Advances in Cellular and Molecular Mechanisms in Immuno-Oncology and Onco-Hematology

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 1909

Special Issue Editor


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Guest Editor
Department of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia, 97, 95123 Catania, Italy
Interests: immunotherapy; oncology; neuroimmunology; autoimmunity; bioinformatics and computational biology
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Special Issue Information

Dear Colleagues,

Research on immune checkpoint inhibitors, such as PD-1/PD-L1 and CTLA-4 blockers, is expanding, revealing new combinations and biomarkers for enhanced efficacy. Understanding the mechanisms of tumor immune evasion is crucial, with studies focusing on the tumor microenvironment and immune escape pathways. Additionally, novel targeted therapies, including CAR T cell therapy—which reprograms immune cells to target cancer cells—are being developed to address specific altered molecular pathways in hematologic malignancies, offering more personalized and effective treatment options. These innovations are driving significant progress in cancer therapy.

We invite you to contribute your research and reviews to this Special Issue, which will serve as a comprehensive resource for researchers, clinicians, and practitioners dedicated to advancing cancer treatment in the rapidly growing fields of oncoimmunology and oncohematology.

Dr. Paolo Fagone
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer immunotherapy
  • inhibitory immune checkpoints
  • CAR T cells
  • tumor immune evasion
  • cancer target therapy

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Published Papers (3 papers)

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Research

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16 pages, 6698 KiB  
Article
Comprehensive Analysis of TSPAN32 Regulatory Networks and Their Role in Immune Cell Biology
by Grazia Scuderi, Katia Mangano, Maria Cristina Petralia, Maria Sofia Basile, Francesco Di Raimondo, Paolo Fagone and Ferdinando Nicoletti
Biomolecules 2025, 15(1), 107; https://doi.org/10.3390/biom15010107 - 11 Jan 2025
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Abstract
Tetraspanin 32 (TSPAN32), a member of the tetraspanin superfamily, is one of several tumor-suppressing subtransferable fragments located in the imprinted gene domain of chromosome 11p15.5, a critical tumor-suppressor gene region. Although the biology of TSPAN32 remains largely unexplored, accumulating evidence suggests its involvement [...] Read more.
Tetraspanin 32 (TSPAN32), a member of the tetraspanin superfamily, is one of several tumor-suppressing subtransferable fragments located in the imprinted gene domain of chromosome 11p15.5, a critical tumor-suppressor gene region. Although the biology of TSPAN32 remains largely unexplored, accumulating evidence suggests its involvement in hematopoietic functions. In this study, we performed a comprehensive analysis of the expression patterns and regulatory roles of TSPAN32. Notably, TSPAN32 is highly expressed in immune cells, particularly in natural killer (NK) cells and CD8+ T cells. The observed downregulation of TSPAN32 during immune cell activation highlights its potential role as a regulator of immune cell activation and metabolic adaptations, which are crucial for effective immune responses against pathogens and tumors. Moreover, the modulation of biological processes following TSPAN32 knockout further supports its critical role in regulating immune cell physiology and responses. These findings not only shed light on the biology of TSPAN32 but also provide the basis for exploring its diagnostic, prognostic, and therapeutic potential in autoimmune and inflammatory disorders, as well as in hematopoietic cancers. Full article
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21 pages, 4172 KiB  
Article
Early-Stage Luminal B-like Breast Cancer Exhibits a More Immunosuppressive Tumor Microenvironment than Luminal A-like Breast Cancer
by Tânia Moura, Olga Caramelo, Isabel Silva, Sandra Silva, Manuela Gonçalo, Maria Antónia Portilha, João N. Moreira, Ana M. Gil, Paula Laranjeira and Artur Paiva
Biomolecules 2025, 15(1), 78; https://doi.org/10.3390/biom15010078 - 7 Jan 2025
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Abstract
Background: Breast cancer is a heterogeneous malignant disease with a varying prognosis and is classified into four molecular subtypes. It remains one of the most prevalent cancers globally, with the tumor microenvironment playing a critical role in disease progression and patient outcomes. Methods: [...] Read more.
Background: Breast cancer is a heterogeneous malignant disease with a varying prognosis and is classified into four molecular subtypes. It remains one of the most prevalent cancers globally, with the tumor microenvironment playing a critical role in disease progression and patient outcomes. Methods: This study evaluated tumor samples from 40 female patients with luminal A and B breast cancer, utilizing flow cytometry to phenotypically characterize the immune cells and tumor cells present within the tumor tissue. Results: The luminal B-like tumor samples exhibited increased infiltration of CD4+ cells, regulatory T cells (Tregs), and Th17 cells and decreased levels of NK cells, γδ T cells, Th1 cells, and follicular T cells, which is indicative of a more immunosuppressive tumor microenvironment. Conclusions: These findings suggest that luminal B-like tumors have a microenvironment that is less supportive of effective anti-tumor immune responses compared to luminal A tumors. This study enhances the understanding of the immunological differences between luminal subtypes of breast cancer and identifies potential new therapeutic targets and biomarkers that could drive advancements in precision medicine for breast cancer management. Full article
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Review

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19 pages, 1548 KiB  
Review
Decoding the Nexus: Cellular and Molecular Mechanisms Linking Stroke and Neurotoxic Microenvironments in Brain Cancer Patients
by Spiro Menounos, Helen Shen, Shraddha Tipirneni and Sonu M. M. Bhaskar
Biomolecules 2024, 14(12), 1507; https://doi.org/10.3390/biom14121507 - 26 Nov 2024
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Abstract
Stroke is an often underrecognized albeit significant complication in patients with brain cancer, arising from the intricate interplay between cancer biology and cerebrovascular health. This review delves into the multifactorial pathophysiological framework linking brain cancer to elevated stroke risk, with particular emphasis on [...] Read more.
Stroke is an often underrecognized albeit significant complication in patients with brain cancer, arising from the intricate interplay between cancer biology and cerebrovascular health. This review delves into the multifactorial pathophysiological framework linking brain cancer to elevated stroke risk, with particular emphasis on the crucial role of the neurotoxic microenvironment (NTME). The NTME, characterized by oxidative stress, neuroinflammation, and blood–brain barrier (BBB) disruption, creates a milieu that promotes and sustains vascular and neuronal injury. Key pathogenic factors driving brain cancer-related stroke include cancer-related hypercoagulability, inflammatory and immunological mechanisms, and other tumor-associated processes, including direct tumor compression, infection-related sequelae, and treatment-related complications. Recent advances in genomic and proteomic profiling present promising opportunities for personalized medicine, enabling the identification of biomarkers—such as oncogenes and tumor suppressor genes—that predict stroke susceptibility and inform individualized therapeutic strategies. Targeting the NTME through antioxidants to alleviate oxidative stress, anti-inflammatory agents to mitigate neuroinflammation, and therapies aimed at reinforcing the BBB could pave the way for more effective stroke prevention and management strategies. This integrative approach holds the potential to reduce both the incidence and severity of stroke, ultimately improving clinical outcomes and quality of life for brain cancer patients. Further research and well-designed clinical trials are essential to validate these strategies and integrate them into routine clinical practice, thereby redefining the management of stroke risk in brain cancer patients. Full article
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