An inhibitor of mTOR reduces neoplasia and normalizes p70/S6 kinase activity in Pten+/- mice

Podsypanina K, Lee RT, Politis C, Hennessy I, Crane A, Puc J, Neshat M, Wang H, Yang L, Gibbons J, Frost P, …, Parsons R · 2001 · PNAS · Atlas ID POD2001

What this study shows

Transformed cells in Pten+/- mice showed raised phosphorylated Akt and active p70 S6 kinase together with faster proliferation. Treating the mice with an mTOR inhibitor reduced neoplastic proliferation, tumour size and S6 kinase activity without changing Akt status. The authors concluded that S6K and possibly other mTOR targets contribute to tumour development downstream of PTEN loss. Boundary: worked from the abstract only (scanned PMC record); mouse model. The abstract does not name the inhibitor.

Abstract

ShowHide

PTEN phosphatase acts as a tumor suppressor by negatively regulating the phosphoinositide 3-kinase (PI3K) signaling pathway. It is unclear which downstream components of this pathway are necessary for oncogenic transformation. In this report we show that transformed cells of PTEN(+/-) mice have elevated levels of phosphorylated Akt and activated p70/S6 kinase associated with an increase in proliferation. Pharmacological inactivation of mTOR/RAFT/FRAP reduced neoplastic proliferation, tumor size, and p70/S6 kinase activity, but did not affect the status of Akt.

Read the full abstract on PubMed →

At a glance

Evidence type	A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Pten+/- mice treated with a pharmacological mTOR inhibitor); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type	4 - Animal Study
Model system	Pten+/- mice treated with a pharmacological mTOR inhibitor
Journal	PNAS
Year	2001
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1073/pnas.171060098 · PMID 11504907 · Free full text (PMC56959)

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	Pharmacological mTOR inhibitor
Target	mTOR -> p70 S6K
Model	Pten+/- mice
Effect	mTOR inhibition reduces neoplasia and normalises S6K activity in Pten+/- mice

In the Atlas

Links in the pathway map

Supports mTORC1 activates S6K1
Supports mTORC1 activates Tumor growth

Cite this paper

ShowHide

Podsypanina, K., Lee, R. T., Politis, C., Hennessy, I., Crane, A., Puc, J., Neshat, M., Wang, H., Yang, L., Gibbons, J., Frost, P., Dreisbach, V., Blenis, J., Gaciong, Z., Fisher, P., Sawyers, C. L., Hedrick-Ellenson, L., & Parsons, R. (2001). An inhibitor of mTOR reduces neoplasia and normalizes p70/S6 kinase activity in Pten+/- mice. PNAS. https://doi.org/10.1073/pnas.171060098

@article{POD2001,
  author       = {Podsypanina, K. and Lee, R. T. and Politis, C. and Hennessy, I. and Crane, A. and Puc, J. and Neshat, M. and Wang, H. and Yang, L. and Gibbons, J. and Frost, P. and Dreisbach, V. and Blenis, J. and Gaciong, Z. and Fisher, P. and Sawyers, C. L. and Hedrick-Ellenson, L. and Parsons, R.},
  title        = {{An inhibitor of mTOR reduces neoplasia and normalizes p70/S6 kinase activity in Pten+/- mice}},
  journal      = {PNAS},
  year         = {2001},
  doi          = {10.1073/pnas.171060098},
  note         = {PMID: 11504907},
}

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 POD2001) [Data set]. https://mtor-atlas.org/study/POD2001/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_POD2001,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record POD2001},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/POD2001/},
  doi          = {10.5281/zenodo.22059963}
}

Was this page useful?