Viruses in Cancers of the Digestive System: Active Contributors or Idle Bystanders?

Marônek, Martin; Link, Rene; Monteleone, Giovanni; Gardlík, Roman; Stolfi, Carmine

doi:10.3390/ijms21218133

Cited by 14 publications

(16 citation statements)

References 229 publications

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“…Changes in the fecal virome, especially the phage population, have been reported recently for CRC patients [7,65,73,90]. It has been suggested that phages may play a causative role in CRC by altering the bacterial populations of the intestine such that pathogenic bacteria can thrive and form biofilms [72,73] (Figure 1B).…”

Section: The Human Intestinal Virome and Its Links To Cancermentioning

confidence: 63%

“…The proposed mechanisms of viral contributions to carcinogenesis also vary widely between viral species and will be briefly discussed in the following subsections. In general, viral infections can contribute to carcinogenesis by any of the following mechanisms: insertional mutation in the host genome, induction of inflammation and modulation of signaling pathways in the infected cells, for example, by viral oncogenes [6,7] (Figure 1A).…”

Section: The Roles Of the Eukaryotic Virome In Cancermentioning

confidence: 99%

“…Moreover, merely associating the presence of specific viral sequences with cancer status does not necessarily indicate a causal role of the virus. [7]. (B) Phages coexist with their host bacteria in a well-balanced equilibrium, for example in the intestinal tract.…”

Section: Papillomaviridaementioning

confidence: 99%

“…The viral genome may also express viral oncogenes, or it activates a near-by host proto-oncogene (not shown). Figure adapted from Marônek et al[7]. (B) Phages coexist with their host bacteria in a well-balanced equilibrium, for example in the intestinal tract.…”

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confidence: 99%

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The Roles of the Virome in Cancer

Broecker¹,

Moelling²

2021

Preprint

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Viral infections as well as changes in the composition of the intestinal microbiota and virome have been linked to cancer. Moreover, the success of cancer immunotherapy with checkpoint inhibitors has been correlated with the intestinal microbial composition of patients. The transfer of feces – which contains mainly bacteria and their viruses (phages) – from immunotherapy responders to non-responders, known as fecal microbiota transplantation (FMT), has been shown to be able convert some non-responders to responders. Since phages may also increase the response to immunotherapy, for example by inducing T cells cross-reacting with cancer antigens, modulating phage populations may provide a new avenue to improve immunotherapy responsiveness. In this review, we summarize the current knowledge on the human virome and its links to cancer, and discuss the potential utility of bacteriophages in increasing the responder rate for cancer immunotherapy.

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Section: The Human Intestinal Virome and Its Links To Cancermentioning

confidence: 63%

Section: The Roles Of the Eukaryotic Virome In Cancermentioning

confidence: 99%

Section: Papillomaviridaementioning

confidence: 99%

mentioning

confidence: 99%

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The Roles of the Virome in Cancer

Broecker¹,

Moelling²

2021

Preprint

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“…Viral infections including HPV, Epstein-Barr virus (EBV), hepatitis B and C viruses, human T-lymphotropic virus-1, and polyomaviruses are considered as the major risk factor for about 20% of all cancers (4)(5)(6). Thus, some studies proposed a possible link between viruses such as EBV, HPV, and cytomegalovirus (CMV) with esophageal carcinoma (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Association of Epstein–Barr Virus and Cytomegalovirus Infections with Esophageal Carcinoma

et al. 2021

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Background: Given the fact that viral infections play an important role, either directly or indirectly, in around 20 percent of human cancers, this study aimed at investigating the potential association of Epstein–Barr virus (EBV) and cytomegalovirus (CMV) infections in esophageal cancer that is the sixth most common cause of cancer-related deaths. Methods: In this case-control study, a total of 200 paraffin-embedded biopsies of cancerous and benign esophageal tissues were gathered from the biopsy bank of Imam Reza Hospital, Tabriz, Iran in 2017. All samples were first deparaffinized, and then subjected to commercial DNA extraction. The quality of extracted DNA was evaluated by amplification of the beta globulin gene. Identification of EBV and CMV DNA was performed using primers designed for the EBER region of EBV and the immediate early (IE) region of the CMV genome, respectively. Results: The mean age of the subjects in the test and control groups was 52.2 (17.1) and 59.9 (18.9), respectively. The distribution of gender (male/female) in patient and control groups was 54/46 and 53/47, respectively. Our results showed that the frequency of EBV (P < 0.001) and CMV (P < 0.001) in cancerous samples was statistically higher than control group. Moreover, in the cancerous group the rate of EBV was significantly higher in the esophageal adenocarcinomas (EAC) sample (12 out of 70) than esophageal squamous cell carcinomas (ESCC) (0 out of 30) (P = 0.016) but, in the ESCC group, 17 out of 30 subjects were positive for CMV which was significantly higher in comparison with EAC patients (1 out of 70) (P < 0.001). Conclusions: Findings indicated that EBV and CMV might be contributed to the pathogenesis of EAC and ESCC types of esophageal carcinoma, respectively, although further studies are warranted.

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Viruses in colorectal cancer

Marongiu

Allgayer

2021

Molecular Oncology

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Increasing evidence suggests that microorganisms might represent at least highly interesting cofactors in colorectal cancer (CRC) oncogenesis and progression. Still, associated mechanisms, specifically in colonocytes and their microenvironmental interactions, are still poorly understood. Although, currently, at least seven viruses are being recognized as human carcinogens, only three of these – Epstein–Barr virus (EBV), human papillomavirus (HPV) and John Cunningham virus (JCV) – have been described, with varying levels of evidence, in CRC. In addition, cytomegalovirus (CMV) has been associated with CRC in some publications, albeit not being a fully acknowledged oncovirus. Moreover, recent microbiome studies set increasing grounds for new hypotheses on bacteriophages as interesting additional modulators in CRC carcinogenesis and progression. The present Review summarizes how particular groups of viruses, including bacteriophages, affect cells and the cellular and microbial microenvironment, thereby putatively contributing to foster CRC. This could be achieved, for example, by promoting several processes – such as DNA damage, chromosomal instability, or molecular aspects of cell proliferation, CRC progression and metastasis – not necessarily by direct infection of epithelial cells only, but also by interaction with the microenvironment of infected cells. In this context, there are striking common features of EBV, CMV, HPV and JCV that are able to promote oncogenesis, in terms of establishing latent infections and affecting p53‐/pRb‐driven, epithelial–mesenchymal transition (EMT)‐/EGFR‐associated and especially Wnt/β‐catenin‐driven pathways. We speculate that, at least in part, such viral impacts on particular pathways might be reflected in lasting (e.g. mutational or further genomic) fingerprints of viruses in cells. Also, the complex interplay between several species within the intestinal microbiome, involving a direct or indirect impact on colorectal and microenvironmental cells but also between, for example, phages and bacterial and viral pathogens, and further novel species certainly might, in part, explain ongoing difficulties to establish unequivocal monocausal links between specific viral infections and CRC.

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Viruses in Cancers of the Digestive System: Active Contributors or Idle Bystanders?

Cited by 14 publications

References 229 publications

The Roles of the Virome in Cancer

The Roles of the Virome in Cancer

Association of Epstein–Barr Virus and Cytomegalovirus Infections with Esophageal Carcinoma

Viruses in colorectal cancer

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