{"entity":{"id":"pi3k-akt-mtor","kind":"pathway","name":"PI3K / AKT / mTOR","aka":[],"tldr":"The cell's 'grow and survive' circuit. Growth signals from the surface switch on PI3K, which switches on AKT, which switches on mTOR, which builds proteins and blocks self-destruction.","summary":"Receptor tyrosine kinases (HER2, EGFR, IGF1R) activate PI3K (p110α, encoded by PIK3CA), producing PIP3, which recruits AKT. PTEN reverses this step and is a tumour suppressor. AKT phosphorylates many targets including TSC2, releasing mTORC1 to drive protein synthesis, and inhibits FOXO and BAD. The most frequently altered pathway in cancer: PIK3CA mutation (~40% HR+ breast, endometrial, head and neck), PTEN loss (prostate, endometrial, glioblastoma), AKT1 E17K. Drugs: alpelisib, inavolisib (PI3Kα), capivasertib (AKT), everolimus (mTOR), gedatolisib (PI3K/mTOR). Feedback: mTOR inhibition releases AKT, so combinations and endocrine partners are needed.","asOf":"2026-09-04","wikipedia":"https://en.wikipedia.org/wiki/PI3K/AKT/mTOR_pathway","links":[{"label":"Wikipedia","url":"https://en.wikipedia.org/wiki/PI3K/AKT/mTOR_pathway"}],"tags":[],"related":[],"cancers":["breast-hr-positive","endometrial","prostate","tnbc","gallbladder"],"sections":[],"technologies":[],"targets":["pik3ca","akt","her2","egfr"],"drugs":["capivasertib","inavolisib","gedatolisib"],"companies":[],"institutions":[],"pathways":[],"terms":[],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"analogy":"Think of a factory: the receptor is the order desk, PI3K and AKT are the managers relaying the order, PTEN is the accountant cancelling orders, and mTOR is the assembly line. Cancer forges orders (PIK3CA mutation) or fires the accountant (PTEN loss).","nodes":[{"id":"rtk","label":"RTK (HER2, EGFR)","x":50,"y":5,"targetId":"her2"},{"id":"pi3k","label":"PI3K (PIK3CA)","x":50,"y":25,"targetId":"pik3ca"},{"id":"pten","label":"PTEN","x":15,"y":40},{"id":"pip3","label":"PIP3","x":50,"y":42},{"id":"akt","label":"AKT","x":50,"y":58,"targetId":"akt"},{"id":"tsc","label":"TSC1/2","x":25,"y":74},{"id":"mtor","label":"mTORC1","x":50,"y":82},{"id":"foxo","label":"FOXO / BAD (apoptosis)","x":85,"y":74},{"id":"growth","label":"Protein synthesis, growth","x":50,"y":97}],"edges":[{"from":"rtk","to":"pi3k","type":"activates"},{"from":"pi3k","to":"pip3","type":"activates"},{"from":"pten","to":"pip3","type":"inhibits"},{"from":"pip3","to":"akt","type":"activates"},{"from":"akt","to":"tsc","type":"inhibits"},{"from":"tsc","to":"mtor","type":"inhibits"},{"from":"akt","to":"foxo","type":"inhibits"},{"from":"mtor","to":"growth","type":"activates"}],"interventions":["PI3Kα inhibitors (alpelisib, inavolisib) for PIK3CA-mutant HR+ breast cancer","AKT inhibitor capivasertib for PIK3CA/AKT1/PTEN-altered breast and PTEN-deficient prostate cancer","mTOR inhibitor everolimus","Dual PI3K/mTOR gedatolisib (2026)","Upstream: anti-HER2, anti-EGFR"]},"route":"/pathways/pi3k-akt-mtor/","neighbours":{"cancer":[{"id":"tnbc-basal-like-2","kind":"cancer","name":"Basal-like 2 triple-negative breast cancer (BL2)","route":"/cancers/tnbc-basal-like-2/"},{"id":"burkitt-lymphoma","kind":"cancer","name":"Burkitt lymphoma","route":"/cancers/burkitt-lymphoma/"},{"id":"cll","kind":"cancer","name":"Chronic lymphocytic leukaemia","route":"/cancers/cll/"},{"id":"cml","kind":"cancer","name":"Chronic myeloid leukaemia (CML)","route":"/cancers/cml/"},{"id":"colorectal","kind":"cancer","name":"Colorectal cancer","route":"/cancers/colorectal/"},{"id":"egfr-mutant-nsclc","kind":"cancer","name":"EGFR-mutated non-small-cell lung 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