An Ae Ri, Kim Kyoung Min, Park Ho Sung, Jang Kyu Yun, Moon Woo Sung, Kang Myoung Jae, Lee Yong Chul, Kim Jong Hun, Chae Han Jung, Chung Myoung Ja
Department of Pathology, Research Institute of Clinical Medicine of Chonbuk National University, Biomedical Research Institute of Chonbuk National University Hospital, Research Institute for Endocrine Sciences, Chonbuk National University Medical School, Jeonju, Korea.
Department of Internal Medicine, Research Institute of Clinical Medicine of Chonbuk National University, Biomedical Research Institute of Chonbuk National University Hospital, Research Institute for Endocrine Sciences, Chonbuk National University Medical School, Jeonju, Korea.
J Pathol Transl Med. 2019 Jul;53(4):217-224. doi: 10.4132/jptm.2019.02.20. Epub 2019 Mar 11.
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).
We investigated the expression of 8-OHdG and p53 in 203 NSCLC tissues using immunohistochemistry and correlated it with clinicopathological features including smoking.
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).
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.
接触香烟烟雾(CS)是肺癌发生的主要危险因素。已知CS会导致氧化性DNA损伤和肿瘤相关基因的突变,这些因素参与致癌过程。8-羟基脱氧鸟苷(8-OHdG)被认为是氧化性DNA损伤的可靠生物标志物。8-OHdG水平升高与包括癌症在内的多种病理状况相关。目前尚无关于非小细胞肺癌(NSCLC)中8-OHdG免疫组化表达的报道。
我们采用免疫组化方法研究了203例NSCLC组织中8-OHdG和p53的表达,并将其与包括吸烟在内的临床病理特征进行关联分析。
83.3%的NSCLC组织中观察到8-OHdG表达。单因素分析显示,其与低T分期、阴性淋巴结状态、从不吸烟者及较长总生存期显著相关(p <.05)。但多因素分析显示,8-OHdG并非NSCLC患者总生存期的独立预后因素。p53的异常表达与吸烟、男性、鳞状细胞癌及Ki-67阳性显著相关(p <.05)。
8-OHdG的表达与良好的预后因素相关。在NSCLC中,它与从不吸烟者呈正相关,提示DNA的氧化性损伤不能仅用吸烟来解释,可能取决于复杂的调控机制。