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Cancers
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Gut Microbiota and Inflammation in Colorectal Tumor Development and Progression
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Gut Microbiota and Inflammation in Colorectal Tumor Development and Progression

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 30 September 2026 | Viewed by 926

Special Issue Editors

Prof. Dr. Giovanni Monteleone

E-Mail Website
Guest Editor
1. Department of Systems Medicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
2. Gastroenterology Unit, Fondazione Policlinico “Tor Vergata”, 00133 Rome, Italy
Interests: colorectal cancer; inflammatory bowel diseases; Crohn’s disease; ulcerative colitis; celiac disease; mucosal immunity; biological therapy; immuno-therapy; gut
Special Issues, Collections and Topics in MDPI journals
Dr. Irene Marafini

E-Mail Website
Guest Editor
1. Department of Systems Medicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
2. Gastroenterology Unit, Fondazione Policlinico “Tor Vergata”, 00133 Rome, Italy
Interests: colorectal cancer; inflammatory bowel diseases; Crohn’s disease; ulcerative colitis; celiac disease; mucosal immunity; biological therapy; immuno-therapy; gut

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to the Special Issue of Cancers entitled “Gut Microbiota and Inflammation in Colorectal Tumor Development and Progression”. This Special Issue aims to explore the mechanistic and clinical links between gut microbiota, mucosal inflammation, and colorectal cancer initiation, progression, and response to therapy. 

We welcome original research articles and reviews addressing basic, translational, and clinical aspects, including immune–microbiota interactions, inflammatory signaling pathways, microbial metabolites, and therapeutic implications. 

Given your expertise, we believe your contributions would be highly valuable to this collection. The submission deadline is 30 September 2026. 

We look forward to receiving your contributions.

Prof. Dr. Giovanni Monteleone
Dr. Irene Marafini
Guest Editors

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 submissions that pass pre-check are 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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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.

Keywords

  • gut microbiota
  • colorectal cancer
  • inflammation
  • tumor microenvironment
  • mucosal immunity
  • microbial metabolites
  • immune–microbiota interactions
  • inflammatory bowel disease
  • cancer progression

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Published Papers (1 paper)

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Review

30 pages, 1037 KB  
Review
Immunologic Drivers and Restraints in Colitis-Associated Colorectal Cancer
by Rachele Frascatani, Federica Laudisi, Carmine Stolfi and Giovanni Monteleone
Cancers 2026, 18(8), 1230; https://doi.org/10.3390/cancers18081230 - 13 Apr 2026
Viewed by 578
Abstract
Inflammatory bowel diseases (IBD), encompassing ulcerative colitis and Crohn’s disease, are associated with an increased risk of colorectal cancer through mechanisms driven by persistent mucosal inflammation. Chronic inflammatory signaling, recurrent epithelial injury, and altered tissue repair processes progressively reshape the intestinal microenvironment, promoting [...] Read more.
Inflammatory bowel diseases (IBD), encompassing ulcerative colitis and Crohn’s disease, are associated with an increased risk of colorectal cancer through mechanisms driven by persistent mucosal inflammation. Chronic inflammatory signaling, recurrent epithelial injury, and altered tissue repair processes progressively reshape the intestinal microenvironment, promoting genomic instability and facilitating the development of colitis-associated colorectal cancer (CAC). Despite the well-established link between inflammation and tumorigenesis, only a subset of patients with long-standing IBD develops malignancy, highlighting the complexity of the regulatory effects of the ongoing inflammation on the tumor initiation and progression. This review discusses the multifaceted roles of innate and adaptive immune responses in CAC pathogenesis. Innate immune signaling mediated by pattern recognition receptors, particularly Toll-like receptors, integrates microbial and damage-associated signals to activate inflammatory pathways that regulate epithelial proliferation, survival, and tumor-promoting cytokine networks. Tumor-associated macrophages, neutrophils, and myeloid-derived suppressor cells contribute to carcinogenesis by sustaining chronic inflammation, promoting immunosuppression, and remodeling the tumor microenvironment, although under specific conditions these cells can also support antitumor immunity. Innate lymphocyte subsets participate in immune surveillance and epithelial homeostasis, yet may also amplify inflammatory circuits that influence tumor development. Adaptive immune populations further shape CAC evolution, as CD4+ T-helper subsets, CD8+ cytotoxic T lymphocytes, regulatory T cells, and B cells exert divergent effects depending on cytokine milieu, immune context, and disease stage. Understanding immune-cell plasticity and the molecular pathways governing these processes may facilitate the identification of predictive biomarkers and the development of targeted immunomodulatory strategies aimed at preventing CAC. Full article
(This article belongs to the Special Issue Gut Microbiota and Inflammation in Colorectal Tumor Development and Progression)
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