Stathmin 1 across neuroendocrine neoplasms: biological, pathological and translational insights

Stathmin 1 (STMN1) is a cytosolic phosphoprotein involved in microtubule dynamics, mitotic progression and cytoskeleton-dependent cellular behaviour. In multiple human malignancies, dysregulated STMN1 expression has been associated with aggressive clinicopathological features, adverse outcomes and, in selected settings, potential therapeutic vulnerability. Its significance in neuroendocrine neoplasms (NENs), however, has not been critically synthesised across anatomical sites. This narrative review examined the available literature on STMN1 in NENs across pulmonary, gastroenteropancreatic, adrenal, cutaneous, pituitary and thyroid settings, with the specific aim of mapping site-specific expression patterns and appraising whether reported associations with aggressive clinicopathological features were descriptive, independently validated, or functionally supported. A literature search was conducted in PubMed, Web of Science, and Scopus from inception to 25 January 2026. Twelve original studies met the inclusion criteria and were narratively synthesised. The available evidence indicates that STMN1 is not a uniform marker of neuroendocrine differentiation across tumour types, but rather a context-dependent signal more often associated with proliferative activity, high-grade morphology and malignant behaviour. The strongest evidence currently derives from pulmonary neuroendocrine neoplasms, where STMN1 has shown diagnostic utility in tissue and bronchoalveolar lavage and where preclinical targeting data are available. Outside the lung, however, the literature is limited and methodologically heterogeneous, and the evidentiary weight varies from descriptive expression studies to functional preclinical observations. Overall, STMN1 emerges as a recurrent molecular signal in several NEN settings, particularly in aggressive and high-grade disease contexts. Its causal biological relevance and clinical value, including potential implications for treatment sensitivity and tumour dissemination, remain to be demonstrated in studies specifically designed for prognostic and therapeutic validation. Current therapeutic evidence remains preclinical and should be regarded as hypothesis-generating rather than clinically actionable.