Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis

By Megan Cully, H. You, Arnold J. Levine, T. Mak. Nature Reviews. Cancer, 2006

1,296 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/000ffc8a24ddd59fd74cdee7275b78bdc6e7101b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

Citations in the corpus

Targeting the ubiquitin system in cancer therapy (2009, background): “PTEN is a lipid phosphatase that negatively regulates the phosphatidylinositol 3-kinase (PI3K)/AKT signalling cascade and is one of the genes most frequently inactivated in human cancers (reviewed in ref”
Regulation of ligands for the NKG2D activating receptor (2013, background): “Among the most common alterations in cancer cells are those that activate the PI3K pathway, which promotes survival and proliferation (42, 43).”
Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “in various tumors, which leads to a constitutive activation of the PI3K pathway [4–6].”
Mitophagy: mechanisms, pathophysiological roles, and analysis (2012, background): “Many known tumor suppressor genes such as Lkt , Ampk , and Pten are positive regulators of autophagy (Cully et al. , 2006 ; Liang et al. , 2007 ; Degtyarev et al. , 2008 ; Hezel and Bardeesy , 2008 ), whereas many oncogenes, including the class I PI3K, Akt, and antiapoptotic Bcl-2 family proteins,…”
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, background): “Under some circumstances, the Ras oncogene or activated receptor tyrosine kinases have also been shown to mediate their transforming potential through aberrant PI3K signaling (16).”
MicroRNA control of signal transduction (2010, background): “The characteristic trait of these pathways is potent signal amplification; this is achieved by numerous kinases acting sequentially and activating one another, as well as by second messengers, such as phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P 3”
Oral squamous cell carcinomas: state of the field and emerging directions (2023, background): “The PI3K/AKT/mTOR pathway leads to the metastasis and proliferation of OSCC cells.(104,105) The PI3K-AKT pathway is frequently activated in OSCC malignancies due to the evaluated phosphorylation levels of AKT and associated mTOR.”
FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis. (2007, neutral): “AKT and the p110a catalytic subunit of PI3K is mutated or amplified and overexpressed in several cancer types, and PTEN, the key PI3K-AKT pathway antagonist , is also inactivated in a broad spectrum of human cancers (Cully et al., 2006).”
Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer (2009, background): “Adaptor PtdIns(4,5)P2 PtdIns(3,4,5)P3 PtdIns(4,5)P2”
The signaling mechanism of ROS in tumor progression (2007, background): “tasis-related genes such as integrins and MMPs [23–25].”