Fig 1: Correlation analysis based on soluble PVR (sPVR) and TIGIT levels in bone marrow plasma from patients with MM. (A) sPVR levels from patients without cancer (n = 3), patients with MGUS, (n = 4), and patients with MM (n = 22). * p < 0.05, ns, not significant; Kruskal–Wallis test. (B) Relationship between sPVR and soluble TIGIT (n = 22). No significant correlations were observed. Positive correlation between sPVR and PVR expression in bone marrow plasma cells as measured by (C) ELISA, (D) IHC, and (E) qPCR (n = 22). Positive correlation between soluble TIGIT and TIGIT expression in bone marrow (F) CD8+ T cells and (G) NK cells (n = 14) measured by FCM. Pearson’s or Spearman’s correlation coefficients (r) were used for analyses. Black ball, raw data; red line, linear fit line; dotted line, 95% confidence band. BM, bone marrow; ELISA, enzyme-linked immunosorbent assay; FCM, flow cytometry; IHC, immunohistochemistry; MGUS, monoclonal gammopathy of undetermined significance; MM, multiple myeloma; PVR, poliovirus receptor; qPCR, quantitative polymerase chain reaction; TIGIT, T cell immunoreceptor with Ig and ITIM domains.
Fig 2: Kaplan–Meier survival curves for OS and PFS according to PVR expression. (A,B) OS and PFS curves for all patients. The median OS was 24 months in the high PVR-expression group and 68 months in the low PVR-expression group (n = 125). The median PFS was 15 and 29 months in the high and low PVR-expression groups, respectively (n = 114). (C,D) OS and PFS curves for the subgroups of patients (n = 50) who received IMiD therapy. The median OS (33 vs. 68 months) and PFS (23 vs. 35 months) showed no significant differences between low and high PVR-expression groups. (E,F) OS (n = 75) and PFS (n = 64) curves for the subgroups of patients who did not receive IMiD therapy. The median OS (24 vs. 54 months) and PFS (8 vs. 24 months) were significantly shorter in the low PVR-expression group relative to the high PVR-expression group. IMiD, immunomodulatory drug; OS, overall survival; PFS, progression-free survival; PVR, poliovirus receptor; TIGIT, T cell immunoreceptor with Ig and ITIM domains.
Fig 3: Assessment of PVR and TIGIT expression in relation to clinical factors in patients with MM. (A) Distribution of PVR expression (H-score) in bone marrow plasma cells in all patients. (B) Representative histogram of TIGIT expression in CD8+ T cells and NK cells. Comparison of PVR expression based on (C) R-ISS, presence of (D) bone lesion, and (E) EMP. * p < 0.05, ** p < 0.01; Kruskal–Wallis and Mann–Whitney U tests. Comparison of clinical factors based on PVR- and TIGIT-expression status. (F) Percentage of bone marrow plasma cells and (G) concentration of ß2-microglobulin in the negative (H-score: 0) and positive (H-score: > 0) PVR-expression groups (n = 125). Error bars indicate the mean ± standard error of the mean. ** p < 0.01, *** p < 0.001; unpaired t-test. (H) Percentage of bone marrow plasma cells in the low (TIGIT-expression groups (n = 14). * p < 0.05; Mann–Whitney U test. BM, bone marrow; EMP, extramedullary plasmacytoma; H-score, histoscore; MM, multiple myeloma; NK, natural killer; PVR, poliovirus receptor; R-ISS, Revised International Staging System; TIGIT, T cell immunoreceptor with Ig and ITIM domains.
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