mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways

Loss of PTEN function leads to activation of phosphoinositide 3-kinase (PI3K) signaling and Akt. Clinical trials are now testing whether mammalian target of rapamycin (mTOR) inhibition is useful in treating PTEN-null cancers. Here, we report that mTOR inhibition induced apoptosis of epithelial cells and the complete reversal of a neoplastic phenotype in the prostate of mice expressing human AKT1 in the ventral prostate. Induction of cell death required the mitochondrial pathway, as prostate-specific coexpression of BCL2 blocked apoptosis.

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Majumder, P. K., et al. (2004). mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways. Nature medicine. https://doi.org/10.1038/nm1052

@article{MAJ2004,
  author       = {Majumder, P. K. and Sellers, W. R. and others},
  title        = {{mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways}},
  journal      = {Nature medicine},
  year         = {2004},
  doi          = {10.1038/nm1052},
  note         = {PMID: 15156201},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record MAJ2004) [Data set]. https://mtor-atlas.org/study/MAJ2004/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_MAJ2004,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record MAJ2004},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/MAJ2004/},
  doi          = {10.5281/zenodo.22059963}
}