ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Interleukin-1α (IL-1α) in pancreatic ductal adenocarcinoma: implications for immunotherapy and molecular biomarkers.
Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with a 5-year survival rate of only 12%, driven by late diagnosis, rapid metastasis, and an immunosuppressive tumor microenvironment (TME). Current therapies, including chemotherapy and immune checkpoint blockade, show limited efficacy due to the "cold" TME. Interleukin-1α (IL-1α) plays a central role in PDAC progression. TCGA (n = 178) and ICGC (n = 267) analyses reveal that high IL1A expression independently predicts poor overall survival (HR = 1.99, 95% CI 1.01-3.93) and progression-free survival (HR = 3.11, 95% CI 1.24-7.80). As a biomarker, IL-1α outperforms traditional CA19-9 for risk stratification and treatment selection. Its detection in serum and exosomes supports potential applications in liquid biopsy for early detection. Therapeutically, IL-1α blockers using agents such as anakinra, canakinumab, and nadunolimab show synergy with immune checkpoint inhibitors and chemotherapy. This combination has been evaluated in preclinical models and early-phase clinical trials. It achieves disease control rates of up to 62% and median progression-free survival of up to 6.8 months, while also reducing fibrosis and enhancing antitumor immunity. This review synthesizes the critical role of interleukin-1α (IL-1α) in PDAC pathogenesis and its potential implications for immunotherapy and molecular biomarker development. IL-1α is highly expressed in PDAC tumor cells and tumor-associated macrophages (TAMs). It activates the NF-κB and MAPK pathways, thereby promoting epithelial-mesenchymal transition (EMT), stromal fibrosis, and immunosuppression. This includes the recruitment of neutrophils and myeloid-derived suppressor cells (MDSCs), which collectively maintain an immunosuppressive ('cold') tumor microenvironment (TME) and contribute to therapeutic resistance. Future multi-omics stratification, targeted delivery systems, and rational combination strategies hold promise for improving PDAC outcomes.
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