Special Issue "Host-Pathogen Interaction in Colorectal Carcinogenesis"

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: 31 December 2020.

Special Issue Editor

Prof. Carlos A Rubio
Guest Editor
Karolinska Institutet,·Gastrointestinal and Liver Pathology Research Laboratory, Karolinska University Hospital, Stockholm, Sweden
Interests: colorectal carcinogenesis; colorectal cancer

Special Issue Information

Dear Colleagues,

For many years it was generally accepted that multiple external environmental risk factors (such as alcohol, diet, life style, soil arsenic and nickel exposure), or hereditary traits, were involved in the development of colorectal cancer (CRC). More recently, mounting literature strongly suggests that alterations of a particular internal risk factor (i.e., dysbiosis in the luminal colonic microenvironment) might be crucial for generating the mucosal changes required for the evolution of sporadic and hereditary CRC.

This notion has been lately substantiated experimentally: gavage of fecal samples from patients with CRC to germ-free and conventional mice promoted intestinal carcinogenesis. Hence, the imbalance of the gut microbiota seems to play a substantial role in the evolution of CRC, not only in humans but also in laboratory animals. However, dysbiosis per se does not fulfil all requirements for that development; the bacterial species implicated in triggering colorectal carcinogenesis have to trespass the mucosal barrier, to reach the host. So far, the mechanisms whereby the gut microbiota reaches the host remains unclear. In inflammatory bowel disease (IBD), the breakdown of the integrity of barrier of macrophages in the lamina propria permits both toxic alien and commensal gut bacteria to trespass that barrier, resulting in host invasion. This leads to alteration of the natural host immunity (that critically controls intestinal carcinogensis) and the development of IBD-associated CRC. A similar defective mucosal barrier might also apply for patients with dysbiosis and hereditary or sporadic CRC.

For this Special Issue of Pathogens, we invite you to submit research articles, review articles, short notes as well as communications related to this part. We look forward to your contribution.

Prof. Carlos A Rubio
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • Colorectal cancer
  • CRC
  • Gut microbiota
  • Inflammatory bowel disease

Published Papers (1 paper)

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Open AccessReview
Human Papillomaviruses and Epstein–Barr Virus Interactions in Colorectal Cancer: A Brief Review
Pathogens 2020, 9(4), 300; https://doi.org/10.3390/pathogens9040300 - 20 Apr 2020
Human papillomaviruses (HPVs) and the Epstein–Barr virus (EBV) are the most common oncoviruses, contributing to approximately 10%–15% of all malignancies. Oncoproteins of high-risk HPVs (E5 and E6/E7), as well as EBV (LMP1, LMP2A and EBNA1), play a principal role in the onset and [...] Read more.
Human papillomaviruses (HPVs) and the Epstein–Barr virus (EBV) are the most common oncoviruses, contributing to approximately 10%–15% of all malignancies. Oncoproteins of high-risk HPVs (E5 and E6/E7), as well as EBV (LMP1, LMP2A and EBNA1), play a principal role in the onset and progression of several human carcinomas, including head and neck, cervical and colorectal. Oncoproteins of high-risk HPVs and EBV can cooperate to initiate and/or enhance epithelial-mesenchymal transition (EMT) events, which represents one of the hallmarks of cancer progression and metastasis. Although the role of these oncoviruses in several cancers is well established, their role in the pathogenesis of colorectal cancer is still nascent. This review presents an overview of the most recent advances related to the presence and role of high-risk HPVs and EBV in colorectal cancer, with an emphasis on their cooperation in colorectal carcinogenesis. Full article
(This article belongs to the Special Issue Host-Pathogen Interaction in Colorectal Carcinogenesis)
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