Role of Inflammatory Cytokines Interleukin-1β and Interleukin-6 in Carcinogenesis, with Particular Emphasis on Gastroenteropancreatic Neuroendocrine Neoplasms.

Inflammation is a hallmark of cancer and contributes to tumour initiation, progression, and therapeutic resistance. Among inflammatory mediators, interleukin-1β (IL-1β) and interleukin-6 (IL-6) are central cytokines linking innate immune responses with oncogenic signalling networks. This narrative review summarizes current experimental and clinical evidence regarding the role of IL-1β and IL-6 in carcinogenesis, with particular emphasis on gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs). We discuss the molecular pathways associated with these cytokines, their interactions within the tumour microenvironment, and their contribution to tumour proliferation, angiogenesis, immune modulation, metastatic dissemination, and resistance to anticancer therapies. Particular attention is given to GEP-NENs, in which chronic inflammation and cytokine dysregulation may influence tumour behaviour, systemic inflammatory activity, and clinical outcomes. Accumulating evidence suggests that IL-6 may represent a promising exploratory biomarker associated with tumour burden, histological grade, disease progression, and systemic inflammation, whereas IL-1β appears to be more closely linked to local inflammatory signalling, microenvironmental remodelling, and potential susceptibility mechanisms. However, current evidence in GEP-NENs remains limited by small study cohorts, heterogeneous patient populations, variable analytical methodologies, and the lack of prospective validation. Further translational and clinical investigations are warranted to determine whether cytokine-based biomarkers and therapeutic modulation of inflammatory pathways may expand current diagnostic, prognostic, and therapeutic approaches in GEP-NENs.