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. 2017 Dec 12;1(5):429–445. doi: 10.1042/ETLS20170142

Figure 4. The immunogenic conversion.

Figure 4.

Immune-silent breast cancer characterized by low TIL density or low expression of genes included in the immunologic constant of rejection (ICR Low) frequently displays dysregulation of MAPK pathways, either caused by genomic alterations (in purple) [i.e. MAP2K4 or MAP3K1 mutations in luminal breast cancer; Hendrickx et al. [31]] and MAPK-activating alterations (e.g. amplifications in KRAS, BRAF, and RAF1, and truncations in NF1) in basal-like tumors (Loi et al. [42]), or by alternative mechanisms. To convert these tumors into an immune-active phenotype characterized by high expression of ICR genes (ICR High) and then trigger tumor rejection, combination therapy consisting of MEK inhibition (MEKi), immune checkpoint inhibition (e.g. PD1 blockade; Dushyanthen et al. [115]), and perhaps other checkpoint inhibitions and immune agonist antibodies (Dushyanthen et al. [115]) is suggested. We refer to this as the ‘immunogenic conversion’.