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Advances in the Molecular Mechanisms in Gastrointestinal Tumorigenesis and Treatment

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 (15 June 2024) | Viewed by 2918

Special Issue Editor


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Guest Editor
Cellular and Molecular Immunology Lab, Department of Biotechnology and Biosciences, Univesità degli studi Milano – Bicocca, Piazza della Scienza, 2, 20126 Milano, Italy
Interests: chronic inflammation in inflammatory bowel disease and gastric cancer
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Special Issue Information

Dear Colleagues,

We are editing a Special Issue for the International Journal of Molecular Science on "Advances in the Molecular Mechanisms in Gastrointestinal Tumorigenesis and Treatment". We would like to invite you to contribute a research article or review article in an area related to this topic.

Acute inflammation is a response to a pathogen or a physical or chemical insult that aims to eliminate the source of the damage and restore homeostasis. In the physiological context, after tissue repair or pathogen elimination, the inflammation is reduced and the homeostatic state recovered. However, if inflammation is unregulated, it can become chronic, inducing malignant cell transformation in the surrounding tissue. It is widely accepted that inadequately resolved chronic inflammation is closely linked to cancer development, more so in the gastrointestinal tract and liver than in any other organs. Some examples include Barrett’s esophagitis being a risk factor for esophageal cancer, Helicobacter pylori (H. pylori) infection for the development of gastric cancer and MALT lymphoma, chronic inflammatory bowel diseases for colorectal cancer development, and chronic viral hepatitis infection for the development of liver cancer. Inflammation-driven malignancies can result from the complex crosstalk between cytokines, chemokines, growth factors and reactive oxygen species (ROS) generated by inflammatory cells and injured parenchymal cells.

Despite a clear causal relationship between inflammation and cancers in the gastrointestinal tract, further studies of the underlying mechanisms and signaling pathways regulated by chronic inflammation activators and inhibitors responsible for this interaction are not fully established.

We aim to develop this Special Issue to contribute and share updates on the advancements in this field.

Themes and questions that we want to address in this Special Issue include, but are not limited to:

  • Biomarker discovery
  • Pathogenesis of GI cancer
  • Omics approach to IBD and GI cancer
  • New treatment strategies
  • The natural history of chronic inflammation in IBD
  • The natural history of chronic inflammation towards GI cancer
  • Risk factors of IBD and GI Cancer
  • Early diagnosis

Dr. Laura Francesca Pisani
Guest Editor

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Published Papers (2 papers)

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Research

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21 pages, 6529 KiB  
Article
Radial Data Visualization-Based Step-by-Step Eliminative Algorithm to Predict Colorectal Cancer Patients’ Response to FOLFOX Therapy
by Jakub Kryczka, Rafał Adam Bachorz, Jolanta Kryczka and Joanna Boncela
Int. J. Mol. Sci. 2024, 25(22), 12149; https://doi.org/10.3390/ijms252212149 - 12 Nov 2024
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Abstract
Application of the FOLFOX scheme to colorectal cancer (CRC) patients often results in the development of chemo-resistance, leading to therapy failure. This study aimed to develop a functional and easy-to-use algorithm to predict patients’ response to FOLFOX treatment. Transcriptomic data of CRC patient’s [...] Read more.
Application of the FOLFOX scheme to colorectal cancer (CRC) patients often results in the development of chemo-resistance, leading to therapy failure. This study aimed to develop a functional and easy-to-use algorithm to predict patients’ response to FOLFOX treatment. Transcriptomic data of CRC patient’s samples treated with FOLFOX were downloaded from the Gene Expression Omnibus database (GSE83129, GSE28702, GSE69657, GSE19860 and GSE41568). Comparing the expression of top up- and downregulated genes in FOLFOX responder and non-responder patients’ groups, we selected 30 potential markers that were used to create a step-by-step eliminative procedure based on modified radial data visualization, which depicts the interplay between the expression level of chosen attributes (genes) to locate data points in low-dimensional space. Our analysis proved that FOLFOX-resistant CRC samples are predominantly characterized by upregulated expression levels of TMEM182 and MCM9 and downregulated LRRFIP1. Additionally, the procedure developed based on expression levels of TMEM182, MCM9, LRRFIP1, LAMP1, FAM161A, KLHL36, ETV5, RNF168, SRSF11, NCKAP5, CRTAP, VAMP2, ZBTB49 and RIMBP2 proved to be capable in predicting FOLFOX therapy response. In conclusion, our approach can give a unique insight into clinical decision-making regarding therapy scheme administration, potentially increasing patients’ survival and, consequently, medical futility due to incorrect therapy application. Full article
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Review

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14 pages, 3171 KiB  
Review
Prognostic Value of B7H4 Expression in Patients with Solid Cancers: A Systematic Review and Meta-Analysis
by Miriam Dawidowicz, Agnieszka Kula, Sylwia Mielcarska, Elżbieta Świętochowska and Dariusz Waniczek
Int. J. Mol. Sci. 2024, 25(9), 5045; https://doi.org/10.3390/ijms25095045 - 6 May 2024
Cited by 1 | Viewed by 1575
Abstract
V-set domain-containing T-cell activation inhibitor 1 (aliases VTCN1, B7H4) participates in tumour immune escape by delivering inhibitory signals to T cells. The purpose of this article was to assess the B7H4 prognostic value in solid cancers. Three databases were searched for relevant articles. [...] Read more.
V-set domain-containing T-cell activation inhibitor 1 (aliases VTCN1, B7H4) participates in tumour immune escape by delivering inhibitory signals to T cells. The purpose of this article was to assess the B7H4 prognostic value in solid cancers. Three databases were searched for relevant articles. The main endpoints were overall survival (OS), disease-specific survival (DSS), progression-free survival (PFS), recurrence-free survival (RFS), and disease-free survival (DFS). Appropriate hazard ratios (HRs) were pooled. The R studio software (version 4.0.3) was used for data analysis. Thirty-one studies met the inclusion criteria. High expression of B7H4 was associated with worse OS (HR = 1.52, 95% CI: 1.37–1.68) but not with DSS (HR = 1.14, 95% CI: 0.49–2.63), RFS (HR = 1.77, 95% CI: 0.75–4.18), DFS (HR = 1.29, 95% CI: 0.8–2.09), or PFS (HR = 1.71, 95% CI: 0.91–3.2) in patients with solid cancers. High expression of B7H4 is associated with a poorer prognosis in patients with solid cancers. B7H4 is a promising prognostic biomarker and immunotherapeutic target for various solid cancers because of its activity in cancer immunity and tumourigenesis. Full article
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