A New Frontier of Hope: Highlighting the Promising Potential of Spliceosome Inhibitor E7107 in Treating SF3B1 Mutant Uveal Melanoma

Doi: 10.36351/pjo.v41i1.1996

Abstract

Dear editor

This letter highlights the promising nature of spliceosome inhibitor E7107 in SF3B1 mutant uveal melanoma and warrants future research to establish its clinical application, safety, and efficacy for these patients.

Uveal melanoma originates from the melanocyte of the uvea and has a metastasis rate of about 25-34% within a span of ten years leading to poor prognosis and a death rate of 80% at 1 year following metastasis.¹ This shows the horrible nature of these melanomas and demand for an inevitable urge of definitive treatment options for these patients. However, unfortunately, the treatment options are very limited and poor. Various prognostic factors have been identified for uveal melanoma including mutations in genes encoding BRCA-1 associated protein (BAP1) being worst, splicing factor 3b subunit 1 (SF3B1) being intermediate, and eukaryotic translation initiating factor 1A X-linked (EIF1AX) being best prognostic factor.^2,3A large percentage of about 15%-35% of uveal melanomas have SF3B1 mutations which make it an important prognostic feature however there is no well-established pharmacological agent targeting or utilizing this major prognostic mutation as a therapeutic fortune. A recently introduced protein Tebetafusp though showed prolonged survival in metastatic carcinoma but available only for metastatic uveal melanoma