A dramatic intersection between the infectious diseases and oncology fields has emerged from the appreciation that many cancers arise in the setting of chronic infection. For certain viral-induced cancers, such as human papilloma virus (HPV)–associated cervical cancer, the integrated virus encodes oncogenes that directly drive the transformation of infected cells. However, the vast majority of infection-associated cancers arise from chronic immune responses that, although ineffective in eliminating the inciting microbe, collaborate with microbial products to drive carcinogenesis. As many as one-third of cancers worldwide, particularly epithelial cancers, are associated with identified single microbial infections, leading to the conceptual paradigm that chronic infection with specific microbes causes these cancers, independent of other components of the ambient microbial community. In addition to cervical cancer and HPV, other well-established examples include gastric cancer and Helicobacter pylori, liver cancer and hepatitis B and C viruses, urinary bladder cancer and Schistosoma hematobium, and biliary tree cancer, Clonorchis sinensis, and Opisthorchis viverrini.

A contrasting view of microbial carcinogenesis has been applied to colon cancer, the second leading cause of death due to cancer among adults in the United States. On the basis of increasingly high through put methods, we now understand that the colon is home to one of the most dense and diverse communities of bacteria in the body and that, although clustering of the colon microbiome sequences may occur in families or under similar close-contact conditions, we are all remarkably unique in our bacterial make up [1–2]. Indeed, beginning in the 1960s, investigators postulated and pursued links between the complex colon commensal flora and colon cancer [3].