The shared endpoint of the pathway's oncogenic lesions, and the outcome every mTOR inhibitor trial in this Atlas was actually measuring.
Cancer growing.
Genotype-dependent: mTORC1 activation is a strong dependency in TSC- and PI3K-pathway-mutant contexts and much weaker elsewhere.
| Tier | What it means | Studies |
|---|---|---|
| B | Direct human evidence | 1 |
| C | Animal in vivo | 1 |
| D | Mechanistic / in vitro / review | 3 |
| Study | Year | Tier | Finding |
|---|---|---|---|
| MOT2008 | 2008 | B | Everolimus extended median progression-free survival from 1.9 to 4.0 months versus placebo in metastatic renal cell carcinoma. |
| NAT2026 | 2026 | C | In syngeneic TP53-mutant HNSCC mouse models, the mTOR inhibitor everolimus reprogrammed the immune-cold tumor microenvironment: it increased CD8+ T cell and dendritic cell infiltration, reduced Tregs |
| VAL2017 | 2017 | D | Hyperactive mTORC1 couples nucleotide synthesis to demand; imbalance drives replication stress in these cells. |
| HSI2012 | 2012 | D | Showed WHY mTOR-driven translation matters for cancer: in prostate cancer, oncogenic mTOR selectively translates a specific set of pro-invasion mRNAs that drive metastasis. An ATP-competitive mTOR inh |
| HSI2010 | 2010 | D | Genetic dissection shows the 4E-BP1-eIF4E axis mediates oncogenic mTOR signalling and is druggable. |