ReviewCell cycle (Georgetown, Tex.)2018
Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis.
Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- RAD18 facilitates cancer progression and immunosuppression via the AKT/mTOR/c-Myc axis: a multi-omics analysis.NPJ precision oncology · 2026Article
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisNAR cancer · 2026Article
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisbioRxiv : the preprint server for biology · 2025Article
- DNA polymerase kappa is the primary translesion synthesis polymerase for aldehyde ICLs.Nucleic acids research · 2025Article
- RAD18 promotes cell malignant behaviors of esophageal squamous cell carcinoma by modulating ATM/STAT3/PD-L1.Chromosoma · 2025Article
- MicroRNA-379-5p attenuates cancer stem cells and reduces cisplatin resistance in ovarian cancer by regulating RAD18/Polη axis.Cell death & disease · 2025Article
- A bispecific antibody targeting EGFR and AXL delays resistance to osimertinib.Cell reports. Medicine · 2024Article
- RAD18 directs DNA double-strand break repair by homologous recombination to post-replicative chromatin.Nucleic acids research · 2024Article
- The DNA Damage Response (DDR) landscape of endometrial cancer defines discrete disease subtypes and reveals therapeutic opportunities.NAR cancer · 2024Article
- RAS-RAF-miR-296-3p signaling axis increases Rad18 expression to augment radioresistance in pancreatic and thyroid cancers.Cancer letters · 2024Article
- RAD18 O-GlcNAcylation promotes translesion DNA synthesis and homologous recombination repair.Cell death & disease · 2024Article
- Role of Rad18 in B cell activation and lymphomagenesis.Scientific reports · 2024Article
- Trans-lesion synthesis and mismatch repair pathway crosstalk defines chemoresistance and hypermutation mechanisms in glioblastoma.Nature communications · 2024Article
- Enzymatic Processing of DNA-Protein Crosslinks.Genes · 2024Review
- Studying Translesion DNA Synthesis Using Xenopus In Vitro Systems.Methods in molecular biology (Clifton, N.J.) · 2024Article
- High-throughput screening of the Saccharomyces cerevisiae genome for 2-amino-3-methylimidazo [4,5-f] quinoline resistance identifies colon cancer-associated genes.G3 (Bethesda, Md.) · 2023Article
- Trans-Lesion Synthesis and Mismatch Repair Pathway Crosstalk Defines Chemoresistance and Hypermutation Mechanisms in Glioblastoma.bioRxiv : the preprint server for biology · 2023Article
- Implication of E3 ligase RAD18 in UV-induced mutagenesis in human induced pluripotent stem cells and neuronal progenitor cells.Journal of radiation research · 2023Article
- Review
- Leveraging the replication stress response to optimize cancer therapy.Nature reviews. Cancer · 2023Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Mutagenesis is a hallmark and enabling characteristic of cancer cells. The E3 ubiquitin ligase RAD18 and its downstream effectors, the 'Y-family' Trans-Lesion Synthesis (TLS) DNA polymerases, confer DNA damage tolerance at the expense of DNA replication fidelity. Thus, RAD18 and TLS polymerases are attractive candidate mediators of mutagenesis and carcinogenesis. The skin cancer-propensity disorder xeroderma pigmentosum-variant (XPV) is caused by defects in the Y-family DNA polymerase Pol eta (Polη). However it is unknown whether TLS dysfunction contributes more generally to other human cancers. Recent analyses of cancer genomes suggest that TLS polymerases generate many of the mutational signatures present in diverse cancers. Moreover biochemical studies suggest that the TLS pathway is often reprogrammed in cancer cells and that TLS facilitates tolerance of oncogene-induced DNA damage. Here we review recent evidence supporting widespread participation of RAD18 and the Y-family DNA polymerases in the different phases of multi-step carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.