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Schematic overview of differential activity of BRAFi/MEKi in BRAF V600E HCL versus RAS mutant pre-malignant lymphoid cells. (A) At steady state, mutant BRAF signals RTK/RAS independently and thereby drives tumor growth of HCL. (B) Upon BRAF and MEK inhibition, the activity of the MAPK pathway is strongly compromised in the HCL context, however, leading to paradoxical activation of the MAPK pathway in the BRAF wildtype, RAS mutant lymphoid clone. RTK, receptor tyrosine kinase.
