2008
DOI: 10.1634/theoncologist.2007-0171
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The Potential Role of mTOR Inhibitors in Non-Small Cell Lung Cancer

Abstract: After completing the course, the reader will be able to:1. Describe the PI3K growth pathway.2. Describe the molecular mechanism of action of mTOR inhibitors. Describe the preliminary clinical results of mTOR inhibitors in NSCLC.Access and take the CME test online and receive 1 AMA PRA Category 1 Credit ™ at CME.TheOncologist.com CME CME ABSTRACTThe mammalian target of rapamycin (mTOR), a serine/threonine kinase, is a downstream mediator in the phosphatidylinositol 3-kinase/Akt signaling pathway, which plays a … Show more

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Cited by 99 publications
(76 citation statements)
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“…The abnormal hyperactivity of EGFR and its downstream mTOR pathways is the leading cause of resistance to TKIs; furthermore, mTOR inhibitors could effectively control the growth of lung adenocarcinoma even after acquiring resistance to TKIs (13,41,42). In order to further unveil the downstream regulatory molecule mechanisms involved in EGFR/mTOR activation, we simultaneously analyzed mRNA expression of EGFR and DEP-TOR, a naturally occurring inhibitor of mTOR, in tumor tissues of patients with lung adenocarcinoma.…”
Section: Mrna Expression Of Egfr Negatively Correlates With Deptor Inmentioning
confidence: 99%
“…The abnormal hyperactivity of EGFR and its downstream mTOR pathways is the leading cause of resistance to TKIs; furthermore, mTOR inhibitors could effectively control the growth of lung adenocarcinoma even after acquiring resistance to TKIs (13,41,42). In order to further unveil the downstream regulatory molecule mechanisms involved in EGFR/mTOR activation, we simultaneously analyzed mRNA expression of EGFR and DEP-TOR, a naturally occurring inhibitor of mTOR, in tumor tissues of patients with lung adenocarcinoma.…”
Section: Mrna Expression Of Egfr Negatively Correlates With Deptor Inmentioning
confidence: 99%
“…By measuring 35 S-labeled methionine incorporation into proteins, we estimated global protein synthesis activity in HT1080 cells treated for 4 h with VST, together with 2DG, thapsigargin, or tunicamycin (Fig. 2d).…”
Section: Hypophosphorylation Of 4e-bp1 and Prevention Of Grp78 Inductmentioning
confidence: 99%
“…The crucial role of the constitutive activation of the PI3K/AKT pathway in the development and maintenance of an EGFR-resistant phenotype supports the hypothesis that a combination of EGFR TKIs and mTOR inhibitors may be the best choice for treatment. Clinical trials testing this strategy in advanced NSCLC are ongoing and only preliminary results are available [18][19][20]. …”
Section: Introductionmentioning
confidence: 99%