Neutrophils, traditionally considered inert bystanders in cancer, are now recognized as dynamic cells with diverse roles in tumor initiation, progression, and metastasis. Recent studies have revealed that tumors can manipulate neutrophils to create different phenotypic and functional states, which can either oppose or potentiate cancer progression. Neutrophils are the most abundant immune cells and their production is regulated by factors such as granulocyte-colony stimulating factor (G-CSF). Tumor microenvironment signals, including cytokines and chemokines, can disrupt normal neutrophil homeostasis, leading to increased neutrophil numbers and altered functions. Neutrophils can promote tumor growth through angiogenesis, immunosuppression, and other mechanisms, but they can also hinder tumor progression by cytotoxic effects. The polarization of neutrophils into 'N1' or 'N2' states, based on nuclear morphology, is a simplified classification that may not fully capture the complexity of their activation states. Neutrophils play crucial roles in tumor initiation, growth, and metastasis, and their functions can be influenced by various factors such as CXCR2 ligands, G-CSF, and TGFβ. Clinical implications of neutrophil activity in cancer include their potential as biomarkers and therapeutic targets. Neutrophil-to-lymphocyte ratios (NLRs) are promising biomarkers, but their interpretation can be complex due to variability in neutrophil levels and the use of different cutoff points. Therapeutic strategies targeting neutrophils, such as CXCR2 antagonists and IL-17 inhibitors, show promise, but further research is needed to optimize their use. Combining neutrophil-targeting therapies with other anti-cancer treatments, such as chemotherapy and immunotherapy, may enhance their efficacy. Understanding the crosstalk between neutrophils and other immune cells is crucial for developing novel anti-cancer therapies.Neutrophils, traditionally considered inert bystanders in cancer, are now recognized as dynamic cells with diverse roles in tumor initiation, progression, and metastasis. Recent studies have revealed that tumors can manipulate neutrophils to create different phenotypic and functional states, which can either oppose or potentiate cancer progression. Neutrophils are the most abundant immune cells and their production is regulated by factors such as granulocyte-colony stimulating factor (G-CSF). Tumor microenvironment signals, including cytokines and chemokines, can disrupt normal neutrophil homeostasis, leading to increased neutrophil numbers and altered functions. Neutrophils can promote tumor growth through angiogenesis, immunosuppression, and other mechanisms, but they can also hinder tumor progression by cytotoxic effects. The polarization of neutrophils into 'N1' or 'N2' states, based on nuclear morphology, is a simplified classification that may not fully capture the complexity of their activation states. Neutrophils play crucial roles in tumor initiation, growth, and metastasis, and their functions can be influenced by various factors such as CXCR2 ligands, G-CSF, and TGFβ. Clinical implications of neutrophil activity in cancer include their potential as biomarkers and therapeutic targets. Neutrophil-to-lymphocyte ratios (NLRs) are promising biomarkers, but their interpretation can be complex due to variability in neutrophil levels and the use of different cutoff points. Therapeutic strategies targeting neutrophils, such as CXCR2 antagonists and IL-17 inhibitors, show promise, but further research is needed to optimize their use. Combining neutrophil-targeting therapies with other anti-cancer treatments, such as chemotherapy and immunotherapy, may enhance their efficacy. Understanding the crosstalk between neutrophils and other immune cells is crucial for developing novel anti-cancer therapies.