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Pharmaceuticals
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Tumor Immunopharmacology, 2nd Edition
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Tumor Immunopharmacology, 2nd Edition

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (27 April 2026) | Viewed by 3296

Special Issue Editors

Dr. Marco A. Velasco-Velázquez

E-Mail Website
Guest Editor
School of Medicine, Universidad Nacional Autónoma de Mexico (UNAM), Mexico City 04510, Mexico
Interests: pharmacology; cancer cell biology; experimental therapeutics
Special Issues, Collections and Topics in MDPI journals
Dr. Nohemí Salinas-Jazmín

E-Mail Website
Guest Editor
School of Medicine, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico
Interests: cancer; drug resistance; chemotherapy; immunotherapy; CSCs; biotherapeutics drugs

Special Issue Information

Dear Colleagues,

Modulation of the immune system has proven to be an effective way to reduce the progression of multiple tumors. Thus, the discovery of new immunotherapeutic agents is a rapidly growing field. At present, the arsenal of immunomodulators with potential clinical application includes multiple modalities of antibodies, small compounds, and peptides targeting immune signaling pathways, vaccines, and adoptive cell transfer.

This Special Issue will provide a comprehensive overview of the development of new immunotherapeutic agents for cancer treatment in the pre-clinical, translational, and clinical settings. We invite authors to submit original research or review articles that analyze the mechanism of action, efficacy, safety, and/or pharmacokinetics of immunotherapeutics in relevant models of neoplastic diseases.

Dr. Marco A. Velasco-Velázquez
Dr. Nohemí Salinas-Jazmín
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 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. Pharmaceuticals is an international peer-reviewed open access monthly 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

  • immunotherapy
  • immunomodulation
  • drug development
  • cytokine receptor antagonist
  • T-cell based therapies
  • therapeutic antibodies
  • drug delivery
  • cancer vaccine
  • immunoresistance
  • tumor-infiltrating lymphocytes (TILs)
  • immune escape
  • immune checkpoint inhibitors
  • cytokine-based therapies
  • small molecule immunomodulators
  • combination therapy
  • precision oncology
  • tumor mutational burden (TMB)
  • antibody-dependent cellular cytotoxicity (ADCC )
  • complement-dependent cytotoxicity (CDC)
  • myeloid-derived suppressor cells (MDSCs)

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Published Papers (3 papers)

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Research

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19 pages, 5675 KB  
Article
A Moderate-Affinity Antibody–Drug Conjugate Targeting B7-H3 Exerts Potent Antitumor Efficacy
by Ziyu Zhang, Huifang Zong, Zhen Li, Shusheng Wang, Xiaodong Xiao, Yueqing Xie and Jianwei Zhu
Pharmaceuticals 2026, 19(4), 596; https://doi.org/10.3390/ph19040596 - 8 Apr 2026
Viewed by 612
Abstract
Background: B7-H3, a type I transmembrane glycoprotein belonging to the B7 superfamily, is an attractive target for antitumor therapies. B7-H3 demonstrates aberrant overexpression in various types of solid tumors while showing limited and low expression in normal human organs. Various types of [...] Read more.
Background: B7-H3, a type I transmembrane glycoprotein belonging to the B7 superfamily, is an attractive target for antitumor therapies. B7-H3 demonstrates aberrant overexpression in various types of solid tumors while showing limited and low expression in normal human organs. Various types of treatment targeting B7-H3 have been reported. Among these treatments, antibody–drug conjugates (ADCs) have shown potent activity, and several clinical trials, including DS7300a and MGC018, are currently ongoing. Methods: Here, we constructed CD276-8 ADC, composed of the anti-B7-H3 antibody CD276-8 with moderate affinity, an enzymatically cleavable tetra-peptide-based linker and DXd. Characteristics, including in vitro binding affinity and internalization activity, were assessed by bio-layer interferometry (BLI), flow cytometry and high content analysis (HCA). The cytotoxicity of CD276-8 ADC was evaluated in cell lines expressing B7-H3. Pharmacokinetic profiles and antitumor activity were evaluated in mouse models in vivo. Finally, the developability of CD276-8 ADC was assessed with plasma stability, accelerated stability and freeze–thaw studies using LC-MS and HPLC. Results: Characterization in vitro demonstrated the moderate affinity and acceptable internalization activity of CD276-8 ADC. In addition, CD276-8 ADC exhibited potent antitumor activities in B7-H3-positive cell line-derived xenograft (CDX) models with acceptable pharmacokinetic profiles, although it showed less potent cytotoxicity in various cell lines in vitro, indicating acceptable developability. Conclusions: We developed CD276-8 ADC, a B7-H3-targeting ADC with moderate affinity, which delivers the TOP1 inhibitor DXd. This design combined moderate affinity and acceptable pharmacokinetics, resulting in potent antitumor efficacy in vivo. Our study suggests that affinity optimization could be a useful consideration for enhancing ADC efficacy, positioning CD276-8 ADC as a promising therapeutic for B7-H3-expressing solid tumors. Full article
(This article belongs to the Special Issue Tumor Immunopharmacology, 2nd Edition)
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Review

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31 pages, 6870 KB  
Review
Decoding the Role of MDSCs in Bone Metastasis: Multicellular Interactions and Clinical Implications
by Samaa Alotab, Mariam Zainab, Labibah Labib Khamies, Rasha Alissa and Khalid Said Mohammad
Pharmaceuticals 2026, 19(5), 723; https://doi.org/10.3390/ph19050723 - 2 May 2026
Viewed by 353
Abstract
Bone metastasis remains a major cause of morbidity in advanced cancer, driven not only by tumor–bone crosstalk but also by profound immune remodeling within the marrow. Myeloid-derived suppressor cells (MDSCs), including polymorphonuclear (PMN-MDSC) and monocytic (M-MDSC) subsets, are increasingly recognized as central effectors [...] Read more.
Bone metastasis remains a major cause of morbidity in advanced cancer, driven not only by tumor–bone crosstalk but also by profound immune remodeling within the marrow. Myeloid-derived suppressor cells (MDSCs), including polymorphonuclear (PMN-MDSC) and monocytic (M-MDSC) subsets, are increasingly recognized as central effectors of this process, integrating inflammatory signals with metabolic and stromal cues to enforce immune suppression and support skeletal colonization. In this review, we synthesize current evidence that bone metastases transform the bone marrow into an “MDSC amplifier,” where vascular and endosteal niches, CXCL12-rich stromal compartments, hypoxia, and adipocyte-derived lipids collectively promote MDSC recruitment, persistence, and functional maturation. We discuss the dominant suppressive programs deployed by MDSCs in bone (e.g., arginase-1 activity, reactive oxygen/nitrogen species, and checkpoint ligand expression), and how these mechanisms converge to impair cytotoxic T-cell and NK-cell responses while fostering regulatory T-cell dominance. Importantly, because the marrow is a hematopoietic organ, bone lesions can also generate systemic consequences through myeloid spillover, providing a mechanistic basis for reduced responsiveness to immune checkpoint blockade in bone-dominant disease. We then evaluate pharmacologic strategies to target MDSCs in the context of bone metastasis, including approaches that block trafficking (e.g., CCR2/CXCR2 axes), deplete or reprogram suppressive myeloid states (e.g., STAT3-directed strategies, differentiation therapy), and disrupt bone-resorptive feedback loops (e.g., receptor activator of NF-κB ligand (RANKL) inhibition and bisphosphonates), emphasizing rational combinations and sequencing to limit marrow toxicity. Finally, we highlight emerging single-cell and spatial profiling tools that can resolve bone-specific heterogeneity in MDSCs and guide biomarker-driven, mechanism-informed therapeutic development. Full article
(This article belongs to the Special Issue Tumor Immunopharmacology, 2nd Edition)
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35 pages, 4824 KB  
Review
Mechanisms of Resistance and Synergy: The Role of Tumor Microenvironment in HER2-Low Breast Cancer Therapy
by Youssef Basem, Alamer Ata, Abanoub Sherif, Shaimaa Abdel-Ghany, Borros Arneth and Hussein Sabit
Pharmaceuticals 2026, 19(4), 541; https://doi.org/10.3390/ph19040541 - 27 Mar 2026
Viewed by 1922
Abstract
HER2-low breast cancer, also known as IHC 1+ or IHC 2+ without ERBB2 amplification, is a new concept in the biology of breast cancer that has removed the binary classification of HER2-positive or HER2-negative breast cancer. The recent introduction of antibody-drug conjugates (ADCs), [...] Read more.
HER2-low breast cancer, also known as IHC 1+ or IHC 2+ without ERBB2 amplification, is a new concept in the biology of breast cancer that has removed the binary classification of HER2-positive or HER2-negative breast cancer. The recent introduction of antibody-drug conjugates (ADCs), such as trastuzumab deruxtecan (T-DXd), has improved therapeutic outcomes for HER2-low breast cancer by demonstrating high efficacy in HER2-low tumors through efficient payload delivery. However, differences in ADC efficacy exist among HER2-low breast cancer patients, with tumor cells showing resistance to ADCs. Recent research indicates that the tumor microenvironment (TME) plays a critical role in determining the efficacy of ADCs against tumor cells. TME creates a barrier to the delivery of ADCs to tumor cells that show resistance to ADCs. This review article aims to highlight the current understanding of the biology of HER2-low breast cancer and its response to ADCs with reference to the tumor microenvironment. Full article
(This article belongs to the Special Issue Tumor Immunopharmacology, 2nd Edition)
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