• Aberrant glycosylation in tumors modulates immune evasion by altering interactions with endogenous lectins, immune checkpoints, and the extracellular matrix.
• Sialic acid-siglec interactions and galectin signaling are key mechanisms that suppress antitumor immunity, promoting Tregs and T-cell exhaustion.
• Glycosylation affects immune checkpoint stability and binding affinity, influencing the efficacy of checkpoint blockade therapies.
• Glycan-based cancer immunotherapies, including targeting glycosylation pathways, represent promising strategies to enhance current immunotherapies.