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Autophagy and Apoptosis in Cancer Progression

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

Deadline for manuscript submissions: 30 June 2026 | Viewed by 1435

Special Issue Editor


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Guest Editor
Anatomic Pathology Unit, Department of Human Pathology in Adult and Developmental Age "Gaetano Barresi", University of Messina, 98125 Messina, Italy
Interests: autophagy; molecular biology; pathology; cancer

Special Issue Information

Dear Colleagues,

Autophagy and apoptosis are key cellular programs that shape tumor initiation, progression, and therapeutic response. While several reviews have discussed their canonical interactions, substantial gaps remain regarding how these pathways integrate within specific tumor ecosystems, evolve under selective pressures, and generate clinically relevant phenotypes. In contrast to previous literature, which has largely emphasized general mechanistic crosstalk, this Special Issue highlights tumor-type specificity, spatial and metabolic constraints, and therapy-induced remodeling of autophagy–apoptosis dynamics, integrating molecular pathology with advanced multi-omics technologies. Particular attention will be dedicated to how these pathways govern intratumoral heterogeneity, immune microenvironmental adaptation, stress-driven dedifferentiation, and resistance to targeted agents, immunotherapies, and conventional treatments. Moreover, this Special Issue aims to provide updated frameworks for biomarker development by incorporating digital pathology, single-cell profiling, and functional readouts that capture cell-death plasticity more accurately than traditional models. By unifying mechanistic, diagnostic, and translational perspectives, the Special Issue will not revisit established concepts but will instead define emerging vulnerabilities and therapeutic opportunities arising from context-dependent regulation of autophagy and apoptosis. Ultimately, it seeks to advance the understanding of how these pathways influence cancer behavior within real tumor architectures and clinical scenarios, with the goal of improving precision oncology strategies.

Dr. Antonio Ieni
Guest Editor

Manuscript Submission Information

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Keywords

  • autophagy
  • apoptosis
  • cancer progression
  • cell death pathways
  • therapeutic resistance

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Published Papers (1 paper)

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Review

15 pages, 1216 KB  
Review
Autophagy Modulates Immunogenic Cell Death in Cancer
by Maiko Matsushita and Miyu Moriwaki
Cancers 2026, 18(2), 205; https://doi.org/10.3390/cancers18020205 - 8 Jan 2026
Cited by 2 | Viewed by 1178
Abstract
Immunogenic cell death (ICD) is a subtype of regulated cell death characterized by the spatiotemporally coordinated emission of damage-associated molecular patterns (DAMPs), such as calreticulin (CALR), ATP, and high-mobility group box-1 (HMGB1), which collectively prime tumor-specific T-cell responses. Autophagy, a lysosome-dependent catabolic process, [...] Read more.
Immunogenic cell death (ICD) is a subtype of regulated cell death characterized by the spatiotemporally coordinated emission of damage-associated molecular patterns (DAMPs), such as calreticulin (CALR), ATP, and high-mobility group box-1 (HMGB1), which collectively prime tumor-specific T-cell responses. Autophagy, a lysosome-dependent catabolic process, is increasingly recognized as a key modifier of antitumor immunity and the tumor microenvironment (TME). In preclinical models, autophagy can not only promote ICD by sustaining endoplasmic reticulum (ER) stress, eukaryotic translation initiation factor-2α (eIF2α) phosphorylation, and secretory pathways, but it can also limit ICD by degrading DAMPs, antigenic cargo, and major histocompatibility complex (MHC) molecules. The net outcome is highly context-dependent and determined by the tumor type, the nature and intensity of the stress, and the level at which autophagy is modulated. Herein, we summarize how autophagy affects the three canonical ICD-associated DAMPs, highlight solid-tumor models in which autophagy supports ICD, and contrast them with systems wherein autophagy inhibition is required for immunogenicity. We then focus on hematological malignancies, especially multiple myeloma, where recent reports implicate the autophagy-related protein GABARAP in bortezomib-induced ICD. Finally, we discuss the translational implications, including rational combinations of autophagy modulators with ICD-inducing chemotherapies, targeted drugs, and cellular immunotherapies, and outline the remaining challenges for safely harnessing the autophagy–ICD axis in the clinical setting. Full article
(This article belongs to the Special Issue Autophagy and Apoptosis in Cancer Progression)
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