A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma.

By Q. Fan, Zachary A. Knight, David D. Goldenberg, Wei Yu, Keith E. Mostov, D. Stokoe, Kevan M. Shokat, W. Weiss. Cancer Cell, 2006

617 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/fea74571f5d13a1d6afa845cee35f4a8c80e0ad2

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Citations in the corpus

A Pharmacological Map of the PI3-K Family Defines a Role for p110α in Insulin Signaling (2006, positive): “These multitargeted compounds possess overlapping yet distinct target selectivities and can complement more selective agents by unmasking hidden synergies between targets within the PI3-K family (Fan et al., 2006).”
Rapamycin passes the torch: a new generation of mTOR inhibitors (2011, background): “, but was quickly recognized also as an mTOR inhibito”
Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer (2009, background): “Subsequently, PI-103, a p110α-specific inhibitor, was shown to have a potent effect in blocking PI3K signalling in glioma cells through its ability to inhibit both p110α and mTO”
Lipid signalling in disease (2008, background): “Limited information is available concerning the in vivo isoform-specificity of novel PI3K inhibitors, and molecules with proven anti-tumour activity in xenograft models (PI-103 (Ref”
Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma (2008, background): “Indeed, one dual PI3K/ mTOR inhibitor has shown superiority to a pure mTOR inhibitor in preclinical models [49].”
Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells (2013, background): “PI3K/AKT signaling is highly active in about 90% of GBM specimens (Fan et al., 2006; Fan and Weiss, 2010; Cancer Genome Atlas Research Network, 2008; Verhaak et al., 2010) and all of GSCs we tested have a high level of activating phosphorylation of AKT (Figure 2C and data not shown).”
Rapamycin differentially inhibits S6Ks and 4E-BP1 to mediate cell-type-specific repression of mRNA translation (2008, background): “The wortmannin/PI-103 sensitivity was observed in both 293 (Fig.”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “…the case is provided by the efficacy of PI-103, a small molecule inhibitor of both p110 (cid:1) and mTOR, which potently blocks the growth of glioma cell lines and of U87EGFRvIII xenografts following subcutaneous injection in nude mice, without discernable toxicity to the animals (Fan et al. 2006).”
Targeting the cancer kinome through polypharmacology (2010, neutral): “For example, mutations in PIK3CA or PTEN are poor predictors of the sensitivity of tumour cell lines to PI3K inhibitors 31,45 .”
Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity (2008, result): “A similar observation has been reported for other PI3K modulators (43, 44).”
Essential function of TORC2 in PKC and Akt turn motif phosphorylation, maturation and signalling (2008, background): “HEK293T cells were transfected with GSTtagged PKCa and Akt in a medium containing PI-103, which is a potent inhibitor of PI3K and mTOR (Fan et al, 2006; Knight et al, 2006).”