Profiling of gene fusion involving targetable genes in Chinese gastric cancer

Figure 1 Flowchart of patient selection. GC: Gastric cancer.

Figure 2 Profile of targetable gene fusions in gastric cancer. A: The types and proportion of 24 gene fusions. Others included targetable ALK, RET, NTRK2, NRG1, and EGFR fusions. Four fusions without targetable genes were excluded from the analysis; B: Comparison of gene fusion frequencies in our cohort and the OrigiMed2020 and The Cancer Genome Atlas (TCGA) cohorts. No statistical differences were found among the cohorts.

Figure 3 Examples of novel gene fusions involving targetable genes in gastric cancer. A-D: Schematic representation and Integrative Genomics Viewer screenshot of FGFR2-PED2A (A), STIM-BRAF (B), OPALIN-RET (C), and NTRK2-ARHGAP10 (D) are shown; A and B: FGFR2 and BRAF fusions were confirmed by fluorescence in situ hybridization using FGFR2 (10q26) or BRAF (7q34) break-apart probes. Red spot: 5′ Probe signal; Green spot: 3′ probe signal; Yellow spot: Target gene without rearrangement. Arrows indicate the cells with separate 5′ (red) and 3′ (green) signals. Bar: 100 μm. TK: Tyrosine kinase domain.

Figure 4 Enrichment of gene fusions in patients with gastric cancer with driver alterations. A: The incidence of gene fusions in patients with and without driver alterations were analyzed, P > 0.05; B: The incidence of gene fusions in patients with and without ERBB2 amplifications were analyzed, P < 0.05; C: The incidence of gene fusions in patients with microsatellite instability-high and microsatellite stability were analyzed, P > 0.05; D: Tumor mutational burden in targetable gene fusion-positive and -negative patients was compared, P > 0.05.