Infectious Agents and Colorectal Cancer: A Review of Helicobacter pylori, Streptococcus bovis, JC Virus, and Human Papillomavirus

Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, 1100 Fairview Avenue North, M4-B402, Seattle, WA 98109, USA.
Cancer Epidemiology Biomarkers & Prevention (Impact Factor: 4.13). 12/2008; 17(11):2970-9. DOI: 10.1158/1055-9965.EPI-08-0571
Source: PubMed


Based on the high volume of bacteria and viruses that the intestine is exposed to and the importance of infectious agents in some gastrointestinal and anogenital cancers, it is not surprising the many studies have evaluated the association between colorectal cancer and infectious agents. This review highlights investigations of four agents in relation to colorectal cancer. Helicobacter pylori, Streptococcus bovis, JC virus, and human papillomavirus have all been evaluated as possible etiologic agents for colorectal cancer. For each of these agents, a review of possible mechanisms for carcinogenesis and epidemiologic evidence is discussed, and future directions for research are proposed.

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    • "Several species of bacteria have been linked to chronic infections of colon and have been shown to increase the risk of colon cancer. Streptococcus bovis has been evaluated as one of the possible etiologic agents for colorectal cancer [1]. S. bovis is a Gram-positive bacterium, which is considered as a normal inhabitant of the human gastrointestinal tract but is less frequently present than other Streptococcus species [2]. "
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    ABSTRACT: Streptococcus bovis is a Gram-positive bacterium causing serious human infections, including endocarditis and bacteremia, and is usually associated with underlying disease. The aims of the current study were to compare prevalence of the bacterium associated with malignant and nonmalignant gastrointestinal diseases and to determine the susceptibility of the isolated strains to different antimicrobial agents. The result showed that the prevalence of S. bovis in stool specimens from patients with malignant or with nonmalignant gastrointestinal diseases was statistically significant. This result may support the idea that there is correlation between S. bovis and the malignant gastrointestinal diseases.
    Full-text · Article · Oct 2011 · International Journal of Microbiology
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    • "As in the case of prevalence of HPV in CRCs, the papers published on the presence of JCV T-antigen sequence in CRCs display contradictory results with frequencies ranging from 0% in Italian and Spanish study, through 26% in Japanese cases to 77% in American patients [13, 34–36]. Given the all above-cited studies based on relatively similar PCR approaches, the discrepancies of JCV frequencies in CRC may reflect ethnic-dependent epidemiology of JCV or lack of reliable and reproducible test for the detection of JCV DNA [37]. A previous study by Goel et al. [13] reported an association between JCV T-antigen expression and methylation of the promoter region of various cancer-related genes in colorectal cancer. "
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    ABSTRACT: There is evidence that insertion of viral DNA into a mammalian genome can lead to alterations of methylation patterns. The aim of the present study was to examine the presence of DNA sequences of five human DNA viruses (assessed by PCR): JC polyoma virus (JCV), human adenovirus (AdV), Epstein-Barr virus (EBV), Kaposi sarcoma-associated herpesvirus (KSHV/HHV8) and human papillomavirus (HPV) in a cohort of 186 sporadic colorectal cancers (CRCs) and related these data with the methylation status of six CpG island methylator phenotype (CIMP)-specific genes (MLH1, CACNA1G, NEUROG1, IGF2, SOCS1, RUNX3) and seven cancer-related genes markers (p16, MINT1, MINT2, MINT31, EN1, SCTR and INHBB) assessed by methylation-specific PCR in 186 and 134 CRC cases, respectively. The AdV, KSHV and HPV were detected in four (2%), two (1%) and zero CRC cases, respectively, and thus were excluded from further analyses. Although 19% and 9% of the CRCs were positive for EBV and JCV, respectively, no associations between virus presence and CpG island methylation were found after correction for multiple testing. Our results demonstrate that the presence of DNA sequences of JCV and EBV in CRC is unrelated to the methylation of the 13 cancer-related CpG islands and CIMP.
    Full-text · Article · Apr 2011 · Tumor Biology
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    • "⁄ p < 0.05 vs. sham-operated mice. and pharmacological agents[4]. Intake of pharmacological agents, namely non-steroidal anti-inflammatory drugs (NSAIDs), can be effective; however, long-term intake could cause adverse reactions and even fatal side effects[8]. Considering the reports from epidemiological surveys that indicated an inverse correlation between the intake of fruits/vegetables and tumor development[38,39], we presumed that certain dietary phytochemicals might be suitable candidates that can suppress carcinogenesis[40]. "
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    ABSTRACT: Reducing cancer incidence and mortality by use of cancer-chemopreventive agents is an important goal. We have established an in vitro bioassay that is able to screen large numbers of candidate chemicals that are positive for prevention of inflammation-related carcinogenesis. To accomplish this we have added candidate chemicals or vehicles and freshly isolated, fluorescent dye-labeled inflammatory cells that were overlaid on TNF-alpha-stimulated mouse endothelial cells in a 96-well plate. Inhibition of inflammatory cell attachment to the endothelial cells by the chemicals was quantified by the intensity of fluorescence from the adherent inflammatory cells after removing unattached cells. Using this assay, we selected two chemicals, auraptene and turmerones, for further study. As an in vivo test, diets containing these test chemicals were administered to mice with a piece of foreign body, gelatin sponge, that had been implanted to cause inflammation, and we found that the number of inflammatory cells that infiltrated into the subcutaneously implanted gelatin sponge was reduced compared to that found in the mice fed with a control diet. Moreover, diets containing either of the two chemicals prevented inflammation-based carcinogenesis in a mouse model. We found that the compounds reduced not only the number of infiltrating cells but also the expression of inducible nitric oxide synthase (iNOS) or formation of 8-hydroxy-2'-deoxyguanine (8-OHdG) in the infiltrated cells. Moreover, both compounds but not controls sustained the reducing activity in the inflammatory lesion, and this finding was confirmed by using non-invasive in vivo electron spin resonance. The newly established in vitro screening assay will be useful for finding biologically effective chemopreventive agents against inflammation-related carcinogenesis.
    Full-text · Article · Feb 2011 · Nitric Oxide
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