ArticleJapanese journal of cancer research : Gann2002
Frequent epigenetic silencing of the p16 gene in non-small cell lung cancers of tobacco smokers.
Article in Japanese journal of cancer research : Gann, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Cigarette smoking and p16INK4α gene promoter hypermethylation in non-small cell lung carcinoma patients: a meta-analysis.PloS one · 2011Pooled it
- Epstein-Barr Virus Infection in Lung Cancer: Insights and Perspectives.Pathogens (Basel, Switzerland) · 2022Review
- Article
- Smoking exposure induces human lung endothelial cell adaptation to apoptotic stress.American journal of respiratory cell and molecular biology · 2014Article
- Epigenetic therapy in lung cancer.Frontiers in oncology · 2013Article
- DNA promoter methylation as a diagnostic and therapeutic biomarker in gallbladder cancer.Clinical epigenetics · 2012Article
- Detection of methylation of the RAR-β gene in patients with non-small cell lung cancer.Oncology letters · 2012Article
- Methylation of Wnt7a is modulated by DNMT1 and cigarette smoke condensate in non-small cell lung cancer.PloS one · 2012Article
- Environmental epigenetics of asthma: an update.The Journal of allergy and clinical immunology · 2010Review
- Promoter hypermethylation of DAP-kinase is associated with poor survival in primary biliary tract carcinoma patients.Cancer science · 2004Article
- Promoter hypermethylation of tumor suppressor and tumor-related genes in non-small cell lung cancers.Cancer science · 2003Article
- Age-related methylation of tumor suppressor and tumor-related genes: an analysis of autopsy samples.Oncogene · 2003Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies have demonstrated a causal link between tobacco smoking and lung cancer. We investigated the association between inactivation of the p16 gene and tobacco smoking in 51 non-small cell lung cancers (NSCLCs). Aberrations of the p16 gene were studied by PCR single-strand conformation polymorphism analysis, followed by direct sequencing, microsatellite analysis, methylation-specific PCR, and immunohistochemistry. Mutations were detected in 3.9% (2/51) of the tumors; the tumors carrying mutations were from smokers. The incidences of loss of heterozygosity, homozygous deletion, and promoter methylation in 37 smokers vs. 14 non-smokers were; 45.9% vs. 28.6%, 16.2% vs. 7.1%, and 35.1% vs. 7.1%, respectively. Among these, only the association between promoter methylation and tobacco smoking was statistically significant (P < 0.05). Therefore, epigenetic aberration is considered to be a major causative event in p16 silencing by tobacco smoking. Loss of p16 protein expression was apparent in 49% (25/51) of the tumors, and was associated with tobacco smoking (P < 0.05) and with histological type (P < 0.05). These findings suggest that tobacco smoking leads to inactivation of the p16 gene mainly through the epigenetic mechanism, ultimately increasing the risk of NSCLC, especially the squamous cell histological type.
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