mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways
What this study shows
mTOR inhibition (rapamycin/RAD001) reverses Akt-driven prostate intraepithelial neoplasia in mice.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse (prostate)); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse (prostate) |
| Journal | Nature medicine |
| Year | 2004 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1038/nm1052 · PMID 15156201 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | mTOR inhibition (rapamycin) |
| Target | mTOR / Akt / HIF-1 |
| Model | Mouse (prostate, AKT1 transgenic) |
| Effect | mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia via apoptotic and HIF-1-dependent pathways |
In the Atlas
Related topics
Links in the pathway map
- Supports mTORC1 activates Prostate cancer
- Supports mTORC1 activates HIF-1α
More studies on this topic
- mTOR complex 2 is required for the development of prostate cancer induced by Pten loss in mice (2009)
- The translational landscape of mTOR signalling steers cancer initiation and metastasis (2012)
- Activation of a metabolic gene regulatory network downstream of mTOR complex 1 (2010)
- Rapamycin attenuates age-related atrial remodeling and fibrillation by targeting HIF-1α-mediated metabolic dysregulation. (2026)
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