
IndraLab
Statements
sparser
"Analysis of the mechanisms of cutaneous toxicities (notably, cuSCC) suggest that in BRAF wt cells, BRAF inhibitors cause formation of RAF dimers that lead to signaling through CRAF, particularly in those with an upstream mutation such as RAS . xref – xref Studies have shown frequent mutations in HRAS , and to a lesser extent NRAS , in benign and malignant (cuSCCs) proliferative lesions resected from patients on BRAF inhibitors, at higher rates than in lesions from patients not treated with inhibitors. xref – xref "
sparser
"The results of both groups support a model in which the BRAF-specific inhibitors induce RAS-GTP-dependent RAF1 activation via the formation of BRAF-RAF heterodimers or RAF1 homodimers followed by recruitment of RAF1 to the plasma membrane, triggering the MEK-ERK pathway ( xref ; xref )."