mTOR

Scientific explanation

mTORC1 integrates growth-factor and nutrient signals to drive protein synthesis, lipid synthesis and suppression. It sits downstream of PI3K/AKT and amino-acid sensing.

Cancers where relevant

Breast cancer ER+ breast cancer PR+ breast cancer HER2+ breast cancer EGFR-mutant NSCLC Hepatocellular carcinoma Endometrial cancer Prostate cancer Androgen-sensitive prostate cancer Castration-resistant prostate cancer Kidney / renal cell carcinoma Non-Hodgkin lymphoma Glioblastoma Neuroendocrine tumors

Compounds that intersect this pathway

Metformin

Modest complex I inhibition raises AMP:ATP, activating and restraining hepatic and -linked anabolism. Direct antineoplastic efficacy is not established from that pharmacology alone.

Evidence in mapped cancers: Clinical / Human Evidence · In Vivo · In Vitro · Mechanistically Plausible

Niclosamide

uncoupler in cestodes; mammalian models report , Wnt/β-catenin and modulation. Those host-signalling findings are investigational/preclinical.

Evidence in mapped cancers: In Vitro · In Vivo · Mechanistically Plausible

AICAR

AMP mimetic that activates in experimental systems. Research tool, not an approved oncology medicine.

Evidence in mapped cancers: In Vitro · In Vivo · Hypothesis-Generating

Berberine

Isoquinoline alkaloid that can inhibit complex I and activate in metabolic models, with additional -independent reports. Not an approved antineoplastic.

Evidence in mapped cancers: In Vitro · In Vivo · Mechanistically Plausible

Convergence partners

Other pathways that co-occur with mTOR on mapped adjunct records: AMPK, Glycolysis, Mitochondrial oxidative phosphorylation, Wnt/β-catenin, JAK/STAT.

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.