Topic: Cellular Inflammation and Immune Evasion as Drivers of Cancer Drug Resistance

While the significance of inflammation in cancer development/progression has been long appreciated, the classic paradigm of inflammation-cancer association typically casts immune cells as protagonists, relegating cancer cells to the role of passive recipients of extrinsic inflammatory effects.

However, emerging evidence reveals a more complex reality: classical inflammatory signaling hubs such as TNF-α/NF-κB and IL-6/ JAK/STAT signaling are usually constitutively and aberrantly activated within tumor cells, and even in precancerous lesions, and these cells autonomously secrete robust profiles of inflammatory cytokines, acting as the primary architects of their niche, utilizing these intrinsic networks to simultaneously entrench their own malignant traits and actively orchestrate the reciprocal reprogramming of the TME, intrinsically exhibiting inflammatory phenotypes analogous to “professional” immune cells. Such a pathological state of cancer cells characterized by full-spectrum inflammatory mimicry and functional locking, driven by intrinsic or extrinsic factors, is recently proposed as the "tumor cell inflammation" theory. Interestingly, chronic cellular inflammation and immune evasion can become drivers of therapeutic resistance of cancer.

Inflammatory signaling within tumor cells reshapes the TME, facilitates immune suppression, and impairs responses to therapies. Understanding how inflammation-associated pathways interact with tumor evolution and immune escape may reveal novel therapeutic vulnerabilities for overcoming resistance.

Topics of interest include, but are not limited to:

● General Mechanisms underlying Tumor Cell Inflammation;

● Mechanistic Insights into Cancer Drug Resistance Driven by Tumor Cell Inflammation;

● Immune Escape and Therapy Resistance;

● Biomarkers and Early Detection for Therapy Resistance;

● Therapeutic Strategies to Overcome Inflammation- and Immune-Mediated Resistance;

● Other Subtopics Relevant to Cellular Inflammation.

Tumor cell inflammation, inflammatory signaling (NF-κB/JAK-STAT), tumor microenvironment reprogramming, immune evasion and therapy resistance, inflammation-driven biomarkers and targeted therapy strategies