Article Figures & Data
Figures
- Figure 1.
Functional Interaction Network from analysis of genes upregulated in prostate tumors from AAM or EAM. The network derived from Ingenuity Pathways analysis shows a high degree of inherent, functional interrelatedness for a subset of factors from the analyzed gene expression datasets (AAM blue, EAM yellow). Results suggest that AAM and EAM prostate tumors are distinguished at gene level with NFKB and inflammatory cytokine factors primarily upregulated in PCa from AAM; EAM-upregulated genes are centered on TNF. Edges (lines) linking members of both sets to P38MAPK, TNF, and PI3K/AKT genes suggests that the associated pathways are operating to some extent in both EAM and AAM contexts.
- Figure 2.
Boxplots of the log base 2 expression levels for genes mapped to the functional interaction network. The genes identified in the functional interaction network in Fig. 1 were stratified by race and the individual genes measured by the DASL assay identified as the PI3K complex genes are named. The stars at the bottom of the graph indicate statistically significant differences between races. As TNF is a central hub in the network, it is included in the graph even though it is not statistically significant.
- Figure 3.
Plot of the first 2 principal components, computed from all 517 genes on 639 tumor samples (270 AAM, 369 EAM) and 165 control samples (82 AAM, 83 EAM). Although all of the control samples had a matching tumor sample and thus are expected to be highly correlated with the respective tumor sample, the samples clustered by tumor/control status, regardless of race. This implies that the expression profile of the tumor samples is similar across races and different than the profile of the control samples, which are also similar across races.
Tables
- Table 1.
Descriptive statistics of the samples under study
Variable AAM (n = 270) EAM (n = 369) P-value Age 62.76 (6.35) 61.74 (6.82) 0.054 Variable Levels AAM (n = 270) EAM (n = 369) P-value Gleason's grade 0.177 ≤6 92 (0.34) 139 (0.38) 7 (3 + 4) 77 (0.29) 122 (0.33) 7 (4 + 3) 60 (0.22) 61 (0.17) ≥8 41 (0.15) 47 (0.13) Gleason's grade categorized 0.030 Nonaggressive 169 (0.63) 261 (0.71) Aggressive 101 (0.37) 108 (0.29) NOTE: Age is described as mean and SD, whereas the Gleason's grade variables are presented as number of observations and percentage. The P-values in the table are a result of a test of the difference between races using a t-test for age and a χ2 test for the Gleason's grade variables.
- Table 2.
Mean expression ratio of EAM as compared to AAM for the functionally linked genes from the network in Fig. 1
Gene Mean EAM relative to AAM expression P-value ADIPOQ 1.12 0.002 AKT1 0.94 0.026 ALOX12 1.09 0.003 ALOX15 1.24 <0.001 ALOX15B 0.88 0.022 BMP2 0.91 0.030 CGA 1.12 0.001 CXCR4 0.87 <0.001 CYP19A1 1.06 0.029 ERG 1.62 <0.001 FASN 0.90 0.009 IL1B 0.89 0.001 IL6 0.78 <0.001 IL8 0.84 <0.001 NFKB1 0.96 0.048 PIK3C3 1.05 0.033 PIK3CA 1.08 0.004 PIK3R1 1.07 0.018 PLA2G2A 1.16 <0.001 TGFB1 0.91 <0.001 TIMP3 1.07 0.017 TNF 0.97 0.445 NOTE: The t test P-value testing the difference in expression between races is included in the table. Individual genes measured on the assay that were associated with the PI3K complex are named in the table.
Supplementary Data
Files in this Data Supplement:
- Supplementary Tables 1 - 2, Figure 1 - PDF file - 114K, Suppl Table 1 - List of the 517 genes whose expression was measured by DASL microarray analysis of RNA from FFPE specimens. Supplemental Table 2. Mean difference and t-test p-value between the computed DDCt from EAM minus the computed DDCt from AAM from the validation sample of 16 AAM and 16 EAM. Supplemental Figure 1. Plot of the first 2 principal components, computed from all 517 genes on 163 patient tumor samples (80 AAM, 83 EAM) with the corresponding matched normal samples.
Volume 22, Issue 5
