Cigarette smoking, TP53 Arg72Pro, TP53BP1 Asp353Glu and the risk of lung cancer in a Japanese population

2010 ◽  
Vol 23 (5) ◽  
Author(s):  
Kiyohara
2010 ◽  
Vol 5 (3) ◽  
pp. 299-304 ◽  
Author(s):  
Chikako Kiyohara ◽  
Takahiko Horiuchi ◽  
Koichi Takayama ◽  
Yoichi Nakanishi

1963 ◽  
Vol 2 (01) ◽  
pp. 13-19 ◽  
Author(s):  
R. Doll

The evidence that cigarette smoking and atmospheric pcllution are causes of lung cancer is largely statistical. The first evidence was indirect; that is, i1. was noticed that in many countries the incidence of lung cancer had increased and that the increase could be correlated with changes in the prevalence of cigarette smoking and of certain types of atmospheric pollution.Since then much direct evidence has been obtained. The relationship between cigarette smoking and lung cancer has been demonstrated retrospectively by comparing the smoking habits of patients with and without lung cancer and prospectively by observing the mortality from lung cancer in groups of persons of known smoking habits. Conclusions can be drawn from these studies only after careful examination of the results. In particular it is important in retrospective studies to test a) the reproducibility of the data, b) the representativeness of the data, and c) the comparability of the special series and their controls. The resul1.s of retrospective studies are all similar and all show a close relationship between cigarette smoking and the disease.The results have been confirmed by pro~pective studies which are lesF. open to bias. The results can be explained if cigarette smoking causes lung cancer or if both are related to some third common factor. Ancillary data (pathological changes in the bronchial mucosa, animal experiments, etc.) support the causal hypothesis.The evidence relating to atmospheric pollution is less definite and it is difficult to get direct evidence of a relationship in the individual. It is clear that pollution has little effect in the absence of smoking, but the mortality associated with a given amount of smoking is generally greater in large towns than in the countryside and among men who have emigrated from Britain than among men who have lived all their lives in less polluted countries.


2007 ◽  
Vol 22 (3) ◽  
pp. 508 ◽  
Author(s):  
Jong-Myon Bae ◽  
Moo-Song Lee ◽  
Myung-Hee Shin ◽  
Dong-Hyun Kim ◽  
Zhong-Min Li ◽  
...  

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Chen Yao ◽  
Roby Joehanes ◽  
Rory Wilson ◽  
Toshiko Tanaka ◽  
Luigi Ferrucci ◽  
...  

Abstract Background DNA methylation is a key epigenetic modification that can directly affect gene regulation. DNA methylation is highly influenced by environmental factors such as cigarette smoking, which is causally related to chronic obstructive pulmonary disease (COPD) and lung cancer. To date, there have been few large-scale, combined analyses of DNA methylation and gene expression and their interrelations with lung diseases. Results We performed an epigenome-wide association study of whole blood gene expression in ~ 6000 individuals from four cohorts. We discovered and replicated numerous CpGs associated with the expression of cis genes within 500 kb of each CpG, with 148 to 1,741 cis CpG-transcript pairs identified across cohorts. We found that the closer a CpG resided to a transcription start site, the larger its effect size, and that 36% of cis CpG-transcript pairs share the same causal genetic variant. Mendelian randomization analyses revealed that hypomethylation and lower expression of CHRNA5, which encodes a smoking-related nicotinic receptor, are causally linked to increased risk of COPD and lung cancer. This putatively causal relationship was further validated in lung tissue data. Conclusions Our results provide a large and comprehensive association study of whole blood DNA methylation with gene expression. Expression platform differences rather than population differences are critical to the replication of cis CpG-transcript pairs. The low reproducibility of trans CpG-transcript pairs suggests that DNA methylation regulates nearby rather than remote gene expression. The putatively causal roles of methylation and expression of CHRNA5 in relation to COPD and lung cancer provide evidence for a mechanistic link between patterns of smoking-related epigenetic variation and lung diseases, and highlight potential therapeutic targets for lung diseases and smoking cessation.


2007 ◽  
Vol 37 (3) ◽  
pp. 168-174 ◽  
Author(s):  
Kenji Wakai ◽  
Chisato Nagata ◽  
Tetsuya Mizoue ◽  
Keitaro Tanaka ◽  
Yoshikazu Nishino ◽  
...  

JAMA ◽  
2004 ◽  
Vol 292 (24) ◽  
pp. 2984 ◽  
Author(s):  
Chi-Ling Chen ◽  
Lin-I Hsu ◽  
Hung-Yi Chiou ◽  
Yu-Mei Hsueh ◽  
Shu-Yuan Chen ◽  
...  

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