Research Papers:

Chronic inflammation-associated genomic instability paves the way for human esophageal carcinogenesis

Runhua Lin, Chong Zhang, Jiaxuan Zheng, Dongping Tian, Zhijin Lei, Donglin Chen, Zexin Xu and Min Su _

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Oncotarget. 2016; 7:24564-24571. https://doi.org/10.18632/oncotarget.8356

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Runhua Lin1,*, Chong Zhang1,*, Jiaxuan Zheng1,*, Dongping Tian1, Zhijin Lei1, Donglin Chen1, Zexin Xu1, Min Su1

1Institute of Clinical Pathology, Guangdong Provincial Key Laboratory of Infectious Disease and Molecular Immunopathology, Shantou University Medical College, Shantou, Guangdong, 515031, PR China

*These authors contributed equally to this work

Correspondence to:

Min Su, e-mail: minsu@stu.edu.cn

Keywords: esophageal carcinogenesis, chronic inflammation, oxidative DNA damage, DNA double-strand breaks, genomic instability

Received: November 16, 2015     Accepted: March 06, 2016     Published: March 25, 2016


Chronic inflammation is associated with increased risk of cancer development, whereas the link between chronic inflammation and esophageal carcinogenesis is still obscure heretofore. This study aimed to investigate the relationship between chronic inflammation and DNA damage, as well as the possible role of DNA damage in esophageal carcinogenic process. Endoscopic esophageal biopsies from 109 individuals from Chaoshan littoral, a high-risk region for esophageal squamous cell carcinoma (ESCC), were examined to evaluate the association between chronic inflammation and histological severity, while additional 204 esophageal non-tumor samples from patients with ESCC were collected. Immunohistochemistry was performed to detect the oxidative DNA damage and DNA double-strand breaks (DSBs). Significantly positive correlation was observed between degree of chronic inflammation and esophageal precursor lesions (rs = 0.37, P < 0.01). Immunohistochemical analysis showed that oxidative DNA damage level was positively correlated with the degree of chronic inflammation (rs = 0.21, P < 0.05). Moreover, the level of oxidative DNA damage positively correlated with histological severity (rs = 0.49, P < 0.01). We found that the extent of DSBs was progressively increased with inflammation degree (P < 0.01) and the progression of precancerous lesions (P < 0.001). Collectively, these findings provide evidence linking chronic inflammation-associated genomic instability with esophageal carcinogenesis and suggest possibilities for early detection and intervention of esophageal carcinogenesis.

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