Journal of Pathology and Translational Medicine

Brief Case Report

Pseudomesotheliomatous carcinoma of the lung in the parietal pleura: Ae Ri An, Kyoung Min Kim, Jong Hun Kim, Gong Yong Jin, Young Hoon Choe, Myoung Ja Chung; J Pathol Transl Med. 2020;54(2):192-195. Published online January 29, 2020; DOI: https://doi.org/10.4132/jptm.2019.11.14

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Original Article

Association between Expression of 8-OHdG and Cigarette Smoking in Non-small Cell Lung Cancer: Ae Ri An, 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; J Pathol Transl Med. 2019;53(4):217-224. Published online March 11, 2019; DOI: https://doi.org/10.4132/jptm.2019.02.20

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Abstract PDF

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.

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