PI3K/AKT

Scientific explanation

phosphorylates PIP2 to PIP3, recruiting . supports growth, survival, glucose uptake and mTORC1 input. Pathway activation is common via PIK3CA mutation, PTEN loss or -tyrosine- signalling.

Cancers where relevant

Breast cancer ER+ breast cancer PR+ breast cancer HER2+ breast cancer Triple-negative breast cancer Lung cancer Non-small-cell lung cancer EGFR-mutant NSCLC ALK-rearranged NSCLC KRAS-driven NSCLC ROS1-rearranged NSCLC MET-altered NSCLC RET-rearranged NSCLC Mesothelioma KRAS-mutant colorectal cancer HER2-amplified colorectal cancer Pancreatic cancer Gastric cancer Esophageal cancer Hepatocellular carcinoma Ovarian cancer Cervical cancer Endometrial cancer Uterine cancer Prostate cancer Androgen-sensitive prostate cancer Castration-resistant prostate cancer Kidney / renal cell carcinoma Bladder cancer Testicular cancer Leukemias Acute myeloid leukemia Acute lymphoblastic leukemia Non-Hodgkin lymphoma Multiple myeloma Brain tumors Glioblastoma IDH-mutant glioma IDH-wildtype glioma Melanoma BRAF-driven melanoma NRAS-driven melanoma KIT-associated melanoma Head and neck cancers Thyroid cancer Neuroendocrine tumors Sarcomas Bone cancers

Compounds that intersect this pathway

EGCG

Green-tea catechin with in-vitro effects on RTKs, epigenetic enzymes and redox. Clinical anticancer efficacy is not established.

Evidence in mapped cancers: In Vitro · Mechanistically Plausible

Quercetin

Flavonol with -related and antioxidant in-vitro activity. Not a clinical oncology agent.

Convergence partners

Other pathways that co-occur with PI3K/AKT on mapped adjunct records: EGFR.

This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.