Table 2.
Phosphatidylinositol‐3 kinase (PI3K)–AKT pathway genes with significantly increased somatic mutation rates (% of tumour samples) compared with background mutation rate in tumour specimens, by tumour type (The Cancer Genome Atlas data)
| Cancer type | PIK3CA | PTEN | PIK3R1 | PIK3CG | AKT1 |
|---|---|---|---|---|---|
| Breast | 33.6 | 3.8 | 2.5 | 0.4 | 2.5 |
| Lung adenocarcinoma | 4.4 | 2.2 | 1.3 | 0.7 | 0.5 |
| Lung‐squamous | 14.9 | 8.1 | 0.6 | 7.5 | 0.6 |
| Colorectal | 17.6 | 1.0 | 2.1 | 0.5 | 0.0 |
| Endometrial | 52.2 | 63.5 | 39 | 1.3 | 1.3 |
| Ovarian | 0.6 | 0.6 | 0.3 | 1.0 | 0.0 |
| Head and neck | 20.6 | 1.3 | 1.7 | 2.7 | 0.7 |
| Renal | 2.9 | 4.3 | 0.5 | 0.7 | 0.5 |
| Glioblastoma | 11.0 | 30.7 | 11.4 | 2.4 | 0.3 |
| AML | 0 | 0 | 0.0 | 0.0 | 0.0 |
| Bladder | 17.4 | 3.1 | 1.0 | 2.0 | 0.0 |
| Combined | 17.8 | 9.7 | 4.4 | 1.7 | 0.9 |
Adapted from Kandoth et al. 39, based on N = 3281 total specimens. The results shown here are in whole based upon data generated by The Cancer Genome Atlas Research Network: (http://cancergenome.nih.gov/). AML, acute myeloid leukaemia; PIK3CA, PIK3 catalytic subunit alpha; PIK3CG, phosphatidylinositol‐4, 5‐bisphosphate 3‐kinase catalytic subunit gamma isoform; PIK3R1, phosphoinositide‐3‐kinase, regulatory subunit 1; PTEN, phosphatase and tensin homologue deleted on chromosome 10