ArticleProceedings of the National Academy of Sciences of the United States of America2000
Human lung cancer and p53: the interplay between mutagenesis and selection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
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
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.
- P53 codon 72 Arg/Pro polymorphism and lung cancer risk in Asians: an updated meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Pooled it
- Pooled it
- Review
- Lung cancer associated with combustion particles and fine particulate matter (PMBiochemical pharmacology · 2023Review
- Insights into Allosteric Mechanisms of the Lung-Enriched p53 Mutants V157F and R158L.International journal of molecular sciences · 2022Article
- The lung-enriched p53 mutants V157F and R158L/P regulate a gain of function transcriptome in lung cancer.Carcinogenesis · 2020Article
- Exposure to Dimethyl Selenide (DMSe)-Derived Secondary Organic Aerosol Alters Transcriptomic Profiles in Human Airway Epithelial Cells.Environmental science & technology · 2019Article
- Lung-Enriched Mutations in the p53 Tumor Suppressor: A Paradigm for Tissue-Specific Gain of Oncogenic Function.Molecular cancer research : MCR · 2019Review
- Changing mutational and adaptive landscapes and the genesis of cancer.Biochimica et biophysica acta. Reviews on cancer · 2017Review
- The RNA-binding protein Sam68 is critical for non-small cell lung cancer cell proliferation by regulating Wnt/β-catenin pathway.International journal of clinical and experimental pathology · 2017Article
- Preclinical Murine Models for Lung Cancer: Clinical Trial Applications.BioMed research international · 2015Review
- Human aldo-keto reductases and the metabolic activation of polycyclic aromatic hydrocarbons.Chemical research in toxicology · 2014Review
- Promotion and selection by serum growth factors drive field cancerization, which is anticipated in vivo by type 2 diabetes and obesity.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- [Advances of hypoxia and lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2013Review
- The role of base excision repair genes OGG1, APN1 and APN2 in benzo[a]pyrene-7,8-dione induced p53 mutagenesis.Mutation research · 2013Article
- p53 Mutagenesis by benzo[a]pyrene derived radical cations.Chemical research in toxicology · 2012Article
- Nuclear factor-κB: a key regulator in health and disease of lungs.Archivum immunologiae et therapiae experimentalis · 2011Review
- P53 polymorphism and lung cancer susceptibility: a pooled analysis of 32 case-control studies.Human genetics · 2009Article
- The pattern of p53 mutations caused by PAH o-quinones is driven by 8-oxo-dGuo formation while the spectrum of mutations is determined by biological selection for dominance.Chemical research in toxicology · 2008Article
- Cell-cell contact interactions conditionally determine suppression and selection of the neoplastic phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
It is an almost consensus opinion that the major carcinogenic risk of tobacco smoke is in its direct mutagenic action on DNA of cancer-related genes. The key data supposedly linking smoke-induced mutations to lung cancer were obtained from the adduct spectrum of the p53 tumor suppressor gene. Results of our analysis of p53 mutations compiled from the International Agency for Research on Cancer p53 database (April 1999 update) and from the literature point to a different causative link. Our new analytical tests focused on complementary base substitutions and showed that it is strand-specific repair of primary lesions and site-specific selection of the resultant mutations that determine the lung cancer-specific hot spots of G:C to T:A transversions along the p53 gene and also their increased abundance in lung tissues as compared with smoke-inaccessible tissues. However, on each of the two strands of p53 DNA, our tests revealed no significant difference between smokers and nonsmokers, either in the frequency of different types of mutations or in the frequency of their occurrence along the p53 gene. Moreover, in both smokers and nonsmokers, there was the same frequency of lung tumors with silent p53 mutations. Accordingly, we offer here a selection-based explanation of why lung cancers with nonsilent p53 mutations are more common in smokers than in nonsmokers. We conclude that physiological stresses (not necessarily genotoxic) aggravated by smoking are the leading risk factor in the p53-associated etiology of lung cancer.
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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.