Fig 1: Fluorescence-activated cell sorting analysis. (A) Autofluorescence of HCT116 cells at 530nm (FL1). (B) Fluorescence of HCT116 cells after incubation with FITC-CaIX-P1. (C) Autofluorescence of HCT116 cells at 590nm (FL2). (D) Fluorescence of HCT116 cells after incubation with rhodamine-labeled anti-CAIX-mAb.
Fig 2: Fluorescence microscopy of FITC-labeled CaIX-P1. Images were performed from two different regions after incubation of HCT116 cells with FITC-CaIX-P1.
Fig 3: Fluorescence-activated cell sorting analysis. (A) Autofluorescence of HT29 cells at 530nm (FL1). (B) Fluorescence of HT29 cells after incubation with FITC-CaIX-P1. (C) Autofluorescence of HT29 cells at 590nm (FL2). (D) Fluorescence of HT29 cells after incubation with rhodamine-labeled anti-CAIX-mAb.
Fig 4: Relationships between CA9 expression and CLDN18-ARHGAP26 fusion status evaluated by immunohistochemistryYounger age patients (under 60 years) (A), and older age patients (older than 60 years) (B) were evaluated separately. Fusion-positive DGC cases showed significantly higher CA9 expression than fusion-negative cases, only in the younger age group (P = 0.042). Numbers under each plot indicate the sample sizes of each group.
Fig 5: Correlation of CAIX, HIF-1a, GLUT1, and VEGF expression with breast cancer recurrence. A, Human breast tumors samples were stained with CAIX, GLUT1, HIF-1a and VEGF antibodies using immunohistochemistry. Magnification × 100, Scale bars: 100 µm. B, Kaplan-Meier plot showed a correlation between HIF-1a, CAIX, GLUT1, and VEGF and breast cancer recurrence for patients treated with tamoxifen
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