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Special Issue "Biological Interfaces in Gastrointestinal Cancer 2.0"

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

Deadline for manuscript submissions: 31 October 2021.

Special Issue Editors

Dr. Andre Lechel
E-Mail Website
Guest Editor
Department of Internal Medicine I, Ulm University, 89081 Ulm, Germany
Interests: liver carcinogenesis; tumor differentiation; chronic liver disease; liver stem cells; tumor stem cells; p53-signalling; aging; telomeres
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Reinhold Schirmbeck
E-Mail Website
Guest Editor
Department of Internal Medicine I, Ulm University, 89081 Ulm, Germany
Interests: CD8 T cells; Genetic vaccines; Mouse models of chronic HBV infection; Development of novel immune therapies against tumors and autoimmune type 1 diabetes; The aging immune system

Special Issue Information

Dear Colleagues,

The focus of this Special Issue is on the role of communication in gastrointestinal cancers, involving cell-to-cell communication, like communication between the microenvironment or the immune system and the tumor cell, as well as communication on the molecular level, like Wnt, NF-kB, and Mtor, which play major roles in signal transduction.

Gastrointestinal cancer, like colorectal cancer, pancreatic cancer, and hepatocellular cancer, belong to the most common causes of cancer mortality and therfore present a major health problem. Gastrointestinal cancers are characterized by their huge heterogeneity, even if many mutations are present in several tumor entities.  

A detailed molecular tumor analysis on biological interfaces is increasingly fundamental in choosing the most appropriate anti-cancer therapy for patients and opening new doors for the development of precision medicine. Interdisciplinary teamwork with colleagues in pathology, bioinformatics, immunology, molecular biology, and other disciplines will help oncologists, integrating data and expertise from the work of professionals involved in prevention, early-diagnosis, and basic and translational cancer research.

In this Special Issue, we invite your contributions, either in the form of original research articles, reviews, or shorter perspective articles on all aspects related to the theme of “Biological Interfaces in Gastrointestinal Cancer”.

Dr. Andre Lechel
Prof. Dr. Reinhold Schirmbeck
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 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. 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

  • Liver cancer
  • Pancreatic cancer
  • Intestinal cancer
  • Gastric cancer
  • Tissue inflammation
  • Microenvironment
  • Innate and adaptive immune responses
  • Checkpoint inhibitors
  • Immunotherapy
  • Precision medicine
  • Model systems (e.g., transgenic mouse models, organoid culture)

Published Papers (2 papers)

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Research

Article
Recruitment of M1 Macrophages May Not Be Critical for Protection against Colitis-Associated Tumorigenesis
Int. J. Mol. Sci. 2021, 22(20), 11204; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011204 - 18 Oct 2021
Viewed by 228
Abstract
A close connection between inflammation and the risk of developing colon cancer has been suggested in the last few years. It has been estimated that patients diagnosed with some types of inflammatory bowel disease, such as ulcerative colitis or Crohn’s disease, have up [...] Read more.
A close connection between inflammation and the risk of developing colon cancer has been suggested in the last few years. It has been estimated that patients diagnosed with some types of inflammatory bowel disease, such as ulcerative colitis or Crohn’s disease, have up to a 30% increased risk of developing colon cancer. However, there is also evidence showing that the activation of anti-inflammatory pathways, such as the IL-4 receptor-mediated pathway, may favor the development of colon tumors. Using an experimental model of colitis-associated colon cancer (CAC), we found that the decrease in tumor development in global IL4Rα knockout mice (IL4RαKO) was apparently associated with an inflammatory response mediated by the infiltration of M1 macrophages (F480+TLR2+STAT1+) and iNOS expression in colon tissue. However, when we developed mice with a specific deletion of IL4Rα in macrophages (LysMcreIL4Rα−/lox mice) and subjected them to CAC, it was found that despite presenting a large infiltration of M1 macrophages into the colon, these mice were as susceptible to colon-tumorigenesis as WT mice. These data suggest that in the tumor microenvironment the absence of IL4Rα expression on macrophages, as well as the recruitment of M1 macrophages, may not be directly associated with resistance to developing colon tumors. Therefore, it is possible that IL4Rα expression in other cell types, such as colonic epithelial cells, could have an important role in promoting the development of colitis-associated colon tumorigenesis. Full article
(This article belongs to the Special Issue Biological Interfaces in Gastrointestinal Cancer 2.0)
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Article
MIR29A Impedes Metastatic Behaviors in Hepatocellular Carcinoma via Targeting LOX, LOXL2, and VEGFA
Int. J. Mol. Sci. 2021, 22(11), 6001; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22116001 - 01 Jun 2021
Cited by 1 | Viewed by 1212
Abstract
Primary liver cancer accounts for the third most deadly type of malignant tumor globally, and approximately 80% of the cases are hepatocellular carcinoma (HCC), which highly relies on the activity of hypoxia responsive pathways to bolster its metastatic behaviors. MicroRNA-29a (MIR29A) [...] Read more.
Primary liver cancer accounts for the third most deadly type of malignant tumor globally, and approximately 80% of the cases are hepatocellular carcinoma (HCC), which highly relies on the activity of hypoxia responsive pathways to bolster its metastatic behaviors. MicroRNA-29a (MIR29A) has been shown to exert a hepatoprotective effect on hepatocellular damage and liver fibrosis induced by cholestasis and diet stress, while its clinical and biological role on the activity hypoxia responsive genes including LOX, LOXL2, and VEGFA remains unclear. TCGA datasets were retrieved to confirm the differential expression and prognostic significance of all genes in the HCC and normal tissue. The Gene Expression Omnibus (GEO) dataset was used to corroborate the differential expression and diagnostic value of MIR29A. The bioinformatic identification were conducted to examine the interaction of MIR29A with LOX, LOXL2, and VEGFA. The suppressive activity of MIR29A on LOX, LOXL2, and VEGF was verified by qPCR, immunoblotting, and luciferase. The effect of overexpression of MIR29A-3p mimics in vitro on apoptosis markers (caspase-9, -3, and poly (ADP-ribose) polymerase (PARP)); cell viability and wound healing performance were examined using immunoblot and a WST-1 assay and a wound healing assay, respectively. The HCC tissue presented low expression of MIR29A, yet high expression of LOX, LOXL2, and VEGFA as compared to normal control. Serum MIR29A of HCC patients showed decreased levels as compared to that of normal control, with an area under curve (AUC) of 0.751 of a receiver operating characteristic (ROC) curve. Low expression of MIR29A and high expression of LOX, LOXL2, and VEGFA indicated poor overall survival (OS). MIR29A-3p was shown to target the 3′UTR of LOX, LOXL2, and VEGFA. Overexpression of MIR29A-3p mimic in HepG2 cells led to downregulated gene and protein expression levels of LOX, LOXL2, and VEGFA, wherein luciferase reporter assay confirmed that MIR29A-3p exerts the inhibitory activity via directly binding to the 3′UTR of LOX and VEGFA. Furthermore, overexpression of MIR29A-3p mimic induced the activity of caspase-9 and -3 and PARP, while it inhibited the cell viability and wound healing performance. Collectively, this study provides novel insight into a clinical-applicable panel consisting of MIR29, LOX, LOXL2, and VEGFA and demonstrates an anti-HCC effect of MIR29A via comprehensively suppressing the expression of LOX, LOXL2, and VEGFA, paving the way to a prospective theragnostic approach for HCC. Full article
(This article belongs to the Special Issue Biological Interfaces in Gastrointestinal Cancer 2.0)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title 1: Immunotherapy in Esophageal Cancer

Title 2: Differential Actions of Muscarinic Receptor Subtypes in Gastric, Pancreatic, and Colon Cancer

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