Comorbid development of infection and cancer

Abstract

Infectious diseases remain the leading cause of death around the world, causing more than 12 million deaths each year. The long-term effects of these illnesses, as a major public health problem, have raised particular concerns since some infectious agents have been associated with different types of chronic diseases, including cancer. Although cancer development can be multi-factorial in origin, several types of solid organ or hematologic cancers are caused by infectious agents (Shurin MR, Immunol Targets Ther 1:1–6, 2012). Approximately 15 % of all cancers occurring worldwide could be attributed to infections, a global total of 1.2 million cases per year (Kuper H, Adami HO, Trichopoulos D et al., J Intern Med 248:171–183, 2000). A substantial body of evidence also support the notion that infection itself or associated production of pro-infl ammatory cytokines such as tumor necrosis factor (TNF), which can cause genetic mutations, thus promoting cancer development or enhancing epithelial-mesynchymal transition (EMT), an important mechanism that enable cancer metastasis (Voronov E et al., Proc Natl Acad Sci USA 100:2645–2650, 2003; Grivennikov SI and Karin M, Curr Opin Genet Dev 20:65–71, 2010). On the other hand, immunosuppression caused by the cancer itself or immunosuppressive drugs used for cancer treatment increase the risk and severity of infections, which in turn provide positive feedback mechanism that further enhance cancer metastasis (Khayr W, Haddad RY, Noor SA, Dis Mon 58:239–249, 2012). For instance, ~50–80 % of patients suffering from various hematological malignancies develop infections, which contribute to a higher incidence of mortality in these patients (Yadegarynia D, Tarrand J, Raad I, Rolston K, Clin Infect Dis 37:1144–1145, 2003).