Table 1 Common mutations in the PI3K/Akt/mTOR pathway [[14]]
From: Akt inhibitors: mechanism of action and implications for anticancer therapeutics
Targets | Genetic alteration | Cancer type |
|---|---|---|
PIK3CA (phosphoinositide-3-kinase, catalytic, α-polypeptide) | Mutations | Breast, endometrial, colon, upper digestive tract, gastric, pancreas, ovarian, liver, brain, oesophageal, lung, melanoma, urinary tract, prostate, thyroid |
| Â | Amplifications | Lung (squamous cell), lung (adenocarcinoma), lung (small cell), lung (non-small cell), cervical, breast, head and neck, gastric, thyroid, oesophageal, endometrial, ovarian, glioblastoma |
PIK3CB (phosphoinositide-3-kinase, catalytic, β-polypeptide) | Amplifications | Ovarian, breast |
| Â | Increase in activity and expression | Colon, bladder |
PDPK1 (3-phosphoinositide dependent protein kinase-1) | Amplifications and overexpression | Breast |
AKT (v-akt murine thymoma viral oncogene homologue) | AKT homologue 1 mutation (E17K) or amplifications | Breast, colon, ovarian, lung, gastric |
| Â | AKT homologue 2 amplifications | Ovarian, pancreas, head and neck, breast |
| Â | AKT homologue 3 mutation (E17K) or amplifications | Skin, glioblastoma |
PIK3R1 (phosphoinositide-3-kinase, regulatory subunit-1) | Mutations | Glioblastoma, ovarian, colon |
PTEN (phosphatase and tensin homologue) | Loss of heterozygosity | Gastric, breast, melanoma, prostate, glioblastoma |
| Â | Mutations | Endometrial, brain, skin, prostate, colon, ovary, breast, haematopoietic and lymphoid tissue, stomach, liver, kidney, vulva, urinary tract, thyroid, lung |