Epigenetic and epitranscriptomic regulation of immune dysfunction in cancer and chronic inflammatory disease

The regulation of immune responses by epigenetic and epitranscriptomic mechanisms plays a fundamental role in cancer and chronic inflammatory diseases. Recent evidence shows that immune cell fate, functional plasticity, and tissue-specific immune suppression are critically shaped by modifications such as DNA methylation, chromatin remodeling, histone modifications, and RNA marks like N6-methyladenosine (m6A). Within the tumor microenvironment or chronic inflammatory lesions, these processes affect both malignant and non-malignant cells, dictating phenomena such as tumor immune evasion, resistance or sensitivity to immunotherapies, formation of immunosuppressive niches, and the persistence of pathological inflammation. Yet, there remain significant gaps in linking specific chromatin and RNA modification pathways to immune dysfunction, disease progression, and patient response to therapy.This Research Topic aims to advance our understanding of how epigenetic and epitranscriptomic regulation drives immune escape and dysfunction in the contexts of cancer and chronic inflammatory disorders. We seek research and review articles that detail how regulatory pathways—such as chromatin state transitions affecting T cell exhaustion, m6A RNA modification in tumor-infiltrating myeloid cells, epigenetic control of cytokine signaling, and tumor microenvironment remodeling—impact disease progression and clinical outcomes. Special priority will be given to work that connects these mechanisms with therapeutic strategies, identifies actionable biomarkers for immunotherapy response, or uncovers resistance pathways amenable to intervention. The Topic encourages submissions supported by patient-derived models, clinically annotated data, and studies with translational potential, as well as state-of-the-art analytical approaches relevant to disease setting.The scope is limited to disease-specific studies in cancer and chronic inflammatory disorders. Manuscripts focused primarily on general innate immunity, broad inflammation models without a defined disease context, or animal models lacking translational orientation will not be considered. To explore this focused landscape, we welcome articles addressing, but not limited to, the following themes:o Mechanistic interrogation of tumor immune evasion via chromatin remodeling or RNA modification pathwayso Disease-relevant roles of m6A and other RNA methylation marks in shaping immune responseso Chromatin state and immune exhaustion in tumor-infiltrating lymphocyteso Epigenetic reprogramming of myeloid cells and its impact on the tumor microenvironmento Functional genomics of immune–stromal cross-talk in the cancer milieuo Discovery and validation of epigenetic biomarkers for immunotherapy stratification and prognosiso RNA and chromatin-based pathways underlying resistance to checkpoint blockade and other immune therapieso Preclinical and clinical studies exploring therapeutic modulation of epigenetic and epitranscriptomic regulators in cancer or longstanding inflammationo Interaction of epigenetic programs with immunometabolism and chronic inflammatory signalsWe encourage comprehensive reviews, translational perspectives, and technology innovations if tightly linked to the disease-relevant immune dysregulation or therapeutic application in cancer and chronic inflammatory disease. Topic editors: Munish Kumar, Girish C Shukla, Sivakumar Vijayaraghavalu Source: https://www.frontiersin.org/research-topics/81350/epigenetic-and-epitranscriptomic-regulation-of-immune-dysfunction-in-cancer-and-chronic-inflammatory-disease