In addition a case report described a Korean patient

In addition, a case report described a Korean patient presenting with both S. stercoralis infection and early gastric adenocarcinoma. Further analysis revealed that the gastric adenocarcinoma and adenoma tissues were positive for S. stercoralis suggesting a causative effect of S. stercoralis (Seo et al., 2015). An association of colorectal cancer with chronic S. stercoralis infection has also been reported in a Columbian patient (Tomaino et al., 2015). These observations suggest that S. stercoralis may not only serve as a cofactor for induction of HTLV-1-related lymphoid cancers, but also stimulates induction of colon adenocarcinoma probably by interacting with the host and/or activating the host immune response.

Paradoxical Dual Impacts of Chagas Disease in Carcinogenesis
Chagas disease (CD), a parasitic disease caused by the flagellated protozoan Trypanosoma cruzi, occurs throughout South and Central America, and affects approximately 15 million people (Coura, 2013). Successful transmission of T. cruzi primarily occurs through triatomine insects (kissing bugs). People become infected when ci-1033 of the kissing bug containing the trypomastigote stage of T. cruzi are deposited on the human skin while the insect feeds on blood; the T. cruzi containing insect feces contaminate mucous membranes, conjunctivae, or skin breaks, and initiate human infection (Stevens et al., 2011).
Approximately 40% of persons infected with T. cruzi are asymptomatic or present with indeterminate forms. About 2–5% progress annually to symptomatic forms with irreversible cardiac and/or digestive disorders, mostly presenting as megaorgans (Nunes et al., 2013). <1% develop severe acute disease with the clinical manifestations of acute myocarditis, pericardial effusion, and/or meningoencephalitis (Nunes et al., 2013).
Conclusions and Perspectives
The associations between infections with parasites and human cancers are well-evidenced. S. haematobium, O. viverrini, and C. sinensis are highly carcinogenic while other infectious species of the genera Opisthorchis (O. felineus) and Schistosoma (S. japonicum and S. mansoni) demonstrate their carcinogenic potential in humans (Table 1). Three main carcinogenic mechanisms have been described for these blood and liver flukes, including chronic inflammation, metabolic oxidative stress induced by parasite-derived products and host tissue damage during parasite development, along with the active wound healing (Fig. 1). However, detailed insights have not yet been obtained into these relationships, and/or into understanding functional consequences of both parasitic and host factors. Studies focusing on the identification of carcinogenic parasite factors and by which mechanisms host signaling pathways or oncogenes contribute to promote tumorgenesis are further warranted.
In malaria-related endemic Burkitt lymphoma, the AID protein appears to be an important factor that contribute to control chronic malaria and to induce human genomic instability (Fig. 2). Future clarification of AID in controlling Plasmodium infection and in its interaction with host chromosomes during B cell differentiation needs to be studied. In addition, the mechanisms by which S. stercoralis can induce malignancy together with HTLV-1 and/or directly induce carcinogenesis require further studies. While the carcinogenic role and mechanism of T. cruzi are not understood, anticancer properties of T. cruzi are mediated via the TcCRT and probably due to an effective response to oxidative stress (Fig. 3). Functional studies are required to warrant the antiangiogenic and antitumor properties of T. cruzi including studies of TcCRT and other molecules, which are potentially involved.


Declaration of Interests

PJB gratefully acknowledges support from awards R01CA155297 and R01CA164719 from the National Cancer Institute (NCI),P50AI098639 from the National Institute of Allergy and Infectious Diseases (NIAID), CA164719, CA155297 and AI098639 from National Institutes of Health (NIH). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NCI, NIAID, or NIH.