Genome maintenance mechanisms for preventing cancer

Hoeijmakers, Jan H. J.

doi:10.1038/35077232

Cited by 3,939DNA Repair MechanismsCancer-related Molecular PathwaysGenetic factors in colorectal cancer

Genome maintenance mechanisms for preventing cancer

Hoeijmakers, Jan H. J.·2001·Nature

DOI 10.1038/35077232

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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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CS patients, defective in the TCR branch of NER, present developmental defects and neurodegeneration; many but not all are photosensitive, some developing blistering sunburns.
“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]
Both XP and CS patients have defects in NER.
“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]
UV light induces DNA damage that blocks replication and transcription, triggering either cell death or genetic instability.
“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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Authors: Hoeijmakers, J. H. J.
Affiliations: Erasmus University Rotterdam (NL)
Corresponding author: Hoeijmakers, Jan H. J.
ORCID: Hoeijmakers, Jan H. J.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2001-05-01
Volume: 411
Issue: 6835
Pages: 366-374
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/35077232
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
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
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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