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. Author manuscript; available in PMC: 2017 Jul 31.
Published in final edited form as: Science. 2015 Apr 3;348(6230):80–86. doi: 10.1126/science.aaa4972

Fig. 2. Mechanisms by which microbes influence cancer development and progression.

Fig. 2

(A) Bacterial toxins can directly damage host DNA. Bacteria also damage DNA indirectly via host-produced reactive oxygen and nitrogen species. When DNA damage exceeds host cell repair capacity, cell death or cancer-enabling mutations occur. (B) β-Catenin signaling alterations are a frequent target of cancer-associated microbes. Some microbes bind E-cadherin on colonic epithelial cells, with altered polarity or within a disrupted barrier, and trigger β-catenin activation. Other microbes inject effectors (e.g., CagA or AvrA) that activate β-catenin signaling, resulting in dysregulated cell growth, acquisition of stem cell–like qualities, and loss of cell polarity. (C) Proinflammatory pathways are engaged upon mucosal barrier breach in an evolving tumor. Loss of boundaries between host and microbe engages pattern recognition receptors and their signaling cascades. Feedforward loops of chronic inflammation mediated by NF-κB and STAT3 signaling fuel carcinogenesis within both transforming and nonneoplastic cells within the tumors.