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 at the University of Michigan Rogel Cancer Center identified a gene that plays a key role in prostate cancer cells that have transitioned to a more aggressive, treatment-resistant form. The gene can be indirectly targeted with an existing class of drugs, suggesting a potential treatment strategy for patients with aggressive subtypes of prostate cancer.