ArticleOncotarget2017
Error-prone DNA polymerase and oxidative stress increase the incidences of A to G mutations in tumors.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- A missense mutation in acyl-CoA synthetase ACSL4 reveals essential residues for catalytic activity in ferroptosis.The Journal of biological chemistry · 2026Article
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- Role of pretreatment 18F-FDG PET/CT parameters in predicting outcome of non-endemic EBV DNA-related nasopharyngeal cancer (NPC) patients treated with IMRT and chemotherapy.La Radiologia medica · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutational processes for A→G mutations in tumors are not well understood. To uncover the mutational mechanisms, we analyzed molecular profiles of more than 9,000 tumor samples from The Cancer Genome Atlas (TCGA). The present study found that error-prone DNA polymerases were involved in stomach tumors with high fraction of A→G mutations. High levels of apoptosis in kidney cancers and high levels of energy metabolism in thyroid cancers increased A→G mutation rate, which was associated with high oxidative stress. We also found that the frequencies of RAS gene mutations were increased in thyroid cancers with high level of energy metabolism because of high-frequency A→G mutations.
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