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. Author manuscript; available in PMC: 2018 Aug 1.
Published in final edited form as: Parasitol Int. 2016 Dec 3;66(4):383–389. doi: 10.1016/j.parint.2016.11.016

Figure 3. Hypothesized pathways of pathogenesis of opisthorchiasis/H. pylori-induced cholangiocarcinoma.

Figure 3

The liver fluke Opisthorchis viverrini/Helicobacter damages bile duct tissue via at least three distinct pathways: 1) mechanical damage to biliary epithelia caused by parasites sucking; 2) inflammation-induced immunopathology, particularly due to reactive oxygen intermediates (ROI) and nitric oxide (NO); and 3) direct effects of fluke/Helicobacter secreted proteins on biliary epithelia including cell proliferation induced by parasite-derived growth factors. These pathways converge, resulting in genetic lesions and unregulated proliferation. Damaged DNA/genes after successive replications become fixed, leading to malignant transformation of cholangiocytes. Adapted from [32].