Targeting the PI3K/Akt/mTOR pathway: effective combinations and clinical considerations.

By J. LoPiccolo, G. Blumenthal, W. Bernstein, P. Dennis. Drug resistance updates, 2008

801 citations recorded by the source corpus.

Subfields: Molecular Biology, Organic Chemistry, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/7f4080a28c1618ceeb21a63d05387657dd66f708

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In Molecular Biology

1. Arkaitz Carracedo
2. P. Pandolfi
3. T. Franke
4. Qingxiang Zeng
5. Junjiang Liu
6. Jin Yang
7. J. Mu
8. Shuzhi Deng

In Pathology and Forensic Medicine

1. P. Pandolfi

Citations in the corpus

• β‐caryophyllene and β‐caryophyllene oxide—natural compounds of anticancer and analgesic properties (2016, background): “Moreover, it induced ROS generation, MAPK activation, and inhibition of PI3K/AKT/mTOR/S6K1 signaling pathway in these cells, a pathway which is essential in cell survival, proliferation, and angiogenesis of the tumor [41].”
• The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Whereas in physiological conditions the proper functioning of this feedback might be of importance for the metabolic processes, re-activation of this brake in conditions of inhibition of mTORC1 could represent a very attractive therapeutic target to oppose tumor progression (Lopiccolo et al., 2007).”
• Strategies to improve radiotherapy with targeted drugs (2011, background): “Activation of AKT by phosphorylation occurs through growth factor receptor pathways, leading in turn to phosphorylation and thereby activation of a host of downstream proteins that are involved in processes such as cell cycle progression, apoptosis suppression, and glucose uptake and metabolis”
• PI3K/Akt: getting it right matters (2008, background): “Thus, the pathological finding of hyperactivated Akt in primary tumors is considered to be a negative prognostic marker for disease outcome (for review, see LoPiccolo et al., 2008).”
• Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer (2021, background): “and can activate PI3K and then phosphorylate phosphatidylinositol-4,5-bisphosphate (PIP2) to phosphatidylinositol-3,4,5-trisphosphate (PIP3).(118,119) Then, PIP3 binds to the phosphoinositide-dependent kinase 1 (PDK1) and PDK2, and subsequently recruits AKT to the plasma membrane and phosphorylates ”