Abstract
Uveal melanoma is a rare neoplasm with an incidence of 5 cases per 1 million, with a risk of developing metastatic disease in 20-30% of patients within 5 years. Considering the low mutational load (TMB) the results of treatment with the use of checkpoint inhibitor immunotherapy are not as good as in cutaneous melanoma.
The essential molecule for the treatment of this diagnosis in the group of patients with HLA-A*02:01 is tebentafusp. It is a bispecific fusion protein that has a TCR receptor-like domain for binding to the gp100 antigen presented within the human leukocyte antigens (HLA) HLA-A*02:01 complex on the surface of a uveal melanoma tumor cell, and which also has an effector anti-CD3 part that binds and activates the circulating cytotoxic T lymphocyte inducing the release of cytokines and the subsequent death of the tumor cell.