Translesion DNA Polymerases and Cancer
Open accessAbstract
DNA repair has been regarded as an important barrier to carcinogenesis. The newly discovered field of translesion synthesis (TLS) has made it apparent that mammalian cells need distinct polymerases to efficiently and accurately bypass DNA lesions. Perturbation of TLS polymerase activity by mutation, loss of expression, etc. is expected to result in the accumulation of mutations in cells exposed to specific carcinogens. Furthermore, several TLS polymerases can modulate cellular sensitivity to chemotherapeutic agents. TLS genes and TLS gene variations may thus be attractive pharmacologic and/or pharmacogenetic targets. We review herein current data with regards to the potential contribution of the primary TLS polymerase genes to cancer, their interaction with pharmacologic agents, and identify areas of interest for further research.
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POLH is highly expressed only in a subset of TCGA tumor cohorts.
“The observed high variability in POLH gene expression suggests that the gene is highly expressed only in a subset of TCGA tumor cohorts (Supplementary Figure 1) which is consistent with previous studies 44 .”
From DNA polymerase <b>η</b> mutational signatures are found in a variety of different types of cancer (2018) · cites this paper as [44]
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References 85 · Cited by 70
Research works printed but not linked: 8
- Efrati E. Tocco G. Eritja R. Wilson S. H. Goodman M. F. (1997). Abasic translesion synthesis by DNA polymerase beta violates the “A-rule.” Novel types of nucleotide incorporation by human DNA polymerase beta at an abasic lesion in different sequence contexts. J. BiolChem. 272, 2559– 2569 8999973
- Friedberg E. C. Walker G. C. Siede W. Wood R. D. Schultz R. A. Ellenberger T. (2005). DNA Repair and Mutagenesis, 2nd Edn Washington, DC: ASM Press
- Guo Z. Zheng L. Dai H. Zhou M. Xu H. Shen B. (2009). Human DNA polymerase beta polymorphism, Arg137Gln, impairs its polymerase activity and interaction with PCNA and the cellular base excision repair capacity. Nucleic Acids Res. 37, 3431– 3441 10.1093/nar/gkn816 19336415 PMC2691839 · DOI
- Starcevic D. Dalal S. Sweasy J. B. (2004). Is there a link between DNA polymerase beta and cancer? Cell Cycle. 3, 998– 1001 [Review]. 10.4161/cc.3.8.1062 15280658 · DOI
- Wang Y. Woodgate R. McManus T. P. Mead S. McCormick J. J. Maher V. M. (2007). Evidence that in xeroderma pigmentosum variant cells, which lack DNA polymerase eta, DNA polymerase iota causes the very high frequency and unique spectrum of UV-induced mutations. Cancer Res. 67, 3018– 3026 10.1158/0008-5472.CAN-06-2480 17409408 · DOI
- Yang J. Chen Z. Liu Y. Hickey R. J. Malkas L. H. (2004). Altered DNA polymerase iota expression in breast cancer cells leads to a reduction in DNA replication fidelity and a higher rate of mutagenesis. Cancer Res. 64, 5597– 5607 10.1158/0008-5472.CAN-04-1822 15313897 · DOI
- Yasui M. Suzuki N. Laxmi Y. R. Shibutani S. (2006). Translesion synthesis past tamoxifen-derived DNA adducts by human DNA polymerases eta and kappa. Biochemistry 45, 12167– 12174 10.1021/bi0608461 17002316 PMC2593916 · DOI
- Zheng H. Wang X. Warren A. J. Legerski R. J. Nairn R. S. Hamilton J. W. Li L. (2003). Nucleotide excision repair- and polymerase eta-mediated error-prone removal of mitomycin C interstrand cross-links. Mol. Cell. Biol. 23, 754– 761 10.1128/MCB.23.5.1590-1601.2003 12509472 PMC151552 · DOI
- Authors
- Makridakis, N. M., & Reichardt, J. K. V.
- Affiliations
- Tulane University (US)
- James Cook University (AU)
- Corresponding author
- Makridakis, Nick M.
- Venue
- Frontiers in Genetics
- Publisher
- Frontiers Media SA
- Published
- 2012
- Volume
- 3
- Pages
- 174-174
- ISSN
- 1664-8021 (ISSN-L)
- PMC
- PMC3434439
- OpenAlex
- W2052954221
- Cited by
- 70
- References
- 85
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 5 · 2023: 7 · 2022: 6 · 2021: 3 · 2020: 7 · 2019: 4 · 2018: 3 · 2017: 5 · 2016: 6 · 2015: 2 · 2014: 6 · 2013: 8 · 2012: 1
- FWCI
- 2.19
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Genetics (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Defense (P20GM103518, PC094628)
- National Institutes of Health
- National Institute of General Medical Sciences (P20GM103518)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- translesion synthesis, DNA polymerase, DNA repair, carcinogenesis, DNA damage bypass, mutation accumulation, chemosensitivity, pharmacogenetics, pharmacologic targets, cancer
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