- Author:
Ae Ri AN
1
;
Kyoung Min KIM
;
Ho Sung PARK
;
Kyu Yun JANG
;
Woo Sung MOON
;
Myoung Jae KANG
;
Yong Chul LEE
;
Jong Hun KIM
;
Han Jung CHAE
;
Myoung Ja CHUNG
Author Information
- Publication Type:Original Article
- Keywords: Carcinoma, non-small cell lung; 8-Oxo-7-hydrodeoxyguanosine; p53; Smoking; Immunohistochemistry
- MeSH: Carcinogenesis; Carcinoma, Non-Small-Cell Lung; Carcinoma, Squamous Cell; DNA; DNA Damage; Humans; Immunohistochemistry; Lung Neoplasms; Lymph Nodes; Male; Multivariate Analysis; Risk Factors; Smoke; Smoking; Tobacco Products
- From:Journal of Pathology and Translational Medicine 2019;53(4):217-224
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Exposure to cigarette smoking (CS) is a major risk factor for the development of lung cancer. CS is known to cause oxidative DNA damage and mutation of tumor-related genes, and these factors are involved in carcinogenesis. 8-Hydroxydeoxyguanosine (8-OHdG) is considered to be a reliable biomarker for oxidative DNA damage. Increased levels of 8-OHdG are associated with a number of pathological conditions, including cancer. There are no reports on the expression of 8-OHdG by immunohistochemistry in non-small cell lung cancer (NSCLC). METHODS: We investigated the expression of 8-OHdG and p53 in 203 NSCLC tissues using immunohistochemistry and correlated it with clinicopathological features including smoking. RESULTS: The expression of 8-OHdG was observed in 83.3% of NSCLC. It was significantly correlated with a low T category, negative lymph node status, never-smoker, and longer overall survival (p < .05) by univariate analysis. But multivariate analysis revealed that 8-OHdG was not an independent prognostic factor for overall survival in NSCLC patients. The aberrant expression of p53 significantly correlated with smoking, male, squamous cell carcinoma, and Ki-67 positivity (p < .05). CONCLUSIONS: The expression of 8-OHdG was associated with good prognostic factors. It was positively correlated with never-smokers in NSCLC, suggesting that oxidative damage of DNA cannot be explained by smoking alone and may depend on complex control mechanisms.