Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

Neutrophils are abundant innate immune cells with remarkable plasticity, capable of exerting both antitumour and protumour functions. Beyond their local roles in the tumour microenvironment, recent studies highlight tumour-induced granulopoiesis as a systemic process by which cancers rewire haematopoiesis to expand immature neutrophils with immunosuppressive and tumour-promoting activity. Sustained by tumour-derived cytokines, chemokines and alarmins, tumour-induced granulopoiesis activates developmental programmes such as STAT3-C/EBPβ and RORC1, driving persistent neutrophilia and systemic immune suppression. Here, we review neutrophil maturation and heterogeneity, their dual roles in tumour initiation and progression, and the emerging recognition of tumour-induced granulopoiesis as a critical axis of tumour-host interaction with clinical and therapeutic implications.