Neutrophils, traditionally seen as inert immune cells, play a complex role in cancer. Recent research shows they can be manipulated by tumors to adopt diverse functional states that influence tumor behavior. Neutrophils can either oppose or promote cancer progression, depending on signals from the tumor microenvironment. They are involved in cancer initiation, progression, and metastasis, and can act as biomarkers or therapeutic targets. Neutrophils originate in the bone marrow and are released into the bloodstream through complex signaling involving chemokines and receptors. Tumors can increase neutrophil production by upregulating cytokines like G-CSF, leading to elevated neutrophil numbers. Neutrophils can be polarized into different states (N1/N2) based on tumor-derived factors, with N1 being pro-tumorigenic and N2 being anti-tumorigenic. Neutrophils contribute to tumor growth by promoting angiogenesis, immunosuppression, and metastasis. They also play a role in tumor metastasis by facilitating cancer cell escape, intravasation, and survival in circulation. Neutrophils can be both pro- and anti-metastatic, depending on the tumor context. Neutrophils are important in cancer progression and can be targeted therapeutically, either by inhibiting their trafficking or by modulating their polarization. Neutrophil-targeting strategies, such as CXCR2 antagonists, may enhance the efficacy of anti-cancer therapies like chemotherapy and radiotherapy. Neutrophils also interact with other immune cells, influencing tumor immune responses. Neutrophil biomarkers, such as neutrophil-to-lymphocyte ratio (NLR), are being explored for cancer risk stratification and treatment decisions. Neutrophils have dual roles in cancer, and their functions can be context-dependent, making them a promising area for further research and therapeutic development.Neutrophils, traditionally seen as inert immune cells, play a complex role in cancer. Recent research shows they can be manipulated by tumors to adopt diverse functional states that influence tumor behavior. Neutrophils can either oppose or promote cancer progression, depending on signals from the tumor microenvironment. They are involved in cancer initiation, progression, and metastasis, and can act as biomarkers or therapeutic targets. Neutrophils originate in the bone marrow and are released into the bloodstream through complex signaling involving chemokines and receptors. Tumors can increase neutrophil production by upregulating cytokines like G-CSF, leading to elevated neutrophil numbers. Neutrophils can be polarized into different states (N1/N2) based on tumor-derived factors, with N1 being pro-tumorigenic and N2 being anti-tumorigenic. Neutrophils contribute to tumor growth by promoting angiogenesis, immunosuppression, and metastasis. They also play a role in tumor metastasis by facilitating cancer cell escape, intravasation, and survival in circulation. Neutrophils can be both pro- and anti-metastatic, depending on the tumor context. Neutrophils are important in cancer progression and can be targeted therapeutically, either by inhibiting their trafficking or by modulating their polarization. Neutrophil-targeting strategies, such as CXCR2 antagonists, may enhance the efficacy of anti-cancer therapies like chemotherapy and radiotherapy. Neutrophils also interact with other immune cells, influencing tumor immune responses. Neutrophil biomarkers, such as neutrophil-to-lymphocyte ratio (NLR), are being explored for cancer risk stratification and treatment decisions. Neutrophils have dual roles in cancer, and their functions can be context-dependent, making them a promising area for further research and therapeutic development.