Somatic mutations in eIF1A, especially in the N-terminal tail (NTT), were recently found to be associated with uveal, thyroid and ovarian cancers. Presently very little is known about the biological function of eIF1A in mammalian cells and how perturbations of its function by the mutations contribute to cancer development. We seek to develop pharmacological tools to selectively interfere with the scanning promoting activity of eIF1A, as a novel personalized therapeutic approach against uveal and thyroid cancers bearing the aforementioned gain-of-function mutations in eIF1A.
Grant type:
Grant scientist:
Rivka Dikstein
Grant year:
2018