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Neutrophils, the most abundant white blood cells in the immune system, play a crucial role in breast cancer progression through their ability to polarize into two distinct phenotypes: N1 and N2. N1 neutrophils are considered antitumor effector cells that promote immune responses and inhibit tumour growth, while N2 neutrophils support tumour progression by promoting inflammation, immune suppression, and metastasis. The balance between these two phenotypes within the tumour microenvironment (TME) can significantly influence breast cancer development and response to treatment. The polarization of neutrophils in the TME is influenced by various factors, including cytokines, growth factors, and interactions with other immune cells. N1 neutrophils exhibit pro-inflammatory and cytotoxic properties that help limit tumour growth, while N2 neutrophils contribute to an immunosuppressive microenvironment that facilitates cancer progression and therapy resistance. Studies suggest that an increased presence of N1 neutrophils correlates with improved prognosis and response to therapies, whereas a predominance of N2 neutrophils is often associated with poor treatment outcomes and increased metastatic potential. This review examines the mechanisms underlying neutrophil polarization and the implications of these phenotypes on treatment responses in breast cancer.
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Obeagu et al. (2025) studied this question.
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