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Cancer Cell Death and Immune Response

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 25 December 2026 | Viewed by 990

Special Issue Editors


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Guest Editor
Department of Cell and Molecular Biology, University of Mississippi Medical Center, Jackson, MS 39216, USA
Interests: inflammation-cancer crosstalk; tumor immune microenvironment; epigenetics; cancer health disparities; cytokine signaling; immune checkpoint response in diverse populations

E-Mail Website
Guest Editor
Department of Cell and Molecular Biology, Cancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MI, USA
Interests: immunogenic cell death; tumor immunity; epigenetics, apoptosis, tumor microenvironment; biomarkers

Special Issue Information

Dear Colleagues,

Cancer cell death mechanisms are central to cancer progression and therapy. Regulated cell death, such as apoptosis, necroptosis, pyroptosis, ferroptosis, and immunogenic cell death (ICD), can activate or suppress antitumor immune responses and remodel the TME. This crosstalk influences therapeutic efficacy, resistance, and durability of response. Although major advances have been made, the dual roles of cell death in promoting both tumor regression and progression remain incompletely understood. By clarifying these mechanisms, we can design strategies that favor immunogenic outcomes and strengthen durable cancer immunotherapies. This Special Issue focuses on the molecular and immunological mechanisms of cancer cell death and their impact on antitumor immunity, therapeutic resistance, and the development of immunotherapy. We aim to highlight both fundamental insights and translational advances that connect cell death pathways to immune activation, biomarkers, and clinical application. The topic aligns with the journal scope by advancing an integrated understanding of tumor-immune interactions and mechanism-based treatment design.

Suggested themes and article types include, but are not limited to:

  • Mechanistic studies of apoptosis, necroptosis, pyroptosis, ferroptosis, and ICD in cancer
  • Impact of cell death pathways on immune cell recruitment, activation, and function
  • TME factors that modulate death-immunity crosstalk
  • Genetic, epigenetic, metabolic, and stress-response regulators of cancer cell death and immunity
  • Therapeutic strategies that target or leverage death pathways, including antibodies, cytokines, and oncolytic approaches
  • Combination strategies to induce ICD and overcome primary or acquired resistance
  • Biomarkers and pharmacodynamic readouts of cell death and immune activation
  • Translational and preclinical studies that advance mechanism-based therapies and clinical trial concepts

Researchers and clinicians are invited to submit original research and review articles that address cellular and immunological dynamics of cancer cell death, translational models, biomarkers, and therapeutic innovations, including rational combinations designed to enhance antitumor immunity.

We look forward to receiving your contributions.

Prof. Dr. Seema Singh
Dr. Amod Sharma
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 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. Cancers 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 2900 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

  • immunogenic cell death
  • tumor immunity
  • epigenetics
  • apoptosis
  • tumor microenvironment
  • biomarkers

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Published Papers (1 paper)

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Review

33 pages, 1983 KB  
Review
Danger or Salvation? The Role of DAMPs in Cancer Therapy
by Anna A. Vedunova, Evgenii L. Guryev, Sergey V. Gudkov, Tatiana A. Mishchenko and Maria V. Vedunova
Cancers 2026, 18(9), 1442; https://doi.org/10.3390/cancers18091442 - 30 Apr 2026
Viewed by 664
Abstract
Background: Modern oncology views immune system dysfunction as a key factor in carcinogenesis. The induction of immunogenic cell death (ICD), a form of regulated cell death capable of activating adaptive immunity, represents a promising therapeutic strategy. Damage-associated molecular patterns (DAMPs) play a central [...] Read more.
Background: Modern oncology views immune system dysfunction as a key factor in carcinogenesis. The induction of immunogenic cell death (ICD), a form of regulated cell death capable of activating adaptive immunity, represents a promising therapeutic strategy. Damage-associated molecular patterns (DAMPs) play a central role in this process. This review aims to summarize current knowledge of DAMPs, their release mechanisms during ICD, their classification, and their prognostic and therapeutic significance in antitumor immunity. Methods: We systematically reviewed and synthesized literature published in Pubmed and Google Scholar on ICD and DAMPs, focusing on distinct forms of DAMPs which were categorized based on recognition mechanisms (five classes) and cellular origin (extracellular, mitochondrial, nuclear, and cytosolic). Key molecules, their receptors, downstream signaling pathways, and clinical associations were analyzed. Results: The spatiotemporally coordinated release of the pattern of DAMPs promotes dendritic cell maturation, antigen presentation, activation of cytotoxic T lymphocytes, and elimination of tumor cells. DAMPs can exhibit a dual role: they are able to induce sterile inflammation essential for antitumor immunity, but may also contribute to metastasis and chronic inflammation. Among all DAMPs, high-mobility group box 1 (HMGB1, a nuclear DAMP) and calreticulin (CRT, a cytosolic protein) demonstrate the greatest prognostic value. Other DAMPs (e.g., extracellular matrix components, uric acid) act as signal amplifiers during various forms of cell death. Conclusions: Understanding the spatiotemporal dynamics of DAMP release is critical for activating immune responses against malignant cells. Monitoring DAMPs may improve patient stratification, predict therapeutic responses, and enable personalized immunotherapeutic strategies. Further investigation of ICD mechanisms and DAMP release represents a fundamental basis for developing novel anticancer therapies. Full article
(This article belongs to the Special Issue Cancer Cell Death and Immune Response)
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