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Cells
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Decoding the Tumor-Immune Intersection: Opportunities for Breakthroughs in Cancer Therapies
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Decoding the Tumor-Immune Intersection: Opportunities for Breakthroughs in Cancer Therapies

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

Deadline for manuscript submissions: 30 August 2026 | Viewed by 5815

Special Issue Editor

Dr. Qiwei Wang

E-Mail Website
Guest Editor
School of Medicine, University of Virginia, Charlottesville, VA, USA
Interests: immuno-oncology; cancer biology; cancer immunology; immunometabolism

Special Issue Information

Dear Colleagues,

As eye-catching headlines about cancer immunotherapy continue to emerge, transforming the landscape of cancer treatment, many advanced cancers remain incurable. Recent studies emphasize the need to investigate tumors as ecosystems composed of diverse cell types and states, highlighting therapeutic opportunities at the intersections between cancer cells and the immune system. Not long ago, cancer biology and immunology were considered separate fields. However, groundbreaking evidence now shows that oncogenic and oncometabolic pathways have a significant impact on the immune system and influence the effectiveness of immunotherapy. Conversely, immune cells also modulate cancer cell signaling and tumor responses to chemotherapy and targeted therapies. Therefore, integrating therapies that target the interface between cancer and immune cells is likely to overcome the limitations of current treatments focused on either type alone. This Special Issue of Cells will highlight the fundamental mechanisms of tumor-immune interactions and feature therapeutic strategies that could harness these interactions to enhance current cancer therapies. It will include a collection of original research articles, reviews, and communications.

Dr. Qiwei Wang
Guest Editor

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 250 words) can be sent to the Editorial Office for assessment.

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

  • immuno-oncology
  • tumor-immune interface
  • tumor microenvironment
  • cancer immunotherapy
  • targeted therapy
  • immunometabolism
  • oncometabolism
  • epigenetics
  • combination strategies

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Published Papers (4 papers)

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Research

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27 pages, 20279 KB  
Article
Novel Taxol-Derivative, STO-1, Induces Selective Anti-Tumor Immunity and Sustained Remission of Glioblastoma Without Triggering Autoimmune Reactions
by Shubhasmita Mohapatra, Adrian Guerrero, Neha Rahman, Khondoker Takia Zaman, Jing Wu, Callistus Onyeagba, Chanyue Hu, Matteo Pellegrini, Jayaram Vankudoth, Seiya Kitamura, Lauren O’Donnell, Youssef Zaim Wadghiri and Probal Banerjee
Cells 2025, 14(21), 1703; https://doi.org/10.3390/cells14211703 - 30 Oct 2025
Cited by 2 | Viewed by 1848
Abstract
Reprogramming of macrophages into the inflammatory state (also known as M1) is currently considered as an effective way of eliminating cancer cells, but systemic deployment of this strategy is likely to induce dangerous autoimmune reactions. Consequently, converting immunosuppressive M2-type macrophages into M1 systemically [...] Read more.
Reprogramming of macrophages into the inflammatory state (also known as M1) is currently considered as an effective way of eliminating cancer cells, but systemic deployment of this strategy is likely to induce dangerous autoimmune reactions. Consequently, converting immunosuppressive M2-type macrophages into M1 systemically is not a safe and effective therapeutic approach against cancer. Through cleavable covalent linking of curcumin to the chemotherapeutic agent Paclitaxel (Taxol), we have created a novel prodrug (STO-1) that, upon intravenous delivery, selectively reprograms tumor-associated microglia and macrophages (TAMs) and eliminates glioblastoma (GBM) without triggering autoimmunity. Demonstrating its therapeutic efficacy, prolonged treatment of six orthotopic GBM-bearing mice with STO-1 resulted in 67% long-term survival, with three surviving mice exhibiting complete tumor clearance and one displaying minimal residual disease, as confirmed by high-resolution ex vivo T2-weighted MRI 85 days after tumor inoculation. In contrast, the vehicle-treated mice displayed extensive intracranial tumors with edema and hemorrhage. Mechanistically, scRNA-seq analysis indicated induction of multiple M1-associated transcripts (ccrl2, cxcl9, ccr2, ccl5) consistent with robust TAMs reprogramming. In striking contrast to the M2⟶M1 reprogramming of TAMs, M1-type macrophages were suppressed in the spleens of STO-1-treated cancer-free mice. Therefore, STO-1 induces selective anti-tumor immunity and GBM elimination without triggering systemic autoimmune reactions. Full article
(This article belongs to the Special Issue Decoding the Tumor-Immune Intersection: Opportunities for Breakthroughs in Cancer Therapies)
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Review

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27 pages, 1813 KB  
Review
Sweet Surprises: Decoding Tumor-Associated Glycosylation in Cancer Progression and Therapeutic Potential
by Eileena F. Giurini, Sam G. Pappas and Kajal H. Gupta
Cells 2026, 15(3), 233; https://doi.org/10.3390/cells15030233 - 26 Jan 2026
Viewed by 1151
Abstract
Tumor-associated glycosylation is a defining hallmark of cancer, exerting profound effects on multiple aspects of tumor biology. This phenomenon arises from the central role of glycosylation in a wide range of cellular processes and its inherently diverse structural complexity. In cancer cells, aberrant [...] Read more.
Tumor-associated glycosylation is a defining hallmark of cancer, exerting profound effects on multiple aspects of tumor biology. This phenomenon arises from the central role of glycosylation in a wide range of cellular processes and its inherently diverse structural complexity. In cancer cells, aberrant glycosylation often results in the modification of glycoconjugate structures, leading to alterations in cell surface architecture that disrupt cellular homeostasis and signaling pathways. These changes can enhance tumor cell proliferation, invasion, and metastasis by modulating cell adhesion, receptor activation, and intracellular communication. Beyond its direct impact on cancer cells, tumor-associated glycosylation plays a pivotal role in shaping the tumor microenvironment. Aberrant glycan structures influence immune cell infiltration by altering antigen presentation and immune checkpoint interactions, contributing to immune evasion. Additionally, these modifications regulate angiogenesis by affecting endothelial cell function and promoting the formation of aberrant vasculature, which supports tumor growth and metastasis. Glycosylation also mediates tumor–stroma interactions, influencing extracellular matrix remodeling and fibroblast activation, further enhancing cancer progression. This interplay between cancer-associated glycan modifications and their functional roles in tumorigenesis presents a promising therapeutic approach. Unlike conventional treatments, glycan-targeting therapies confer high tumor specificity, operate independently of canonical immune checkpoint targets, and help mitigate immune cell exhaustion. This review explores commonly dysregulated glycan motifs implicated in tumorigenesis and delves into their mechanistic contributions to cancer pathogenesis. We then highlight emerging opportunities for therapeutic intervention, including the development of glycan-targeted therapies and biomarker-driven strategies for cancer diagnosis and treatment. We also outline where glycan-targeted agents (e.g., desialylating biologics, glycomimetics, and anti-glycan mAbs) can complement checkpoint blockade and potentially overcome immune escape. Full article
(This article belongs to the Special Issue Decoding the Tumor-Immune Intersection: Opportunities for Breakthroughs in Cancer Therapies)
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34 pages, 1220 KB  
Review
Unraveling the Epigenetic Regulation of Regulatory T Cells in Cancer Immunity
by Kalpana Subedi, Nirmal Parajuli, Xzaviar Kaymar Solone, Jeffrey Cruz, Sahil Kapur, Deyu Fang, Qing-Sheng Mi and Li Zhou
Cells 2026, 15(3), 228; https://doi.org/10.3390/cells15030228 - 25 Jan 2026
Viewed by 1291
Abstract
Regulatory T cells (Tregs) are central mediators of immune tolerance, yet within tumors they adopt specialized phenotypes that confer the potent suppression of anti-tumor immune responses. Emerging evidence indicates that this functional plasticity is not driven by genetic alterations but instead arises from [...] Read more.
Regulatory T cells (Tregs) are central mediators of immune tolerance, yet within tumors they adopt specialized phenotypes that confer the potent suppression of anti-tumor immune responses. Emerging evidence indicates that this functional plasticity is not driven by genetic alterations but instead arises from dynamic and context-dependent epigenetic reprogramming. While individual epigenetic mechanisms controlling Treg development and stability have been described, how tumor-derived cues reshape Treg epigenetic states, how these programs differ across cancer types, and which features distinguish tumor-infiltrating Tregs from their peripheral counterparts remain incompletely understood. In this review, we synthesize recent advances in DNA methylation, histone modifications, chromatin accessibility, and non-coding RNA regulation that govern Treg identity and function with a particular emphasis on tumor-specific epigenetic adaptations. We highlight emerging epigenetic hallmarks of intratumoral Tregs, discuss unresolved mechanistic questions, and evaluate the therapeutic potential and limitations of targeting epigenetic pathways to selectively modulate Tregs in cancer. By integrating mechanistic, cancer-specific, and translational perspectives, this review aims to provide a conceptual framework for understanding how epigenetic regulation shapes Treg behavior in the tumor microenvironment and how it may be exploited for cancer immunotherapy. Full article
(This article belongs to the Special Issue Decoding the Tumor-Immune Intersection: Opportunities for Breakthroughs in Cancer Therapies)
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21 pages, 567 KB  
Review
If Plan A Does Not Work: The CD47 Ectodomain as a Target for Immune Tolerance
by Enrique Montero and Jeffrey S. Isenberg
Cells 2026, 15(1), 71; https://doi.org/10.3390/cells15010071 - 31 Dec 2025
Viewed by 927
Abstract
Cell surface immune checkpoint receptors are objects for therapeutic intervention to stimulate immune cell attack of cancers. Interference between the checking ectodomain (ECD) and the natural ligand lowers constitutive restraints exerted on immune cells. This approach assumes that immune cells can do more, [...] Read more.
Cell surface immune checkpoint receptors are objects for therapeutic intervention to stimulate immune cell attack of cancers. Interference between the checking ectodomain (ECD) and the natural ligand lowers constitutive restraints exerted on immune cells. This approach assumes that immune cells can do more, that a checkpoint blocker will make immune cells more effective at killing cancer cells, and that checkpoint molecules might have limited physiological roles. These assumptions may be warranted, as in the case of checkpoint-blockers towards the programmed death-ligand 1 (PD-L1) ECD, where clinical outcomes are consistently good. However, this does not appear to be the case for the universally expressed CD47 ECD. Much effort has been directed at engineering molecules that bind to the CD47 ECD to increase T cell and macrophage killing of cancers. But a wealth of clinical data do not indicate strong signals, improved killing, or meaningful survival advantages. This suggests that the CD47 ECD is a subpar target for cancer therapy. Consideration of reasons accounting for the modest benefits realized by molecules that bind to the CD47 ECD in cancer, also known as Plan A, is provided. This is followed by thoughts on what might be done, known as plan B, to identify advantages within the CD47 ECD for modulating tolerance in autoimmune diseases. Full article
(This article belongs to the Special Issue Decoding the Tumor-Immune Intersection: Opportunities for Breakthroughs in Cancer Therapies)
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