Infectious Causes of Colorectal Cancer

Hasan, Nazia; Pollack, Ari H.; Cho, Ilseung

doi:10.1016/j.idc.2010.07.009

Cited by 17 publications

(13 citation statements)

References 161 publications

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“…The pathogenesis of this cancer is highly complex and it involves sequential genetic and epigenetic mechanisms [4,5]. A possible contribution of environmental agents, including bacteria and viruses, is also considered [6,7]. However, the search for a pathogenic agent generated conflicting results, possibly related to technical reasons or other unknown factors [6].…”

Section: Resultsmentioning

confidence: 99%

“…Amplification methods consisted of real time (EBV, JCV, BKV, HTLV and HHV-8) [8-11] and qualitative PCR (MCPyV, HPV) [12,13]. Given the very controversial evidence concerning JCV, which was found from 0% to nearly 80% of the tumor samples tested in the literature [6,14-18], JCV was additionally investigated by the specific qualitative PCR described in positive reports [18] and that employed primers spanning a different portion of the large T antigen. Sensitivity for JCV real-time PCR assay was 1 viral copy in 10 5 cells.…”

Section: Resultsmentioning

confidence: 99%

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Systematic analysis of human oncogenic viruses in colon cancer revealed EBV latency in lymphoid infiltrates

Fiorina

Ricotti

Vanoli

et al. 2014

Infect Agents Cancer

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BackgroundEnvironmental factors may play a role in colon cancer. In this view, several studies investigated tumor samples for the presence of various viral DNA with conflicting results.FindingsWe undertook a systematic DNA analysis of 44 consecutive, prospectively collected primary tumor samples by real time and qualitative PCR for viruses of known or potential oncogenic role in humans, including polyomavirus (JCV, BKV, Merkel cell polyomavirus), HPV, HTLV, HHV-8 and EBV. Negative controls consisted of surgical resection margins. No evidence of genomic DNA fragments from tested virus were detected, except for EBV, which was found in a significant portion of tumors (23/44, 52%). Real-time PCR showed that EBV DNA was present at a highly variable content (median 258 copies in 105 cells, range 15–4837). Presence of EBV DNA had a trend to be associated with high lymphocyte infiltration (p = 0.06, χ2 test), and in situ hybridization with EBER1-2 probes revealed latency in a fraction of these lymphoid cells, with just a few scattered plasma cells positive for BZLF-1, an immediate early protein expressed during lytic replication. LMP-1 expression was undetectable by immunohistochemistry.ConclusionsThese results argue against a significant involvement of the tested oncogenic viruses in established colon cancer.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Systematic analysis of human oncogenic viruses in colon cancer revealed EBV latency in lymphoid infiltrates

Fiorina

Ricotti

Vanoli

et al. 2014

Infect Agents Cancer

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“…Investigation of these cancer entities in which the tumour development is poorly understood, and in which a viral contribution is not excluded so far [76,77], revealed, by real-time PCR, the occurrence of HBoV DNA in about 20% of all cases. Confirmation by fluorescence in-situ hybridization revealed that the viral DNA is present in either 'head-to-tail' orientation (episomal form, concatemeres) or a linear form (genome before encapsidation, integrated into host genome).…”

Section: Introductionmentioning

confidence: 99%

Human bocavirus

Schildgen

Khalfaoui

Schildgen

2014

Reviews in Medical Microbiology

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The human bocavirus (HBoV) was initially discovered in 2005 in clinical samples from the respiratory tract of children suffering from respiratory infections of unknown aetiology and would be the second parvovirus that is capable of infecting humans with the potential to cause clinical diseases. HBoV-1 is detected as the fourth most common virus in respiratory infections and is associated with respiratory symptoms and sometimes also gastroenteritis in virtually all age groups [1,2]. Having been shown to form covalently closed circular DNA it appears likely that HBoV has the ability to persist in the infected tissue as other parvoviruses do [3][4][5][6][7], maybe leading to a chronic inflammation on the edge of its detection limit. Consequently HBoV could be detected in chronic lung diseases and, moreover, in tumour tissue of the lung and of the gastrointestinal tract. Therefore, it remains unclear to what extent the virus contributes to the development of such cancers or if the virus infects tumour cells preferentially. In this review we summarize our current knowledge about HBoV and discuss the perspective and challenges of future HBoV research. ß

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“…Apoptosis inhibition and DNA damage are mechanisms involved in inflammation-induced malignancies. Inflammation induces proinflammatory cytokines, which in turn induce oxygen radical formation [4, 31]. The competency of neonates’ immune systems, which differ from those of adults, is another suspect in tumourigenesis [32].…”

Section: Discussionmentioning

confidence: 99%

“…Although the aetiology and pathophysiology of congenital tumours are still unclear, they seem to be multifactorial; some tumours are associated with congenital anomalies, where the role of genetic factors is prominent, while environmental factors could affect the foetus during uterine life [1–4]. …”

Section: Introductionmentioning

confidence: 99%

ecancermedicalscience

Monajemzadeh

Sarmadi

Moeini³

et al.

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Congenital tumours are a group of distinct infrequent disorders whose exact aetiologies have not clearly been understood so far. Viral infection seems to be one of the key factors involved in the carcinogenesis of certain tumours. This study was performed to assess whether viral DNAs are present in the congenital tumours or not. Nucleic acid from 31 congenital tumours was extracted. Detection of Epstein–Barr virus, Cytomegalovirus (CMV), adenovirus, Herpes simplex virus 1 (HSV1) and 2, Human herpes virus 6 (HHV6), and BK virus was performed using polymerase chain reaction. Viral nucleic acid was detected in eight subjects (25.8%), mostly adenovirus, CMV, and HHV6. Despite their low frequencies, a possible role could be identified for viral infections in tumour development or progression.

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Infectious Causes of Colorectal Cancer

Cited by 17 publications

References 161 publications

Systematic analysis of human oncogenic viruses in colon cancer revealed EBV latency in lymphoid infiltrates

Systematic analysis of human oncogenic viruses in colon cancer revealed EBV latency in lymphoid infiltrates

Human bocavirus

ecancermedicalscience

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