Figure 1. Immunological mechanisms underlying the antineoplastic effects of low-dose aspirin. By inactivating cyclooxygenase 1 (COX1) in platelets and/or tumor cells, the conversion of arachidonic acid into thromboxane A₂ (TXA₂) and prostaglandin D₂ (PGD₂) is reduced, leading to a decrease in the number of immature immune cells—including immature dendritic cells (iDCs), myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs)—that infiltrate neoplastic lesions, as well as in the expression of immunosuppressive mediators, such as transforming growth factor β (TGFβ). Ultimately, such immunomodulatory effects limit tumor growth, suggesting that low-dose aspirin might be successfully employed in combinatorial regimens to improve the therapeutic efficacy of immunotherapy.