Figure 4
Figure 4. Specific LCH mutations have differential sensitivity to BRAF and MEK inhibitors. (A,B) HE293 cells transiently transfected with expression plasmids encoding various cDNAs (A) or c.302_307del MAP2K1 lesion biopsy cell suspension (B) were treated with BRAF or MEK inhibitor for 1 hour, and corresponding lysates were subjected to immunoblotting with the indicated antibodies. (C) Median fluorescent intensity (MFI) of p-ERK1/2 in CD207+ cells determined through IFC analyses in patients harboring BRAFV600E (patients LCH5, LCH7, and LCH13) and MAP2K1 c.302_307del (patient LCH24) mutations, and patients with no somatic mutations (LCH30, LCH32, LCH37, LCH38, and LCH40) posttreatment with BRAF or MEK inhibitor.

Specific LCH mutations have differential sensitivity to BRAF and MEK inhibitors. (A,B) HE293 cells transiently transfected with expression plasmids encoding various cDNAs (A) or c.302_307del MAP2K1 lesion biopsy cell suspension (B) were treated with BRAF or MEK inhibitor for 1 hour, and corresponding lysates were subjected to immunoblotting with the indicated antibodies. (C) Median fluorescent intensity (MFI) of p-ERK1/2 in CD207+ cells determined through IFC analyses in patients harboring BRAFV600E (patients LCH5, LCH7, and LCH13) and MAP2K1 c.302_307del (patient LCH24) mutations, and patients with no somatic mutations (LCH30, LCH32, LCH37, LCH38, and LCH40) posttreatment with BRAF or MEK inhibitor.

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