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Fig. 2 | Molecular Cancer

Fig. 2

From: Mutation of neurotrophic tyrosine receptor kinase can promote pan-cancer immunity and the efficacy of immunotherapy

Fig. 2

The characteristics of tumor immune microenvironment in patients with NTRK-mutant and NTRK -non-mutant cancer. (A) Comparison of TMB, non-silent mutation rate, and silent mutation rate between NTRK-mutant and NTRK-non-mutant tumors. (B) Expression of three major immune checkpoints in patients with NTRK-mutant and NTRK-non-mutant tumors. (C) The immune cell infiltration revealed by leukocyte fractions, lymphocytes fraction and tumor-infiltrating lymphocyte fraction in NTRK-mutant and NTRK-non-mutant tumors. (D) The abundances of SNV /Indel neoantigens and the diversity of TCR/BCR in NTRK-mutant and NTRK-non-mutant tumors. (E) Differences of 29 immune signatures estimated by ssGSEA between NTRK-mutant and NTRK-non-mutant tumors. (F) Comparison of 9 immune and 2 stromal cell populations between NTRK-mutant and NTRK-non-mutant tumors. (G) Expression differences of 16 MHC-related antigen-presenting molecules and 25 co-stimulators between NTRK-mutant and NTRK-non-mutant tumors. (H) Comparison of 48 chemokines and their receptors between NTRK-mutant and NTRK-non-mutant tumors. (I) Expression differences of 39 immune-stimulators between NTRK-mutant and NTRK-non-mutant tumors. BCR, B cell receptor; CTLA-4, cytotoxic T-lymphocyte-associated antigen 4; MHC, major histocompatibility complex; PD-1, programmed cell death protein 1; PD-L1, programmed cell death ligand 1; SNV, single nucleotide variants; TCR, T cell receptor; TIL, tumor-infiltrating lymphocyte; TMB, tumor mutation burden

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