Table 2.
Significant pathways associated with genes that are sites of HPV integration and mutated in cervical cancer.
| Significantly Enriched Pathway | Proteins from Network | False Discovery Rate | Nodes |
|---|---|---|---|
| EGFR tyrosine kinase inhibitor resistance | 7 | 1.01 × 10−7 | PTEN, ERBB3, ERBB2, MAPK1, NRG1, PIK3CA, KRAS |
| Human T-cell leukemia virus 1 infection | 9 | 1.01 × 10−7 | PTEN, MAPK1, EP300, HLA-B, HLA-A, TGFBR2, PIK3CA, KRAS, TP53 |
| Cellular senescence | 8 | 1.31 × 10−7 | PTEN, MAPK1, HLA-B, HLA-A, TGFBR2, PIK3CA, KRAS, TP53 |
| Prostate cancer | 7 | 1.31 × 10−7 | PTEN, ERBB2, MAPK1, EP300, PIK3CA, KRAS, TP53 |
| p53 pathway feedback loops 2 | 5 | 1.74 × 10−7 | PTEN, TP63, PIK3CA, KRAS, TP53 |
| Endometrial cancer | 6 | 1.88 × 10−7 | PTEN, ERBB2, MAPK1, PIK3CA, KRAS, TP53 |
| Kaposi sarcoma-associated herpesvirus infection | 8 | 2.26 × 10−7 | CASP8, MAPK1, EP300, HLA-B, HLA-A, PIK3CA, KRAS, TP53 |
| Pathways in cancer | 11 | 2.35 × 10−7 | PTEN, CASP8, MECOM, ERBB2, MAPK1, EP300, TGFBR2, PIK3CA, KRAS, TP53, NFE2L2 |
| Viral carcinogenesis | 8 | 3.15 × 10−7 | CASP8, MAPK1, EP300, HLA-B, HLA-A, PIK3CA, KRAS, TP53 |
| Central carbon metabolism in cancer | 6 | 3.15 × 10−7 | PTEN, ERBB2, MAPK1, PIK3CA, KRAS, TP53 |
| MicroRNAs in cancer | 9 | 3.43 × 10−7 | PTEN, ERBB3, ERBB2, MAPK1, EP300, TP63, PIK3CA, KRAS, TP53 |
| FoxO signaling pathway | 7 | 3.43 × 10−7 | PTEN, STK11, MAPK1, EP300, TGFBR2, PIK3CA, KRAS |
| Chronic myeloid leukemia | 6 | 3.94 × 10−7 | MECOM, MAPK1, TGFBR2, PIK3CA, KRAS, TP53 |
| Human papillomavirus infection | 9 | 4.65 × 10−7 | PTEN, CASP8, MAPK1, EP300, HLA-B, HLA-A, PIK3CA, KRAS, TP53 |
| ErbB2/ErbB3 signaling events | 5 | 4.65 × 10−7 | ERBB3, ERBB2, MAPK1, NRG1, KRAS |