Targeting the PI3K-Akt pathway in human cancer: rationale and promise.

By Ji Luo, B. Manning, Lewis C. Cantley. Cancer Cell, 2003

1,414 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/8af8f11d66b0ddffa6655cd36d622567add83211

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Citations in the corpus

Cholesteryl Ester Accumulation Induced by PTEN Loss and PI3K/AKT Activation Underlies Human Prostate Cancer Aggressiveness (2014, background): “Finally, given that the PI3K pathway is hyperactivated not only in advanced PCa but also in many other human cancers, including brain, breast, renal, lymphocyte, cervical, and lung (Luo et al., 2003), CE accumulation might be a common characteristic of PI3K-driven cancers.”
Perturbations of the AKT signaling pathway in human cancer (2005, background): “Moreover, genetically modified mice have been used as in vivo models to demonstrate that aberrant AKT signaling can contribute to malignancy, either alone or in cooperation with other genetic alterations (Luo et al., 2003; Bjornsti and Houghton, 2004).”
Signal transduction by focal adhesion kinase in cancer (2009, background): “Phospholipid production stimulated by FAK association and activation of PI3K can activate Akt kinase, which inhibits apoptosis by regulating various cell death machinery proteins [31, 32].”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Indeed, several compounds are now being designed and tested in preclinical trials for the treatment of cancer with hyperactive PI3K (Luo et al., 2003), such as the PI3K SF1126 from Semaphore and XL147 from Exelixis.”
NEDD4-1 is a proto-oncogenic ubiquitin ligase for PTEN. (2007, positive): “, 1998), which is required for activation of kinase AKT/PKB and the downstream cellular survival and growth responses (Luo et al., 2003).”
Target of rapamycin (TOR): an integrator of nutrient and growth factor signals and coordinator of cell growth and cell cycle progression (2004, background): “As a result, rapamycin analogs, such as CCI-779 and RAD001, are currently being tested in clinical trials against a variety of human tumors (Elit, 2002; and reviewed in Vivanco and Sawyers, 2002; Huang and Houghton, 2003; Luo et al., 2003).”
Mutant PIK3CA promotes cell growth and invasion of human cancer cells. (2005, background): “Numerous mechanisms by which AKTs suppress apoptosis or facilitate invasion have been suggested (Luo et al., 2003; Majewski et al., 2004; Vivanco and Sawyers, 2002).”
Pten regulates neuronal arborization and social interaction in mice. (2006, background): “Upon activation, AKT phosphorylates a diverse spectrum of substrates, including tuberous sclerosis complex 2 (TSC2) gene product tuberin, glycogen synthase kinase 3b (GSK3b), and the proapoptotic protein BAD (Luo et al., 2003).”