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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1 retracted
Oncogenic activity of Cdc6 through repression of the INK4/ARF locus
González, S., Klatt, P., Delgado, S., Conde, E., López‐Ríos, F., Sánchez‐Céspedes, M., Méndez, J., Antequera, F., & Serrano, M. (2006) · Nature · doi:10.1038/nature04585 · Cited by 186
RetractedHanahan, D., & Weinberg, R. A. (2000) · Cell · doi:10.1016/s0092-8674(00)81683-9 · Cited by 29,219
ROS function in redox signaling and oxidative stress
Schieber, M., & Chandel, N. S. (2014) · Current Biology · doi:10.1016/j.cub.2014.03.034 · Cited by 6,931
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218
Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
Land, H., Parada, L. F., & Weinberg, R. A. (1983) · Nature · doi:10.1038/304596a0 · Cited by 2,804
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
Bartkova, J., Hořejší, Z., Koed, K., Krämer, A., Tort, F., Zieger, K., Guldberg, P., Sehested, M., Nesland, J. M., Lukas, C., et al. (2005) · Nature · doi:10.1038/nature03482 · Cited by 2,688
Genomic instability — an evolving hallmark of cancer
Negrini, S., Gorgoulis, V. G., & Halazonetis, T. D. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2858 · Cited by 2,397
Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis
DeNicola, G. M., Karreth, F. A., Humpton, T. J., Gopinathan, A., Wei, C., Frese, K., Mangal, D., Yu, K. H., Yeo, C. J., Calhoun, E. S., et al. (2011) · Nature · doi:10.1038/nature10189 · Cited by 2,277
Siddiqui-Jain, A., Grand, C. L., Bearss, D. J., & Hurley, L. H. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.182256799 · Cited by 2,274
BRAFE600-associated senescence-like cell cycle arrest of human naevi
Michaloglou, C., Vredeveld, L. C. W., Soengas, M. S., Denoyelle, C., Kuilman, T., van der Horst, C. M. A. M., Majoor, D. M., Shay, J. W., Mooi, W. J., & Peeper, D. S. (2005) · Nature · doi:10.1038/nature03890 · Cited by 2,160
Research works printed but not linked: 4
- Feijoo, 2001, Activation of mammalian Chk1 during DNA replication arrest: a role for Chk1 in the intra-S phase checkpoint monitoring replication origin firing, J Cell Biol, 154, 913, 10.1083/jcb.200104099 · DOI
- Kotsantis, 2015, Cancer therapy and replication stress: forks on the road to perdition, Adv Clin Chem, 69, 91, 10.1016/bs.acc.2014.12.003 · DOI
- Sanjiv, 2016, Cancer-specific synthetic lethality between ATR and CHK1 kinase activities, Cell Rep, 17, 3407, 10.1016/j.celrep.2016.12.031 · DOI
- Vafa, 2002, c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability, Mol Cell, 9, 1031, 10.1016/S1097-2765(02)00520-8 · DOI · Paper page
Cited by
Sorted by citations
ROS and the DNA damage response in cancer
Srinivas, U. S., Tan, B. W. Q., Vellayappan, B. A., & Jeyasekharan, A. D. (2019) · Redox Biology · doi:10.1016/j.redox.2018.101084 · Cited by 2,144
“Modulation of replication stress by ROS has clinical implications, with the development of several agents- notably ATR and WEE1 inhibitors, which target replication stress in tumours [28].”
BackgroundInfluentialThe central role of DNA damage in the ageing process
Schumacher, B., Pothof, J., Vijg, J., & Hoeijmakers, J. H. J. (2021) · Nature · doi:10.1038/s41586-021-03307-7 · Cited by 907
The DNA damage response to transcription stress
Lans, H., Hoeijmakers, J. H. J., Vermeulen, W., & Marteijn, J. A. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0169-4 · Cited by 321
Genomic instability, inflammatory signaling and response to cancer immunotherapy
Chen, M., Linstra, R., & van Vugt, M. A. T. M. (2022) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2021.188661 · Cited by 166
Transcriptional responses to DNA damage
Silva, E., & Ideker, T. (2019) · DNA repair · doi:10.1016/j.dnarep.2019.05.002 · Cited by 31
“Replication is complete when replisomes converge [90,91].”
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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