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Novel Developments on Diagnosis and Treatment of Gastrointestinal Cancer

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Gastroenterology & Hepatopancreatobiliary Medicine".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 380

Special Issue Editor


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Guest Editor
Department of Immunotherapeutics and Biotechnology, Texas Tech University Health Science Center, Abilene, TX 79601, USA
Interests: colorectal cancer; gastric cancer; biomarker; novel therapy; immunotherapy

Special Issue Information

Dear Colleagues,

The rising global burden of gastrointestinal cancers, particularly the increasing incidence among younger populations, is a growing concern. Emerging evidence suggests potential links to lifestyle factors and environmental changes. Current diagnostic methods, including blood tests, ultrasound, and CT scans, often fail to enable early detection, highlighting the urgent need for reliable biomarkers. Furthermore, existing treatment approaches such as surgery, chemotherapy, and radiation therapy remain inadequate in reducing recurrence rates.

To address these challenges, further research is imperative. The development and reassessment of novel and existing diagnostic biomarkers are crucial to improve early detection and treatment outcomes. This Special Issue aims to explore advancements in gastrointestinal cancer diagnosis and therapy, opening new avenues for innovation in the field.

We invite you to contribute original research, systematic reviews, and meta-analyses focusing on novel diagnostic markers, targeted delivery methods, treatment mechanisms, and immunotherapies for gastrointestinal cancers, including gastric, colon, and colorectal cancers.

We look forward to your valuable contributions.

Prof. Dr. Bhaumik Patel
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 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

  • colorectal cancer
  • gastric cancer
  • biomarker
  • novel therapy
  • immune microenvironment
  • gut microbiota
  • molecular mechanisms

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Published Papers (1 paper)

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Research

19 pages, 7071 KiB  
Article
Differential Role of CD318 in Tumor Immunity Affecting Prognosis in Colorectal Cancer Compared to Other Adenocarcinomas
by Bhaumik Patel, Marina Curcic, Mohamed Ashraf Eltokhy and Sahdeo Prasad
J. Clin. Med. 2025, 14(14), 5139; https://doi.org/10.3390/jcm14145139 - 19 Jul 2025
Viewed by 255
Abstract
Background/Objectives: CD318 (also known as CDCP1) is a transmembrane protein that is overexpressed in many cancers and contributes to tumor progression, invasion, and metastasis by activating SRC family kinases through phosphorylation. Emerging evidence also suggests that CD318 plays a role in modulating [...] Read more.
Background/Objectives: CD318 (also known as CDCP1) is a transmembrane protein that is overexpressed in many cancers and contributes to tumor progression, invasion, and metastasis by activating SRC family kinases through phosphorylation. Emerging evidence also suggests that CD318 plays a role in modulating the tumor immune microenvironment, although its precise mechanism in tumor progression is still not well understood. Methods: To investigate this, we analyzed the expression and immune-related functions of CD318 using the publicly available data from The Cancer Genome Atlas (TCGA) across colorectal adenocarcinoma (COAD), cervical squamous cell carcinoma (CESC), lung adenocarcinoma (LUAD), and pancreatic adenocarcinoma (PAAD). Results: All four cancers exhibited a high level of CD318 expression. Notably, in CESC, LUAD, and PAAD, plasmin-mediated cleavage of CD318 leads to phosphorylation of SRC and protein kinase C delta (PKCδ), which activates HIF1α and/or p38 MAPK. These downstream effectors translocate to the nucleus and promote the transcriptional upregulation of TGFβ1, fostering an immunosuppressive tumor microenvironment through Treg cell recruitment. In contrast, this signaling cascade appears to be absent in COAD. Instead, our analysis indicate that intact CD318 in COAD interacts with the surface receptors CD96 and CD160, which are found on CD8+ T cells and NK cells. Conclusions: This interaction enhances cytotoxic immune responses in COAD by promoting CD8+ T cell and NK cell activity, offering a possible explanation for the favorable prognosis associated with high CD318 expression in COAD, compared to the poorer outcomes observed in CESC, LUAD, and PAAD. Full article
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