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After a transplant, cancer is a leading cause of morbidity and mortality. Human leukocyte antigen-G (HLA-G) — an immune checkpoint molecule — reduces allograft rejection by dampening host immune responses. Reports suggest malignant cells utilize HLA-G to evade the immune system and promote cancer development. The objective was to evaluate HLA-G donor-recipient polymorphism matching and development of cancer after a heart transplant.
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