ArticleCell cycle (Georgetown, Tex.)2010
DNA damage response induced by exposure of human lung adenocarcinoma cells to smoke from tobacco- and nicotine-free cigarettes.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Common genetic variants on 3q28 contribute to non-small cell lung cancer susceptibility: evidence from 10 case-control studies.Molecular genetics and genomics : MGG · 2015Pooled it
- DNA repair gene polymorphisms and tobacco smoking in the risk for colorectal adenomas.Carcinogenesis · 2011Trial
- Molecular Effect of Tobacco on Genetic, Epigenetic, and Metabolic Pathways During Cancer Progression.Cureus · 2026Review
- TAAT and the rise of hemp cigarettes.Tobacco control · 2024Article
- The tobacco-free fallacy: What paediatricians should know about herbal smoking products.Paediatrics & child health · 2023Article
- Review
- Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Assessing the lung cancer risk reduction potential of candidate modified risk tobacco products.Internal and emergency medicine · 2019Article
- Tobacco and bone fractures: A review of the facts and issues that every orthopaedic surgeon should know.Bone & joint research · 2019Article
- Cell type-specific properties and environment shape tissue specificity of cancer genes.Scientific reports · 2016Article
- Article
- Assessing tobacco use by cancer patients and facilitating cessation: an American Association for Cancer Research policy statement.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Nicotine and lung cancer.Journal of carcinogenesis · 2013Article
- Construction of a computable network model for DNA damage, autophagy, cell death, and senescence.Bioinformatics and biology insights · 2013Article
- SIRT1 pathway dysregulation in the smoke-exposed airway epithelium and lung tumor tissue.Cancer research · 2012Article
- Analysis of individual molecular events of DNA damage response by flow- and image-assisted cytometry.Methods in cell biology · 2011Review
- New biomarkers probing depth of cell senescence assessed by laser scanning cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2010Article
- DNA damage signaling assessed in individual cells in relation to the cell cycle phase and induction of apoptosis.Critical reviews in clinical laboratory sciencesReview
- LKB1/PEA3/ΔNp63 pathway regulates PTGS-2 (COX-2) transcription in lung cancer cells upon cigarette smoke exposure.Oxidative medicine and cellular longevityArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Cigarette smoke (CS) is the major cause of lung cancer and contributes to the development of other malignancies. Attempts have been made to construct reduced toxicity cigarettes, presumed to have diminished genotoxic potential. One such product on the market is the tobacco and nicotine free (T&N-free) cigarette type made from lettuce and herbal extracts. We have recently developed a sensitive assay of the genotoxicity of CS based on cytometric analysis of induction of the DNA damage response (DDR) in normal human pulmonary endothelial or A549 pulmonary adenocarcinoma cells. In the present study, we observed that exposure of A549 cells to CS from T/N-free cigarettes induced a smoke-dose dependent DDR as evidenced by phosphorylation (activation) of the Ataxia telangiectasia mutated (ATM) protein kinase and of the histone H2AX (γH2AX). The extent of DDR induced by T&N-free smoke was distinctly greater than that induced by comparable doses of CS from reference cigarettes (2R4F) containing tobacco and nicotine. The pattern of DDR induced by T&N-free smoke was similar to that of 2R4F cigarettes in terms of the cell cycle phase specificity and involvement of reactive oxygen species (ROS). The data also imply that similar to 2R4F exposure of cells to T/N-free smoke leads to formation of double-strand DNA breaks (DSBs) resulting from collapse of replication forks upon collision with the primary ssDNA lesions induced by smoke. Since DSBs are potentially carcinogenic our data indicate that smoking tobacco and nicotine-free cigarettes is at least as hazardous as smoking cigarettes containing tobacco and nicotine.
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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.