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The Impact of Cigarette Smoking on the Frequency of and Qualitative Differences in KRAS Mutations in Korean Patients with Lung Adenocarcinoma

 Hye Ryun Kim  ;  Jung Ryun Ahn  ;  Jin Gu Lee  ;  Doo Hee Bang  ;  Sang-Jun Ha  ;  Yun Kyoung Hong  ;  Sun Mi Kim  ;  Ki Chang Nam  ;  Sun Young Rha  ;  Ross A. Soo  ;  Gregory J. Riely  ;  Joo Hang Kim  ;  Byoung Chul Cho 
 YONSEI MEDICAL JOURNAL, Vol.54(4) : 865-874, 2013 
Journal Title
Issue Date
Adenocarcinoma/drug therapy ; Adenocarcinoma/etiology ; Adenocarcinoma/genetics* ; Adenocarcinoma/pathology ; Adult ; Aged ; Aged, 80 and over ; Asian Continental Ancestry Group/genetics ; Female ; Humans ; Incidence ; Lung Neoplasms/drug therapy ; Lung Neoplasms/etiology ; Lung Neoplasms/genetics* ; Lung Neoplasms/pathology ; Male ; Middle Aged ; Mutation* ; Mutation Rate ; Proportional Hazards Models ; Proto-Oncogene Proteins/genetics* ; Proto-Oncogene Proteins p21(ras) ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Receptor, Epidermal Growth Factor/genetics ; Smoking/adverse effects ; Smoking/genetics* ; Treatment Outcome ; ras Proteins/genetics*
EGFR ; KRAS ; pulmonary adenocarcinoma ; cigarette smoking ; EGFR-tyrosine kinase inhibitors
PURPOSE: This study was designed to determine the relationship of cigarette smoking to the frequency and qualitative differences among KRAS mutations in lung adenocarcinomas from Korean patients. MATERIALS AND METHODS: Detailed smoking histories were obtained from 200 consecutively enrolled patients with lung adenocarcinoma according to a standard protocol. EGFR (exons 18 to 21) and KRAS (codons 12/13) mutations were determined via direct-sequencing. RESULTS: The incidence of KRAS mutations was 8% (16 of 200) in patients with lung adenocarcinoma. KRAS mutations were found in 5.8% (7 of 120) of tumors from never-smokers, 15% (6 of 40) from former-smokers, and 7.5% (3 of 40) from current-smokers. The frequency of KRAS mutations did not differ significantly according to smoking history (p=0.435). Never-smokers were significantly more likely than former or current smokers to have a transition mutation (G→A or C→T) rather than a transversion mutation (G→T or G→C) that is known to be smoking-related (p=0.011). In a Cox regression model, the adjusted hazard ratios for the risk of progression with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) were 0.24 (95% CI, 0.14-0.42; p<0.001) for the EGFR mutation and 1.27 (95% CI, 0.58-2.79; p=0.537) for the KRAS mutation. CONCLUSION: Cigarette smoking did not influence the frequency of KRAS mutations in lung adenocarcinomas in Korean patients, but influenced qualitative differences in the KRAS mutations.
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Medical Engineering (의학공학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Thoracic and Cardiovascular Surgery (흉부외과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Joo Hang(김주항)
Kim, Hye Ryun(김혜련) ORCID logo https://orcid.org/0000-0002-1842-9070
Nam, Ki Chang(남기창)
Rha, Sun Young(라선영) ORCID logo https://orcid.org/0000-0002-2512-4531
Ahn, Jung Ryun(안정련)
Lee, Jin Gu(이진구)
Cho, Byoung Chul(조병철) ORCID logo https://orcid.org/0000-0002-5562-270X
Hong, Yun Kyoung(홍윤경)
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