Cited by 273Lung Cancer Treatments and MutationsLung Cancer Research StudiesSmoking Behavior and Cessation

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TP53 and KRAS Mutation Load and Types in Lung Cancers in Relation to Tobacco Smoke: Distinct Patterns in Never, Former, and Current Smokers

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Le Calvez, Florence, Mukeria, Anush, Hunt, Jay D., Kelm, Olaf, Hung, Rayjean J., Tanière, Philippe, Brennan, Paul, Boffetta, Paolo, Zaridze, David G., Hainaut, Pierre·2005·Cancer Research

DOI 10.1158/0008-5472.can-05-0551

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Abstract

TP53 mutations are common in lung cancers of smokers, with high prevalence of G:C-to-T:A transversions generally interpreted as mutagen fingerprints of tobacco smoke. In this study, TP53 (exons 5-9) and KRAS (codon 12) were analyzed in primary lung tumors of never (n = 40), former (n = 27), and current smokers (n = 64; mainly heavy smokers). Expression of p53, cyclooxygenase-2 (Cox-2), and nitrotyrosine (N-Tyr), a marker of protein damage by nitric oxide, were analyzed by immunohistochemistry. TP53 mutations were detected in 47.5% never, 55.6% former, and 77.4% current smokers. The relative risk for mutation increased with tobacco consumption (Plinear trend < 0.0001). G:C-to-T:A transversions (P = 0.06, current versus never smokers) and A:T-to-G:C transitions (P = 0.03, former versus never smokers) were consistently associated with smoking. In contrast, G:C-to-A:T transitions were associated with never smoking (P = 0.02). About half of mutations in current smokers fell within a particular domain of p53 protein, suggesting a common structural effect. KRAS mutations, detected in 20 of 131 (15.3%) cases, were rare in squamous cell carcinoma compared with adenocarcinoma [relative risk (RR), 0.2; 95% confidence interval (95% CI), 0.07-1] and were more frequent in former smokers than in other categories. No significant differences in Cox-2 expression were found between ever and never smokers. However, high levels of N-Tyr were more common in never than ever smokers (RR, 10; 95% CI, 1.6-50). These results support the notion that lung tumorigenesis proceeds through different molecular mechanisms according to smoking status. In never smokers, accumulation of N-Tyr suggests an etiology involving severe inflammation.

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Pfeifer GP, Denissenko MF, Olivier M, Tretyakova N, Hecht SS, Hainaut P. Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers. Oncogene 2002; 21: 7435–51. · DOI

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Authors: Le Calvez, F., Mukeria, A., Hunt, J. D., Kelm, O., Hung, R. J., Tanière, P., Brennan, P., Boffetta, P., Zaridze, D. G., & Hainaut, P.
Affiliations: 1IARC, Lyon, France;
Russian Cancer Research Center NN Blokhin (RU)
Centre international de recherche sur le cancer (FR)
4Department of Cellular Pathology, The Medical School, University of Birmingham, Egbaston, Birmingham, United Kingdom
ORCID: Hunt, Jay D.
Kelm, Olaf
Hung, Rayjean J.
Brennan, Paul
Boffetta, Paolo
Zaridze, David G.
Hainaut, Pierre
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2005-06-15
Volume: 65
Issue: 12
Pages: 5076-5083
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-05-0551
OpenAlex: W2149459560
Cited by: 273
References: 54
Citations by year: 2026: 5 · 2025: 8 · 2024: 8 · 2023: 12 · 2022: 11 · 2021: 12 · 2020: 9 · 2019: 15 · 2018: 4 · 2017: 10 · 2016: 11 · 2015: 9 · 2014: 11 · 2013: 14 · 2012: 27
FWCI: 13.85
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Cancer Research (publishedVersion)
PubMed (publishedVersion)
Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
Funders: European Commission (IC15-CT96-0313)
National Institutes of Health (5k01es000358-03)
National Institute of Environmental Health Sciences (K01‐ES00358)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
Keywords: TP53 mutation, KRAS mutation, lung cancer, smoking, mutation patterns, G:C to T:A transversions, cyclooxygenase-2, nitrotyrosine, nitric oxide, inflammation, never smokers, former smokers, squamous cell carcinoma, adenocarcinoma, lung carcinogenesis
MeSH terms: Aged, Female, Humans, Immunohistochemistry, Lung Neoplasms, Male, Membrane Proteins, Middle Aged, Mutation, Prostaglandin-Endoperoxide Synthases, Genes, ras, Smoking, Tyrosine, Genes, p53, Tumor Suppressor Protein p53, Cyclooxygenase 2

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TP53 and KRAS Mutation Load and Types in Lung Cancers in Relation to Tobacco Smoke: Distinct Patterns in Never, Former, and Current Smokers

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