The DOI matches its Crossref record; 67 of the 68 references it cites were found in a registry or an index.
Genome maintenance mechanisms for preventing cancer
Abstract
The early notion that cancer is caused by mutations in genes critical for the control of cell growth implied that genome stability is important for preventing oncogenesis. During the past decade, knowledge about the mechanisms by which genes erode and the molecular machinery designed to counteract this time-dependent genetic degeneration has increased markedly. At the same time, it has become apparent that inherited or acquired deficiencies in genome maintenance systems contribute significantly to the onset of cancer. This review summarizes the main DNA caretaking systems and their impact on genome stability and carcinogenesis.
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In the citing paper
“CS patients, defective in the TCR branch of NER (1, 27), present a very different clinical picture, one of developmental defects and neurodegeneration; many but not all patients are also photosensitive, some developing blistering sunburns (5, 28).”
From Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency (2016) · cites this paper as [27]
In the citing paper
“Both XP and CS patients have defects in NER.”
From Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency (2016) · cites this paper as [27]
In the citing paper
“Ultraviolet (UV) light induces DNA damage that blocks replication and transcription [1][2][3] triggering either cell death or genetic instability.”
From Gap-filling and bypass at the replication fork are both active mechanisms for tolerance of low-dose ultraviolet-induced DNA damage in the human genome (2014) · cites this paper as [1]
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2 retracted
RETRACTED: Transcription-Coupled Repair of 8-oxoGuanine
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- Bootsma, D., Kraemer, K. H., Cleaver, J. & Hoeijmakers, J. H. J. in The Metabolic and Molecular Basis of Inherited Disease Vol. 1 (eds Scriver, C. R., Beaudet, A. L., Sly, W. S. & Valle, D.) 677–703 (McGraw-Hill, New York, 2001).
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Metadata
- Authors
- Hoeijmakers, J. H. J.
- Affiliations
- Erasmus University Rotterdam (NL)
- Corresponding author
- Hoeijmakers, Jan H. J.
- Venue
- Nature
- Published
- 2001-05-01
- Volume
- 411
- Issue
- 6835
- Pages
- 366-374
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2096136751
- Semantic Scholar
- d0f61e028e7f97375defc2b754e37345af93b400
- Cited by
- 3,939
- References
- 68
- Citations by year
- 2026: 48 · 2025: 65 · 2024: 70 · 2023: 118 · 2022: 99 · 2021: 143 · 2020: 137 · 2019: 146 · 2018: 156 · 2017: 138 · 2016: 179 · 2015: 189 · 2014: 189 · 2013: 201 · 2012: 217
- FWCI
- 11.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- KWF Kankerbestrijding
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- genome maintenance, genome stability, carcinogenesis, DNA repair, DNA damage response, mutagenesis, cancer prevention
- MeSH terms
- Animals, DNA Damage, DNA Repair, Humans, Models, Genetic, Neoplasms, Recombination, Genetic, Syndrome, Transcription, Genetic, Telomere, Genome, Base Pair Mismatch
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