ArticleBMC chemistry2021
Carcinogen-induced DNA structural distortion differences in the RAS gene isoforms; the importance of local sequence.
Article in BMC chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Comprehensive computational analysis via Adverse Outcome Pathways and Aggregate Exposure Pathways in exploring synergistic effects from radon and tobacco smoke on lung cancer.Frontiers in public health · 2025Article
- Local sequence context atFrontiers in molecular biosciences · 2025Article
- Relative genotoxicity of polycyclic aromatic hydrocarbons inferred from free energy perturbation approaches.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Hepatoprotective Effects of Flavonoids against Benzo[a]Pyrene-Induced Oxidative Liver Damage along Its Metabolic Pathways.Antioxidants (Basel, Switzerland) · 2024Review
- Utilizing biological experimental data and molecular dynamics for the classification of mutational hotspots through machine learning.Bioinformatics advances · 2024Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLocal sequence context is known to have an impact on the mutational pattern seen in cancer. The RAS genes and a smoking carcinogen, Benzo[a]pyrene diol epoxide (BPDE), have been utilised to explore these context effects. BPDE is known to form an adduct at the guanines in a number of RAS gene sites, KRAS codons 12, 13 and 14, NRAS codon 12, and HRAS codons 12 and 14.
resultsMolecular modelling techniques, along with multivariate analysis, have been utilised to determine the sequence influenced differences between BPDE-adducted RAS gene sequences as well as the local distortion caused by the adducts.
conclusionsWe conclude that G:C > T:A mutations at KRAS codon 12 in the tumours of lung cancer patients (who smoke), proposed to be predominantly caused by BPDE, are due to the effect of the interaction methyl group at the C5 position of the thymine base in the KRAS sequence with the BPDE carcinogen investigated causing increased distortion. We further suggest methylated cytosine would have a similar effect, showing the importance of methylation in cancer development.
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