Table 2.
Number of CpG sites by location in 14 candidate genes evaluated for differential methylation profiles in prostate cancer patients with recurrence versus no recurrence
| Candidate gene |
Total No. CpG sites evaluateda |
No. CpG sites evaluated in promoter regionb |
No. CpG sites evaluated in 5’ regionb |
No. CpG sites evaluated in gene body regionb |
|---|---|---|---|---|
| ABHD9 | 20 | 12 (7) | 11 (8) | 6 (1) |
| APC | 39 | 26 (0) | 22 (0) | 2 (0) |
| ASC | 19 | 12 (2) | 3 (0) | 4 (0) |
| CD44 | 32 | 5 (0) | 6 (0) | 21 (0) |
| CDH13 | 61 | 10 (0) | 4 (1) | 47 (0) |
| GPR7 | 13 | 10 (4) | 3 (1) | 0 |
| GSTP1 | 19 | 11 (0) | 2 (0) | 6 (0) |
| HOXD3 | 28 | 11 (9) | 10 (9) | 7 (1) |
| MDR1 | 31 | 7 (0) | 25 (3) | 11 (0) |
| PITX2 | 69 | 17 (1) | 13 (0) | 51 (0) |
| PTGS2 | 17 | 9 (3) | 2 (0) | 6 (0) |
| RARâ | 29 | 11 (0) | 11 (0) | 12 (0) |
| RASSF1A | 56 | 40 (0) | 30 (0) | 46 (0) |
| RUNX3 | 91 | 40 (0) | 5 (0) | 74 (0) |
The total number of CpG sites evaluated is greater than the sum of the CpG sites in each region for some genes because certain CpGs have multiple annotations due to alternative transcription start sites. The total number of CpG sites evaluated in each gene was used to determine statistical significance base on t-tests of differential methylation between patients with recurrence versus no recurrence, with Bonferroni correction for multiple testing within each gene.
Shown in parentheses is the number of CpG sites with significantly higher methylation (i.e., hypermethylated) in patients with prostate cancer recurrence compared to those with no evidence of recurrence.