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Biological insights into BRAFV600 mutations in melanoma patient

Not mere therapeutic targets

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Article: e25594 | Received 25 Jun 2013, Accepted 28 Jun 2013, Published online: 03 Jul 2013

Figures & data

Figure 1. Vemurafenib increases interferon γ-induced MHC expression on melanoma cells harboring a masked heterozygous BRAFV600 mutation. (A) MHC expression levels are higher in wild-type melanoma cells that in cells bearing a BRAFV600 mutation. (B) Mutant BRAFV600 suppresses the expression of MHC molecules on the cell surface. (C) The administration of BRAF inhibitors (BRAFis) promotes the interferon γ (IFNγ)-induced expression of MHC molecules by melanoma cells that harbor a “masked” heterozygous BRAFV600 mutation in the context of BRAF amplification or loss-of-heterozygosity (LOH). ERK, extracellular signal-regulated kinase; MEK, MAPK/ERK kinase; TCR, T-cell receptor.

Figure 1. Vemurafenib increases interferon γ-induced MHC expression on melanoma cells harboring a masked heterozygous BRAFV600 mutation. (A) MHC expression levels are higher in wild-type melanoma cells that in cells bearing a BRAFV600 mutation. (B) Mutant BRAFV600 suppresses the expression of MHC molecules on the cell surface. (C) The administration of BRAF inhibitors (BRAFis) promotes the interferon γ (IFNγ)-induced expression of MHC molecules by melanoma cells that harbor a “masked” heterozygous BRAFV600 mutation in the context of BRAF amplification or loss-of-heterozygosity (LOH). ERK, extracellular signal-regulated kinase; MEK, MAPK/ERK kinase; TCR, T-cell receptor.