulton, S. J.
- Affiliations
- The Francis Crick Institute (GB)
- University of Birmingham (GB)
- Corresponding author
- Kotsantis, Panagiotis
- Venue
- Cancer Discovery
- Published
- 2018-04-30
- Volume
- 8
- Issue
- 5
- Pages
- 537-555
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC5935233
- OpenAlex
- W2797725119
- Cited by
- 416
- References
- 232
- Citations by year
- 2026: 43 · 2025: 55 · 2024: 41 · 2023: 59 · 2022: 53 · 2021: 63 · 2020: 58 · 2019: 33 · 2018: 11
- FWCI
- 4.05
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Lancaster EPrints (Lancaster University) (submittedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion, other-oa)
- Funders
- Wellcome Trust (FC0010048, 104558/Z/14/Z)
- Francis Crick Institute (10048)
- Cancer Research UK (FC0010048)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- oncogene-induced replication stress, genomic instability, carcinogenesis, replication origin firing, reactive oxygen species, nucleotide metabolism, cancer therapy targets
- MeSH terms
- Animals, Antineoplastic Agents, Cell Cycle, Cell Transformation, Neoplastic, DNA Damage, DNA Replication, DNA-Binding Proteins, Gene Expression Regulation, Humans, Mutation, Neoplasms, Oncogenes, Oxidation-Reduction, Stress, Physiological, Transcription, Genetic, Signal Transduction, Reactive Oxygen Species, Replication Origin, Genomic Instability, Molecular Targeted Therapy
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