Table 3. Canonical pathways predicted to be significantly altered in both cohorts in B vs. A group samples.
The first three data columns refer to our cohort, and the last three to the Jorissen cohort.
| Ingenuity Canonical Pathways | log(p-value) | Down | Up | log(p-value) (Jorissen) | Down (Jorissen) | Up (Jorissen) |
|---|---|---|---|---|---|---|
| Role of BRCA1 in DNA Damage Response | 10.6 | 0/60 (0%) | 46/60 (77%) | 1.85 | 12/61 (20%) | 17/61 (28%) |
| Protein Ubiquitination Pathway | 9.27 | 20/249 (8%) | 126/249 (51%) | 6.54 | 21/251 (8%) | 101/251 (40%) |
| Cell Cycle: G2/M DNA Damage Checkpoint Regulation | 8.48 | 1/48 (2%) | 32/48 (67%) | 1.79 | 7/49 (14%) | 17/49 (35%) |
| Hereditary Breast Cancer Signaling | 7.29 | 7/111 (6%) | 61/111 (55%) | 1.68 | 16/112 (14%) | 32/112 (29%) |
| Cell Cycle: G1/S Checkpoint Regulation | 4.86 | 7/63 (11%) | 32/63 (51%) | 1.38 | 12/63 (19%) | 16/63 (25%) |
| Regulation of eIF4 and p70S6K Signaling | 4.54 | 10/141 (7%) | 72/141 (51%) | 1.42 | 13/140 (9%) | 44/140 (31%) |
| Cyclins and Cell Cycle Regulation | 4.46 | 10/77 (13%) | 36/77 (47%) | 1.31 | 11/77 (14%) | 22/77 (29%) |
| DNA damage-induced 14-3-3“€ Signaling | 3.47 | 3/19 (16%) | 11/19 (58%) | 1.63 | 2/19 (11%) | 9/19 (47%) |
| Gluconeogenesis I | 2.83 | 2/24 (8%) | 12/24 (50%) | 1.33 | 2/23 (9%) | 10/23 (43%) |
| mTOR Signaling | 2.19 | 16/178 (9%) | 73/178 (41%) | 1.42 | 21/181 (12%) | 51/181 (28%) |
| Polyamine Regulation in Colon Cancer | 2.12 | 1/22 (5%) | 12/22 (55%) | 1.68 | 0/21 (0%) | 12/21 (57%) |
| dTMP De Novo Biosynthesis | 1.86 | 0/5 (0%) | 4/5 (80%) | 1.35 | 0/5 (0%) | 4/5 (80%) |
| Androgen Signaling | 1.44 | 11/109 (10%) | 42/109 (39%) | 1.84 | 13/110 (12%) | 35/110 (32%) |
| Calcium Transport I | 1.37 | 3/9 (33%) | 2/9 (22%) | 1.38 | 2/9 (22%) | 4/9 (44%) |
| Endoplasmic Reticulum Stress Pathway | 1.34 | 0/21 (0%) | 12/21 (57%) | 1.68 | 2/21 (10%) | 10/21 (48%) |