Will mTOR inhibitors make it as cancer drugs? (Q35604822)

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scientific article published on November 2003

Language	Label	Description	Also known as
English	Will mTOR inhibitors make it as cancer drugs?	scientific article published on November 2003

Statements

scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

9 August 2017

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Europe PubMed Central

Will mTOR inhibitors make it as cancer drugs? (English)

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Europe PubMed Central

PubMed publication ID

9 August 2017

author name string

Charles L Sawyers

1

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Europe PubMed Central

PubMed publication ID

9 August 2017

publication date

1 November 2003

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Europe PubMed Central

PubMed publication ID

9 August 2017

1 reference

Europe PubMed Central

PubMed publication ID

9 August 2017

4

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Europe PubMed Central

PubMed publication ID

9 August 2017

5

1 reference

Europe PubMed Central

PubMed publication ID

9 August 2017

343-348

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Europe PubMed Central

PubMed publication ID

9 August 2017

Identification of TOR signaling complexes: more TORC for the cell growth engine

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Loss of PTEN/MMAC1/TEP in EGF receptor-expressing tumor cells counteracts the antitumor action of EGFR tyrosine kinase inhibitors

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The Ras-related protein Rheb is farnesylated and antagonizes Ras signaling and transformation.

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Clinical development of mammalian target of rapamycin inhibitors

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New antitumor substances of natural origin

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Insulin activation of Rheb, a mediator of mTOR/S6K/4E-BP signaling, is inhibited by TSC1 and 2

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AKT activity determines sensitivity to mammalian target of rapamycin (mTOR) inhibitors by regulating cyclin D1 and c-myc expression

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Rapamycin inhibits primary and metastatic tumor growth by antiangiogenesis: involvement of vascular endothelial growth factor

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Raptor, a binding partner of target of rapamycin (TOR), mediates TOR action

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Targets for Cell Cycle Arrest by the Immunosuppressant Rapamycin in Yeast

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Studies on the mechanism of resistance to rapamycin in human cancer cells

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Regulation of hypoxia-inducible factor 1alpha expression and function by the mammalian target of rapamycin.

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Rheb is in a high activation state and inhibits B-Raf kinase in mammalian cells

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TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling

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Molecular basis of the VHL hereditary cancer syndrome

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mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery

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mTor is required for hypertrophy of Pten-deficient neuronal soma in vivo

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TOR deficiency in C. elegans causes developmental arrest and intestinal atrophy by inhibition of mRNA translation

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Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway

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Cyclin D Expression Is Controlled Post-transcriptionally via a Phosphatidylinositol 3-Kinase/Akt-dependent Pathway

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Enhanced sensitivity of PTEN-deficient tumors to inhibition of FRAP/mTOR.

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Genetic and biochemical characterization of dTOR, the Drosophila homolog of the target of rapamycin

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The immunosuppressant rapamycin mimics a starvation-like signal distinct from amino acid and glucose deprivation

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

1 reference

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Akt regulates growth by directly phosphorylating Tsc2

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dS6K-regulated cell growth is dPKB/dPI(3)K-independent, but requires dPDK1.

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Oncogenic Ras and Akt Signaling Contribute to Glioblastoma Formation by Differential Recruitment of Existing mRNAs to Polysomes

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Rheb promotes cell growth as a component of the insulin/TOR signalling network

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TOR, a central controller of cell growth

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Gene expression profiling identifies molecular subtypes of gliomas

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Partitioning the transcriptional program induced by rapamycin among the effectors of the Tor proteins

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Integration of growth factor and nutrient signaling: implications for cancer biology

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Rheb is an essential regulator of S6K in controlling cell growth in Drosophila

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Cyclin D1 expression mediated by phosphatidylinositol 3-kinase through mTOR-p70(S6K)-independent signaling in growth factor-stimulated NIH 3T3 fibroblasts

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The phosphatidylinositol 3-Kinase AKT pathway in human cancer

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A randomized trial of bevacizumab, an anti-vascular endothelial growth factor antibody, for metastatic renal cancer

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MAP kinases, phosphatidylinositol 3-kinase, and p70 S6 kinase mediate the mitogenic response of human endothelial cells to vascular endothelial growth factor

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Regulation of cellular growth by the Drosophila target of rapamycin dTOR

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Rheb is a direct target of the tuberous sclerosis tumour suppressor proteins

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Identifiers

10.1016/S1535-6108(03)00275-7

1 reference

Europe PubMed Central

PubMed publication ID

9 August 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

9 August 2017

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