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PMID: 17045203 Published · ppublish English Journal Article Comment

AKT and cancer--is it all mTOR?

Cancer cell ·Vol. 10 ·No. 4 ·2006-10-00 ·Pages 254-6

Rosen N, She QB

Abstract

AKT, a key regulator of cell proliferation and survival, is commonly dysregulated in human cancers. Activated AKT kinase is oncogenic and required for tumorigenesis in PTEN-deficient animals. However, the importance of AKT in mediating transformation by other oncogenes and which of its targets are necessary for this process are poorly understood. In this issue of Cancer Cell, Skeen et al. show that AKT is required for transformation by mutant H-Ras and for experimental skin carcinogenesis. Moreover, the effects of AKT are mediated predominantly or solely via mTORC1. This suggests that AKT or mTOR inhibitors will be useful treatments for many cancers.

MeSH Terms
Animals Humans Mice Mice, Inbred C57BL Mice, Knockout Neoplasms/etiology,pathology Protein Kinases/genetics,metabolism Proto-Oncogene Proteins c-akt/deficiency,genetics TOR Serine-Threonine Kinases
Chemicals
Protein Kinases MTOR protein, human mTOR protein, mouse Proto-Oncogene Proteins c-akt TOR Serine-Threonine Kinases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Rosen Neal
Department of Medicine and Program in Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA. rosenn@mskcc.org
She Qing-Bai
Article Info
Journal
Cancer cell
Abbr.
Cancer Cell
ISSN
1535-6108
Published
2006-10-00
Pages
254-6
Language
English
Region
United States
NLM ID
101130617
Subset
IM
Corrections
CommentOn
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