AKT and cancer-Is it all mTOR? Journal Article


Authors: Rosen, N.; She, Q. B.
Article Title: AKT and cancer-Is it all mTOR?
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. © 2006 Elsevier Inc. All rights reserved.
Keywords: signal transduction; protein kinase b; clinical trial; advanced cancer; nonhuman; protein function; neoplasms; cell proliferation; animals; mice; mice, knockout; cell survival; imatinib; protein kinases; genetic transcription; chronic myeloid leukemia; phosphatidylinositol 3 kinase; cancer therapy; oncogene h ras; mice, inbred c57bl; carcinogenesis; animalia; sarcoma; mammalian target of rapamycin; proto-oncogene proteins c-akt; short survey; kidney cancer; rapamycin; tor serine-threonine kinases; rapamycin derivative
Journal Title: Cancer Cell
Volume: 10
Issue: 4
ISSN: 1535-6108
Publisher: Cell Press  
Date Published: 2006-10-01
Start Page: 254
End Page: 256
Language: English
DOI: 10.1016/j.ccr.2006.10.001
PUBMED: 17045203
PROVIDER: scopus
DOI/URL:
Notes: --- - "Cited By (since 1996): 25" - "Export Date: 4 June 2012" - "CODEN: CCAEC" - "Source: Scopus"
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  1. Neal Rosen
    426 Rosen
  2. Qing-Bai She
    31 She