B lymphocytes exhibit dual roles in tumorigenesis, acting as both allies and adversaries in the tumor microenvironment (TME). Their anti-tumor functions include recognizing tumor-associated antigens, producing antibodies, activating cytotoxic immune responses, and forming tertiary lymphoid structures (TLS) that enhance immune cell coordination. Tumor-infiltrating B cells (TIL-Bs) within TLS contribute to improved patient survival and immunotherapy responses by facilitating antibody class switching, somatic hypermutation, and cytokine secretion that recruit and activate T cells, natural killer (NK) cells, and dendritic cells (DCs). Antibodies from B cells mediate complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and antibody-dependent cell-mediated cytotoxicity (ADCC), directly eliminating tumor cells. Additionally, B cells present antigens to T cells and secrete cytokines like IFN-γ and CXCL13, amplifying anti-tumor immunity. However, regulatory B cells (Bregs) and other subsets suppress immune responses by secreting IL-10, TGF-β, and VEGF, promoting angiogenesis, recruiting immunosuppressive cells like myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs), and expressing immune checkpoints like PD-L1. This duality underscores the complexity of targeting B cells in cancer therapy.

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.