Fig. 2

PTTG1 is over-expressed in MM patients. In silico analysis was performed on publically available gene expression datasets from CD138⁺ plasma cells isolated by MACS from MM (n = 73) and MGUS (n = 22) patients and healthy controls (n = 15) (E-GEOD-6477) (a), MM (n = 155) and MGUS (n = 5) patients and healthy controls (n = 5) (E-MTAB-363) (b) and MM (n = 133) and MGUS (n = 11) patients and healthy controls (n = 5) (E-GEOD-16122) (c). Box and whiskers plots show the median and interquartile ranges for each cohort. *p < 0.05; **** p < 0.0001; Kruskal-Wallis test with Dunn’s multiple comparison tests. d Representative image of a BM trephine section from an MM patient stained with anti-CD138 (red) and anti-PTTG1 (green), showing plasma cell-specific protein expression of PTTG1. A negative (no primary antibody) control is shown. e Kaplan-Meier plot of PTTG1 high patients (quartile 4; n = 71) vs PTTG1 low patients (quartiles 1–3; n = 214) (TT2 patients from GSE4581). f MM patients from GSE4581 (n = 414) were stratified into subgroups based on the UAMS criteria; namely, patients characterised by increased proliferation-related genes (PR), chromosomal translocations involving cyclin D1 and cyclin D3 (CD1 and CD2), MAF (MF) or MMSET (MS), as well as patients exhibiting hyperdiploidy (HY) and decreased prevalence of lytic bone disease (LB) [4]. The expression of PTTG1 was analysed in each subset. Box and whiskers plots show the median and interquartile ranges for each cohort; ^p < 0.0001 relative to CD1, CD2, MF, MS, HY and LB; #p < 0.01 relative to CD2, MF, MS, LB; Kruskal-Wallis test with Dunn’s multiple comparison tests