Myeloid cells, including TAMs and MDSCs, play crucial roles in the tumor microenvironment, influencing cancer progression and therapeutic resistance through their plasticity and diverse functions.
TAMs and MDSCs are derived from monocytes and bone marrow progenitors, with contributions from extramedullary hematopoiesis driven by tumor-secreted factors.
Metabolic reprogramming is essential for myeloid cell functions in the TME, with TAMs utilizing glycolysis, lactate production, and lipid accumulation to modulate immune responses.
MDSCs impair T cell function through amino acid metabolism, while relying on glutamine and FAO pathways for energy and survival.
Therapeutic approaches target myeloid cell recruitment, survival, and metabolic dependencies to mitigate their pro-tumoral effects.
Advancements in single-cell transcriptomics reveal myeloid heterogeneity, with subsets exhibiting distinct roles and responses to therapy based on tumor type and microenvironment.
Interactions between myeloid cells and other immune/stromal constituents shape complex ecosystems that influence tumor fate and therapeutic responses.
Reprogramming myeloid function through metabolic interventions and drug repurposing offers promising avenues to enhance anti-tumor immunity.
Precision immunomodulation targeting myeloid subsets can transform the therapeutic landscape by reversing immune suppression and improving T cell efficacy.
Understanding myeloid cell biology in oncology paves the way for personalized immunotherapy, emphasizing their pivotal role in fighting cancer.