Precision Immuno-Oncology Across Organ Systems: Cytokine–lncRNA Networks Linking Chronic Inflammation, Neurodegeneration, and Cancer

Saleem Iqbal; Jing Chen; Debnath Pal; Bairong Shen

doi:10.1016/j.eng.2026.05.009

Engineering ›› :202605009 DOI: 10.1016/j.eng.2026.05.009

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Precision Immuno-Oncology Across Organ Systems: Cytokine–lncRNA Networks Linking Chronic Inflammation, Neurodegeneration, and Cancer

Saleem Iqbal ^a^,^b^,^c^,^*
, Jing Chen ^d
, Debnath Pal ^c
, Bairong Shen ^a^,^*

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Abstract

Psoriasis, atopic dermatitis (AtD), and Alzheimer’s disease (AD) are chronic inflammatory disorders traditionally examined within isolated organ systems, but are increasingly recognized as manifestations of a shared immunometabolic architecture with direct relevance to cancer biology. Synthesizing multi-omics with transcriptomic and clinical evidence, this review delineated the conserved cytokine-driven networks linking cutaneous, neural, and oncologic inflammation. Core inflammatory loops centered on interleukin (IL)-1b, tumor necrosis factor-a (TNF-a), IL-6, IL-17A/F, and IL-23 were found to converge on Janus kinase (JAK)–signal transducer and activator of transcription (STAT), nuclear factor jB (NF-jB), and mitogen-activated protein kinase (MAPK) signaling across keratinocytes-, microglia-, and tumor-associated immune cells. Transcription factors (peroxisome proliferator activated receptor c (PPARG), zinc finger protein, FOG family member 2 (ZFPM2), zinc finger protein 415 (ZNF415), H2.0 like homeobox (HLX), and anomalous homeobox (ANHX)) and long non-coding RNAs (metastasis associated lung adenocarcinoma transcript 1 (MALAT1), nuclear enriched abundant transcript 1 (NEAT1), psoriasis susceptibility-related induced by stress (PRANS), and b-site APP cleaving enzyme 1 antisense transcript (BACE1-AS)) were found to form feed-forward regulatory circuits that sustained immune activation across tissues. Comparative immunogenomic analyses revealed overlapping inflammatory states among lesional skin, the Alzheimer’s brain, and tumor microenvironments, supporting a unified inflammatory continuum. Biologic agents and JAK inhibitors, originally developed for dermatologic diseases, were observed to provide mechanistic and therapeutic entry points for modulating neuroinflammation and tumor-promoting immune niches. These findings demonstrate that integrative systems biology and artificial intelligence (AI)-driven multimodal modeling frameworks enable immune-state stratification beyond organ boundaries, offering a precision-guided paradigm for cross-disease immunomodulation in neurodegeneration and cancer.

Keywords

Neuroendocrine–immune interaction / Cytokine networks / Systems immunology / Long non-coding RNAs / JAK–STAT signaling / Artificial intelligence / Precision neuroinflammation

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Saleem Iqbal, Jing Chen, Debnath Pal, Bairong Shen. Precision Immuno-Oncology Across Organ Systems: Cytokine–lncRNA Networks Linking Chronic Inflammation, Neurodegeneration, and Cancer. Engineering 202605009 DOI:10.1016/j.eng.2026.05.009

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