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Cells
Special Issues
Gastrointestinal Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities
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Gastrointestinal Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 7166

Special Issue Editors

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
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

Special Issue Information

Dear Colleagues,

Gastrointestinal cancer includes all cancers arising in the digestive tract organs, such as esophageal and gastric cancers, hepatobiliary cancers, pancreatic cancers, and colorectal cancers. When combined together, gastrointestinal cancers account for more new cases and deaths per year than cancers occurring in any other system of the body, and their incidence continues to increase. Additionally, in most cases, these malignancies are diagnosed at an advanced stage, leading to a poor prognosis despite the availability of different therapeutic approaches (e.g., chemotherapy, immunotherapy, radiotherapy). Even in patients with potentially curative cancer, almost half of them will develop recurrent disease. Despite recent technological advances and major scientific efforts, the cellular and molecular pathways that underpin the pathogenesis and progression of these malignancies are still being uncovered. Better knowledge of these mechanisms can definitely improve our understanding of gastrointestinal cancer cell biology and offer opportunities for the design of new and more effective therapeutic strategies.

In this Special Issue, we invite scholars working on gastrointestinal cancer to submit original research papers or review articles dealing with novel mechanistic insights and details of the molecular signatures of oncogenic transformation and disease progression. We also encourage the submission of manuscripts that focus on translating basic molecular knowledge to new medical applications. Articles focusing on diagnostic and prognostic biomarkers, as well as novel drug targets or targeted treatments, including possible clinical trials, are also welcomed.

Dr. Federica Laudisi
Dr. Carmine Stolfi
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. Cells 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 2700 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
  • liver cancer
  • pancreatic cancer
  • tumor microenvironment
  • cytokines
  • epigenetic
  • checkpoint inhibitors
  • biomarkers
  • immunotherapy

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Published Papers (4 papers)

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Research

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17 pages, 2609 KB  
Article
Residual Tumor Resection After Anti-PD-1 Therapy: A Promising Treatment Strategy for Overcoming Immune Evasive Phenotype Induced by Anti-PD-1 Therapy in Gastric Cancer
by Hajime Matsuida, Kosaku Mimura, Shotaro Nakajima, Katsuharu Saito, Sohei Hayashishita, Chiaki Takiguchi, Azuma Nirei, Tomohiro Kikuchi, Hiroyuki Hanayama, Hirokazu Okayama, Motonobu Saito, Tomoyuki Momma, Zenichiro Saze and Koji Kono
Cells 2025, 14(15), 1212; https://doi.org/10.3390/cells14151212 - 6 Aug 2025
Viewed by 656
Abstract
Background: Anti-programmed death 1 receptor (PD-1) therapy is a promising treatment strategy for patients with unresectable advanced or recurrent gastric/gastroesophageal junction (G/GEJ) cancer. However, its response rate and survival benefits are still limited; an immunological analysis of the residual tumor after anti-PD-1 therapy [...] Read more.
Background: Anti-programmed death 1 receptor (PD-1) therapy is a promising treatment strategy for patients with unresectable advanced or recurrent gastric/gastroesophageal junction (G/GEJ) cancer. However, its response rate and survival benefits are still limited; an immunological analysis of the residual tumor after anti-PD-1 therapy would be important. Methods: We evaluated the clinical efficacy of tumor resection (TR) after chemotherapy or anti-PD-1 therapy in patients with unresectable advanced or recurrent G/GEJ cancer and analyzed the immune status of tumor microenvironment (TME) by immunohistochemistry using their surgically resected specimens. Results: Patients treated with TR after anti-PD-1 therapy had significantly longer survival compared to those treated with chemotherapy and anti-PD-1 therapy alone. Expression of human leukocyte antigen (HLA) class I and major histocompatibility complex (MHC) class II on tumor cells was markedly downregulated after anti-PD-1 therapy compared to chemotherapy. Furthermore, the downregulation of HLA class I may be associated with the activation of transforming growth factor-β signaling pathway in the TME. Conclusions: Immune escape from cytotoxic T lymphocytes may be induced in the TME in patients with unresectable advanced or recurrent G/GEJ cancer after anti-PD-1 therapy due to the downregulation of HLA class I and MHC class II expression on tumor cells. TR may be a promising treatment strategy for these patients when TR is feasible after anti-PD-1 therapy. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities)
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Review

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16 pages, 682 KB  
Review
Claudin18.2 as a Promising Therapeutic Target in Gastric Cancer
by Agata Poniewierska-Baran, Paulina Plewa, Zuzanna Żabicka and Andrzej Pawlik
Cells 2025, 14(16), 1285; https://doi.org/10.3390/cells14161285 - 19 Aug 2025
Cited by 1 | Viewed by 1367
Abstract
Claudin-18.2 (CLDN18.2) is an isoform of a tight junction protein and has emerged as a promising therapeutic target in gastric cancer (GC). CLDN18.2 is responsible for gastric homeostasis and protects epithelial cells from low pH conditions. Interestingly, CLDN18.2 expression is strictly restricted to [...] Read more.
Claudin-18.2 (CLDN18.2) is an isoform of a tight junction protein and has emerged as a promising therapeutic target in gastric cancer (GC). CLDN18.2 is responsible for gastric homeostasis and protects epithelial cells from low pH conditions. Interestingly, CLDN18.2 expression is strictly restricted to the stomach, making it an ideal tumor marker. This narrative review presents the characterization and role of claudin 18.2 (CLDN18.2) as a promising biomarker in GC and a target for clinical therapies, more specifically CLDN18.2-targeted drugs and therapies including mABs (e.g., Zolbetuximab, Osemitamab, ZL-1211), bsAB, and CAR-T cell-based immunotherapies. We also summarize numerous ongoing worldwide clinical trials that are evaluating CLDN18.2 as a target for GC treatment. What seems to be crucial is that preclinical and clinical data indicate their high efficacy and safety. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities)
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16 pages, 716 KB  
Review
Unconventional T Cells’ Role in Cancer: Unlocking Their Hidden Potential to Guide Tumor Immunity and Therapy
by Paola Pinco and Federica Facciotti
Cells 2025, 14(10), 720; https://doi.org/10.3390/cells14100720 - 15 May 2025
Cited by 1 | Viewed by 1513
Abstract
Unconventional T (UC T) cells, including invariant natural killer T (iNKT) cells, mucosal-associated invariant T (MAIT) cells, γδ T cells, and double-negative (DN) T cells, are key players in immune surveillance and response due to their properties combining innate-like and adaptive-like features. These [...] Read more.
Unconventional T (UC T) cells, including invariant natural killer T (iNKT) cells, mucosal-associated invariant T (MAIT) cells, γδ T cells, and double-negative (DN) T cells, are key players in immune surveillance and response due to their properties combining innate-like and adaptive-like features. These cells are widely present in mucosal tissues, where they can rapidly respond to infections and tumor-associated changes. In fact, UC T cells can have both pro- and anti-tumoral effects, with their activity influenced by factors such as microbial composition and the tumor microenvironment. In particular, intratumoral microbiota significantly impacts the development, function, and activation of UC T cells, influencing cytokine production and shaping the immune response in various cancers. The complex crosstalk between UC T cells and the surrounding factors is discussed in this review, with a focus on how these cells might be interesting candidates to explore and exploit as anticancer therapeutic agents. However, the great potential of UC T cells, not only demonstrated in the context of adoptive cell transfer, but also enhanced through techniques of engineering, is still flanked by different challenges, like the immunosuppressive tumor microenvironment and heterogeneity of target molecules associated with some specific categories of tumors, like gastrointestinal cancers. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities)
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30 pages, 1092 KB  
Review
B7H3 in Gastrointestinal Tumors: Role in Immune Modulation and Cancer Progression: A Review of the Literature
by Sylwia Mielcarska, Anna Kot, Agnieszka Kula, Miriam Dawidowicz, Piotr Sobków, Daria Kłaczka, Dariusz Waniczek and Elżbieta Świętochowska
Cells 2025, 14(7), 530; https://doi.org/10.3390/cells14070530 - 2 Apr 2025
Cited by 1 | Viewed by 2576
Abstract
B7-H3 (CD276), a member of the B7 immune checkpoint family, plays a critical role in modulating immune responses and has emerged as a promising target in cancer therapy. It is highly expressed in various malignancies, where it promotes tumor evasion from T cell [...] Read more.
B7-H3 (CD276), a member of the B7 immune checkpoint family, plays a critical role in modulating immune responses and has emerged as a promising target in cancer therapy. It is highly expressed in various malignancies, where it promotes tumor evasion from T cell surveillance and contributes to cancer progression, metastasis, and therapeutic resistance, showing a correlation with the poor prognosis of patients. Although its receptors were not fully identified, B7-H3 signaling involves key intracellular pathways, including JAK/STAT, NF-κB, PI3K/Akt, and MAPK, driving processes crucial for supporting tumor growth such as cell proliferation, invasion, and apoptosis inhibition. Beyond immune modulation, B7-H3 influences cancer cell metabolism, angiogenesis, and epithelial-to-mesenchymal transition, further exacerbating tumor aggressiveness. The development of B7-H3-targeting therapies, including monoclonal antibodies, antibody–drug conjugates, and CAR-T cells, offers promising avenues for treatment. This review provides an up-to-date summary of the B7H3 mechanisms of action, putative receptors, and ongoing clinical trials evaluating therapies targeting B7H3, focusing on the molecule’s role in gastrointestinal tumors. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities)
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