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Inflammation and Gastrointestinal Cancers: Molecular Mechanisms and Therapies 2.0
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Inflammation and Gastrointestinal Cancers: Molecular Mechanisms and Therapies 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 19621

Special Issue Editors

Dr. Carmine Stolfi

E-Mail Website
Guest Editor
Department of Systems Medicine, University of Rome “Tor Vergata”, Rome, Italy
Interests: colorectal cancer; immunotherapy; inflammatory bowel diseases; anti-cancer drugs
Special Issues, Collections and Topics in MDPI journals
Dr. Federica Laudisi

E-Mail Website
Guest Editor
Department of Systems Medicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
Interests: colorectal cancer; inflammatory bowel disease; intestinal inflammation; intestinal epithelial barrier; microbiota; immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous special issue "Inflammation and Gastrointestinal Cancers: Molecular Mechanisms and Therapies".

Many epidemiologic and molecular studies showed that chronic inflammation is an independent risk factor for the development of gastrointestinal cancers (e.g., chronic gastritis for gastric cancer, chronic hepatitis for liver cancer, inflammatory bowel diseases for colorectal cancer). Moreover, the infiltration of immune/inflammatory cells is known to occur in all the stages of gastrointestinal carcinogenesis and to play a major role in such a process. Although inflammatory cell-derived cytokines/factors can either directly or indirectly promote cancer cell growth and invasion, under specific inflammatory conditions, immune cells can mediate antitumor responses with the downstream effect of eliminating dysplastic and cancerous cells. The specific nature of the inflammatory response and the tissue context may thus determine the beneficial versus the detrimental effects of inflammation in both tumor initiation and progression.

Despite recent scientific advances, the molecular and cellular pathways connecting inflammation and cancer are still being uncovered. A better understanding of this liaison may definitely improve our knowledge about cancer cell biology and offer opportunities for the design of new therapeutic interventions.

In this Special Issue, we invite investigators working on inflammation and gastrointestinal cancers to submit original papers or reviews to shed further light on this complex field. Potential topics include but are not limited to:

- Mechanistic studies on esophageal, liver, pancreatic, gastric, and colorectal carcinogenesis;

- Role of epigenetic alterations in gastrointestinal cancers;

- Effects of dietary and/or lifestyle changes on gastrointestinal inflammation and tumorigenesis;

- Effects of the microbiota on inflammation, carcinogenesis, and cancer therapy;

- Role of inflammatory cell-derived factors on cancer immunosurveillance and immunoediting;

- Therapeutic strategies and novel clinical approaches for gastrointestinal cancers (e.g., chemotherapeutics, immunotherapy, natural compounds, drug repositioning, precision medicine);

- Prognostic and predictive biomarkers reflecting qualitative and quantitative disease activity, progression of cancer, and prediction of the outcome of the treatment.

Dr. Carmine Stolfi
Dr. Federica Laudisi
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • colorectal cancer
  • gastric cancer
  • liver cancer
  • inflammatory bowel diseases
  • tumor microenvironment
  • mucosal immunology
  • inflammasome
  • cytokines
  • microbiota
  • diet and lifestyle
  • epigenetic
  • drug repositioning
  • natural compounds
  • checkpoint inhibitors
  • prognostic biomarkers
  • immunotherapy
  • autophagy

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Published Papers (4 papers)

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14 pages, 5651 KiB  
Article
Cell Type-Specific Induction of Inflammation-Associated Genes in Crohn’s Disease and Colorectal Cancer
by Dominik Saul, Luísa Leite Barros, Alexander Q. Wixom, Benjamin Gellhaus, Hunter R. Gibbons, William A. Faubion and Robyn Laura Kosinsky
Int. J. Mol. Sci. 2022, 23(6), 3082; https://doi.org/10.3390/ijms23063082 - 12 Mar 2022
Cited by 9 | Viewed by 4671
Abstract
Based on the rapid increase in incidence of inflammatory bowel disease (IBD), the identification of susceptibility genes and cell populations contributing to this condition is essential. Previous studies suggested multiple genes associated with the susceptibility of IBD; however, due to the analysis of [...] Read more.
Based on the rapid increase in incidence of inflammatory bowel disease (IBD), the identification of susceptibility genes and cell populations contributing to this condition is essential. Previous studies suggested multiple genes associated with the susceptibility of IBD; however, due to the analysis of whole-tissue samples, the contribution of individual cell populations remains widely unresolved. Single-cell RNA sequencing (scRNA-seq) provides the opportunity to identify underlying cellular populations. We determined the enrichment of Crohn’s disease (CD)-induced genes in a publicly available Crohn’s disease scRNA-seq dataset and detected the strongest induction of these genes in innate lymphoid cells (ILC1), highly activated T cells and dendritic cells, pericytes and activated fibroblasts, as well as epithelial cells. Notably, these genes were highly enriched in IBD-associated neoplasia, as well as sporadic colorectal cancer (CRC). Indeed, the same six cell populations displayed an upregulation of CD-induced genes in a CRC scRNA-seq dataset. Finally, after integrating and harmonizing the CD and CRC scRNA-seq data, we demonstrated that these six cell types display a gradual increase in gene expression levels from a healthy state to an inflammatory and tumorous state. Together, we identified cell populations that specifically upregulate CD-induced genes in CD and CRC patients and could, therefore, contribute to inflammation-associated tumor development. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal Cancers: Molecular Mechanisms and Therapies 2.0)
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Review

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17 pages, 2418 KiB  
Review
NK Cells and Other Cytotoxic Innate Lymphocytes in Colorectal Cancer Progression and Metastasis
by Cinzia Fionda, Gianluca Scarno, Helena Stabile, Rosa Molfetta, Chiara Di Censo, Angela Gismondi, Rossella Paolini, Silvano Sozzani, Angela Santoni and Giuseppe Sciumè
Int. J. Mol. Sci. 2022, 23(14), 7859; https://doi.org/10.3390/ijms23147859 - 16 Jul 2022
Cited by 13 | Viewed by 3241
Abstract
Colorectal cancer (CRC) is one of the most common malignancies and leading causes of cancer-related deaths worldwide. Despite its complex pathogenesis and progression, CRC represents a well-fitting example of how the immune contexture can dictate the disease outcome. The presence of cytotoxic lymphocytes, [...] Read more.
Colorectal cancer (CRC) is one of the most common malignancies and leading causes of cancer-related deaths worldwide. Despite its complex pathogenesis and progression, CRC represents a well-fitting example of how the immune contexture can dictate the disease outcome. The presence of cytotoxic lymphocytes, both CD8+ T cells and natural killer (NK) cells, represents a relevant prognostic factor in CRC and is associated with a better overall survival. Together with NK cells, other innate lymphocytes, namely, innate lymphoid cells (ILCs), have been found both in biopsies of CRC patients and in murine models of intestinal cancer, playing both pro- and anti-tumor activities. In particular, several type 1 innate lymphoid cells (ILC1) with cytotoxic functions have been recently described, and evidence in mice shows a role for both NK cells and ILC1 in controlling CRC metastasis. In this review, we provide an overview of the features of NK cells and the expanding spectrum of innate lymphocytes with cytotoxic functions. We also comment on both the described and the potential roles these innate lymphocytes can play during the progression of intestinal cancer leading to metastasis. Finally, we discuss recent advances in the molecular mechanisms underlying the functional regulation of cytotoxic innate lymphocytes in CRC. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal Cancers: Molecular Mechanisms and Therapies 2.0)
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35 pages, 3261 KiB  
Review
Molecular Mechanisms of Tumor Immunomodulation in the Microenvironment of Colorectal Cancer
by Dorothea Plundrich, Sophia Chikhladze, Stefan Fichtner-Feigl, Reinhild Feuerstein and Priscilla S. Briquez
Int. J. Mol. Sci. 2022, 23(5), 2782; https://doi.org/10.3390/ijms23052782 - 3 Mar 2022
Cited by 13 | Viewed by 5975
Abstract
Colorectal cancer remains one of the most important health challenges in our society. The development of cancer immunotherapies has fostered the need to better understand the anti-tumor immune mechanisms at play in the tumor microenvironment and the strategies by which the tumor escapes [...] Read more.
Colorectal cancer remains one of the most important health challenges in our society. The development of cancer immunotherapies has fostered the need to better understand the anti-tumor immune mechanisms at play in the tumor microenvironment and the strategies by which the tumor escapes them. In this review, we provide an overview of the molecular interactions that regulate tumor inflammation. We particularly discuss immunomodulatory cell-cell interactions, cell-soluble factor interactions, cell-extracellular matrix interactions and cell-microbiome interactions. While doing so, we highlight relevant examples of tumor immunomodulation in colorectal cancer. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal Cancers: Molecular Mechanisms and Therapies 2.0)
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33 pages, 859 KiB  
Review
Systemic Interleukins’ Profile in Early and Advanced Colorectal Cancer
by Paulina Czajka-Francuz, Sylwia Cisoń-Jurek, Aleksander Czajka, Maciej Kozaczka, Jerzy Wojnar, Jerzy Chudek and Tomasz Francuz
Int. J. Mol. Sci. 2022, 23(1), 124; https://doi.org/10.3390/ijms23010124 - 23 Dec 2021
Cited by 17 | Viewed by 4733
Abstract
Tumor microenvironment (TME) is characterized by mutual interactions of the tumor, stromal and immune cells. Early and advanced colorectal tumors differ in structure and present altered serum cytokine levels. Mutual crosstalk among TME infiltrating cells may shift the balance into immune suppressive or [...] Read more.
Tumor microenvironment (TME) is characterized by mutual interactions of the tumor, stromal and immune cells. Early and advanced colorectal tumors differ in structure and present altered serum cytokine levels. Mutual crosstalk among TME infiltrating cells may shift the balance into immune suppressive or pro-inflammatory, antitumor response this way influencing patients’ prognosis. Cancer-related inflammation affects all the body and this way, the systemic level of cytokines could reflect TME processes. Despite numerous studies, it is still not known how systemic cytokines levels change during colorectal cancer (CRC) tumor development. Better understanding tumor microenvironment processes could help in planning therapeutic interventions and more accurate patient prognosis. To contribute to the comprehension of these processes within TME, we reviewed cytokines levels from clinical trials in early and advanced colorectal cancer. Presented data were analyzed in the context of experimental studies and studies analyzing tumor infiltration with immune cells. The review summarizes clinical data of cytokines secreted by tumor microenvironment cells: lymphocytes T helper 1 (Th1), lymphocytes T helper 2 (Th2), lymphocytes T helper 17 (Th17), regulatory T cells (Treg cells), regulatory T cells (Breg cells), M1/M2 macrophages, N1/N2 neutrophils, myeloid-derived suppressor cells (MDSC), dendritic cells (DC), innate lymphoid cells (ILC) natural killer (NK) cells and tumor cells. Full article
(This article belongs to the Special Issue Inflammation and Gastrointestinal Cancers: Molecular Mechanisms and Therapies 2.0)
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