Recent advances in cancer research have underscored the critical role of myeloid cells in shaping tumor microenvironments (TME), influencing tumor progression, immune evasion, and therapeutic resistance. Myeloid cells, including tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), exhibit functional plasticity driven by interactions with tumor cells, stromal components, and metabolic adaptations. These cells not only directly promote tumor growth by enhancing angiogenesis, matrix remodeling, and metastasis but also suppress anti-tumor immunity through nutrient deprivation, oxidative stress, and cytokine-mediated inhibition of T and NK cells. Their dual roles—both pro-tumorigenic and occasionally anti-tumorigenic—highlight their complexity and context-dependent behavior across cancer types.

Researchers from The University of Osaka found that PM_2.5 air pollutants negatively affect mucociliary clearance, a protective mechanism of the respiratory tract. Air pollution led to the formation of lipid peroxide-derived aldehydes, known to damage protective cells in the airway and increase the risk of infections. ALDH1A1 was found to play an important role in protection against aldehydes, making it a potential therapeutic target to diminish the negative effects of air pollution.