Document resource
Despite the transformative impact of immune checkpoint inhibitors in oncology, hepatocellular carcinoma (HCC) remains stubbornly resistant in many patients, with durable responses to combination regimens such as atezolizumab plus bevacizumab occurring in a minority.1 2 Neutrophils, long regarded as short-lived bystanders in tumour biology, have emerged as functionally diverse and often pro-tumoural players, capable of suppressing T cell-mediated killing, promoting angiogenesis and fostering therapeutic resistance.3 4 In HCC specifically, the heterogeneity of tumour-associated neutrophils is increasingly recognised, with distinct subpopulations exhibiting pro-tumoural functions including promotion of angiogenesis and maintenance of an immunosuppressive microenvironment.5 Yet the molecular mechanisms by which the tumour microenvironment coerces neutrophils into these roles have remained unclear. The relationship between selenium status and HCC risk has been debated for decades, with epidemiological data consistently linking low circulating selenium to increased incidence.6 In Gut, Jiao et al make a compelling case that the missing link is not the tumour cell itself, but the immunosuppressive neutrophil niche that selenium deficiency creates.7