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.
    International Journal of Microbiology 10/2011; 2011:792019. DOI:10.1155/2011/792019
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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.
    Tumor Biology 04/2011; 32(4):653-9. DOI:10.1007/s13277-011-0165-6 · 3.61 Impact Factor
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    • "Infectious diseases are acquiring relevance as important pathogenic elements in human cancer, since almost one fifth of human cancers are associated with infectious agent, either bacteria or viruses, particularly in the gastrointestinal tract [2], but do not represent mainstream oncologic research. The development of several types of human cancers can be triggered by the exposure to different infectious agents, viruses or bacteria, such as Human Papilloma Virus (HPV) infection associated to cervical carcinoma [3], hepatitis B virus to liver carcinoma [4], Epstein-Barr virus to Burkitt lymphomas [5], HTVL-1 to ATL [6], Helicobacter pylori to gastric carcinoma [7] and more recently a human retrovirus, XMRV, has been associated to sporadic prostate cancer [8-10]. More recently, it has been reported the association between the development of lower gastrointestinal tract neoplasias and infectious agents [7], such as between colorectal cancer (CRC) and JCV infection. "
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    ABSTRACT: JCV infection occurs early in childhood and last throughout life. JCV has been associated to colorectal cancer and might contribute to the cancer phenotype by several mechanisms. Among JCV proteins, particularly two of them, large T-antigen and agnoprotein, can interfere with cell cycle control and genomic instability mechanisms, but other viral proteins might also contribute to the process. Part of viral DNA sequences are detected in carcinoma lesions, but less frequently in adenomas, and not in the normal surrounding tissue, suggesting they are integrated in the host cell genome and these integrations have been selected; in addition viral integration can cause a gene, or chromosomal damage. The inflammatory infiltration caused by a local chronic viral infection in the intestine can contribute to the selection and expansion of a tumor prone cell in a cytokine rich microenvironment. JCV may not be the cause of colorectal cancer, but it can be a relevant risk factor and able to facilitate progression at one or several stages in tumor progression. JCV transient effects might lead to selective expansion of tumor cells. Since there is not a direct cause and effect relationship, JCV infection may be an alternative to low frequency cancer predisposition genes.
    Virology Journal 02/2010; 7(1):42. DOI:10.1186/1743-422X-7-42 · 2.18 Impact Factor
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