Figure 4 Molecular signalling and immunological

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Figure 4 Molecular signalling and immunological interactions relevant to the clinical treatment of melanoma Figure 4 | Molecular signalling and immunological interactions relevant to the clinical treatment of melanoma. a | Schematic summary of the key molecular signalling pathways related to melanoma tumorigenesis. Advanced-stage melanoma can be categorized according to mutational profiles. These include mutations in either the BRAF, RAS, or NF1 genes in approximately 50%, 20%, and 15% of patients, respectively, and rarer mutations in KIT, GNAQ, or GNA11. Generally, these mutations result in activation of ERK signalling, and most melanomas are, therefore, broadly amendable to therapeutic inhibition at the levels of BRAF, MEK, or KIT. b | Summary of immune interactions in the tumour microenvironment of melanoma. Following priming by activated dendritic cells (DCs), antigen-specific T cells can migrate to melanoma tumours. In response to cytokines, particularly of IFNγ, T-cell-inflamed tumours upregulate immune-inhibitory molecules, such as programmed cell-death 1 ligand 1 (PD-L1). Binding of PD-L1 to programmed cell-death protein 1 (PD-1) on T cells at the invasive margins of melanomas can suppresses their antitumour activity. Upon the application of anti-PD1 antibody, however, these T cells are released from inhibition leading to tumour infiltration and antitumour activity. Mechanisms of resistance to anti-PD1 immunotherapy have been described to involve loss of IFNγ signalling via JAK mutations, loss of antigen presentation owing to mutations in β2 microglobulin (a component of the major histocompatibility complex class I (MHC I)), and activation of β-catenin signalling (leading to loss of DC recruitment and T-cell priming). BATF3, basic leucine zipper transcriptional factor ATF-like 3; CCL4, C–C chemokine 4; CCR5, C–C-chemokine receptor 5; TCR, T-cell receptor. Luke, J. J. et al. (2017) Targeted agents and immunotherapies: optimizing outcomes in melanoma Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2017.43