Molecular mechanism of infection/inflammation-associatedcarcinogenesis and cancer prevention

由生物、化学和物理因素引起的慢性炎症已被发现与癌症风险增加有关。我们发现，考克斯-2的核定位，这是报告作为一个转录因子的功能，是显着相关的干细胞标志物在寄生虫感染的癌组织中的上调。考克斯-2活化可能参与炎症介导的肿瘤发生中干细胞的增殖/分化。8-硝基鸟嘌呤在炎症相关癌组织中的干细胞标志物阳性细胞中形成。炎症可增加突变干细胞的数量，其中通过NF-κB活化发生iNOS依赖性DNA损伤，导致肿瘤发展。

Chronic inflammation induced by biological, chemical, and physical factors has been found to be associated with the increased risk of cancer. We revealed that the nuclear localization of COX-2, which was reported to function as a transcription factor, was significantly associated with the up-regulation of stem cell marker in cancer tissues with parasite infection. COX-2 activation may be involved in stem cell proliferation/differentiation in inflammation-mediated carcinogenesis. 8-Nitroguanine was formed in stem cell marker-positive cells in inflammation-associated cancer tissues. Inflammation may increase the number of mutant stem cells, in which iNOS-dependent DNA damage occurs via NF-κB activation, leading to tumor development.