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Targeting NF-κB Signaling to Enhance Combination Cancer Therapies

Submission Deadline: 30 April 2026 View: 227 Submit to Special Issue

Guest Editors

Dr. Kamoru A. Adedokun

Email: kamoru.adedokun@roswellpark.org

Affiliation: Department of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, New York, 14263, United States

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Research Interests: cancer metastasis, immunotherapy, radioimmunotherapy

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Assist. Prof. Dr. Sheu K. Rahamon

Email: sk.rahamon@ui.edu.ng

Affiliation: Department of Immunology, College of Medicine, University of Ibadan, Ibadan, 200212, Nigeria

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Research Interests: psychoneuroimmunology, immunometabolism, tumor immunology

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Prof. Ibrahim Bello

Email: ibello@ksu.edu.sa

Affiliation: Department of Oral Medicine and Diagnostic Sciences, College of Dentistry, King Saud University, Riyadh, 11545, Saudi Arabia; Department of Pathology, Haartman Institute, University of Helsinki, Helsinki, 00014, Finland

Homepage:

Research Interests: oral pathology, head and neck cancer

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Summary

NF-κB is a master regulator of inflammation, immune response, and cell survival, with pivotal roles in cancer development, progression, and therapeutic resistance. Its complex crosstalk with the tumor microenvironment (TME) makes it both a challenge and an opportunity for therapeutic modulation. While classically activated through Toll-like receptors (TLRs), NF-κB is also downstream of diverse signaling axes including TNF receptors, IL-1R family members, STING, CD40, and other immune or stromal triggers—each with implications for therapy resistance, immune suppression, or activation.

 

This thematic collection will spotlight innovative strategies to modulate NF-κB signaling in combination with cancer treatments such as:

· Immune checkpoint inhibitors (ICIs), where NF-κB-driven cytokine reprogramming may influence T cell infiltration and myeloid cell phenotypes

· Chemotherapy or targeted agents, where blocking NF-κB may reverse resistance or sensitize cells to apoptosis

· Innate immune agonists (TLRs, STING, CD40, etc.) that activate or redirect NF-κB-mediated antitumor immunity

 

Submission topics include but not limited to:

· Mechanistic studies exploring NF-κB signaling in the context of combination therapies

· Use of NF-κB modulators (inhibitors or agonists) to enhance therapeutic efficacy

· Tumor-type or immune-cell-type-specific profiling of NF-κB activation patterns

· NF-κB as a predictive biomarker for response to immunotherapy

· Engineering of novel agonists (e.g., TLR ligands, CD40 antibodies, STING agonists) that interface with the NF-κB network

· Development of chemical probes and biosensors to monitor NF-κB activity in vivo

 

This collection aims to consolidate insights from chemical biology, immuno-oncology, and systems immunology, offering new paths to overcome resistance and achieve durable tumor regression through rationally designed combination therapies involving NF-κB pathway control.


Keywords

NF-κB signaling, toll-like receptors (TLRs), combination cancer therapy, tumor immunology, radiosensitizers and immunomodulators, innate immune activation, tumor microenvironment reprogramming

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