The phosphatidylinositol 3-Kinase–AKT pathway in human cancer

By I. Vivanco, C. Sawyers. Nature Reviews. Cancer, 2002

6,297 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d37212ad1f70a3c566216bd0d474048bf86b49a2

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Citations in the corpus

Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer. (2003, background): “…cells will eventually in human prostate cancers, making them promising targets for therapeutic strategies (DeMarzo et al., 2003; Sellers and Saw-relapse and develop into hormone refractory prostate cancer (HRPC) (Denis and Murphy, 1993; Landis et al., 1999). yers, 2002; Vivanco and Sawyers, 2002).”
Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks (2004, background): “(#2; C3): In response to survival signals, p110 and p85 are both targeted to the plasma membrane where the stimulatory binding of p85 to p110 is favoured (#3, B2): Alternatively, PI3K can be activated by binding of p110 to Ras (when Ras is bound to GTP) (Vivanco and Sawyers, 2002).”
PTEN and the PI3-kinase pathway in cancer. (2009, background): “For other substrates such as MDM2, which promotes degradation of the tumor-suppressor p53, or the transcription factor nuclear factor–kappa B (NF-κB), AKT-mediated phosphorylation enhances activity (13).”
Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer (2009, background): “gif" NDATA ITEM> ]> Since its discovery in the 1980s, the family of lipid kinases termed phosphoinositide 3-kinases (PI3Ks) has been found to have key regulatory roles in many cellular processes, including cell survival, proliferation and differentiatio”
Cholesteryl Ester Accumulation Induced by PTEN Loss and PI3K/AKT Activation Underlies Human Prostate Cancer Aggressiveness (2014, background): “, 2011), which leads to enhanced cell survival, metastasis, and castration-resistant growth (Liu et al., 2011; Mulholland et al., 2011; Vivanco and Sawyers, 2002).”
Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “in various tumors, which leads to a constitutive activation of the PI3K pathway [4–6].”
A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma. (2006, positive): “Class 1A PI3 kinases are hetero-dimers of a catalytic p110 lipid kinase subunit and an adaptor p85 subunit that recruits PI3 kinase to tyrosine phosphorylated membrane docking sites (Vivanco and Sawyers, 2002).”
Hyperactive Ras in developmental disorders and cancer (2007, background): “Akt is a kinase that promotes survival in many cell types by phosphorylating and therefore inactivating several pro-apoptotic proteins including BAD and Forkhead ( FKHR ) transcription factor”
PI3K/Akt/mTOR Pathway and Its Role in Cancer Therapeutics: Are We Making Headway? (2022, background): “AKT1 activation mutations and AKT1 infrequent amplification enableAKT1 activation independent of phosphoinositide (14, 35, 36).”
Exploiting the PI3K/AKT Pathway for Cancer Drug Discovery (2005, background): “Previous reviews have provided depth and focus on the role of the PI3K/AKT pathway in cell proliferation and surviva”
Mechanisms of type-I- and type-II-interferon-mediated signalling (2005, background): “It is well established that AKT, a downstream effector of PI3K, mediates anti-apoptotic and pro-survival signal”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Second, AKT activates cell proliferation by inactivating p27 (Fujita et al., 2002) and inhibiting glycogen synthase kinase 3 (GSK3)mediated Myc and cyclin D1 inhibition (Vivanco and Sawyers, 2002).”
Mechanisms of BCR–ABL in the pathogenesis of chronic myelogenous leukaemia (2005, neutral): “DH p185 (1-426) p210 (1-902–927) p230 (1–1,176) Y177 Myr GAG BCR F G 1a 1b”
Activation of Akt and eIF4E survival pathways by rapamycin-mediated mammalian target of rapamycin inhibition. (2005, background): “Because Akt and eIF4E are often associated with cell survival and resistance to cancer therapy (4, 14), our findings imply that the activation of Akt and eIF4E through mTOR inhibition may counteract mTOR inhibitors’ anticancer efficacy and confers resistance to mTOR-targeted cancer therapy.”
Control of apoptosis by p53 (2003, background): “Prosurvival cytokines lead to the activation of PI3 kinase, the production of phosphotidyl inositol-3,4-P2 and -3,4,5-P3, and activation of downstream effectors, including Akt/PKB. Akt, in turn, phosphorylates effector molecules that can regulate survival in several ways (Vivanco and Sawyers, 2002).”