Perturbations of the AKT signaling pathway in human cancer

By D. Altomare, J. Testa. Oncogene, 2005

1,360 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/7086168f034e1d0e6c0ad024ac8628c33eb9003e

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

1. Tianyan Gao
2. A. Newton
3. Ping Wee
4. Gautam Sethi
5. Zhixiang Wang
6. N. Turner
7. P. Chiarugi
8. E. Giannoni

In Pathology and Forensic Medicine

1. A. Newton
2. Ping Wee
3. Zhixiang Wang

Citations in the corpus

• Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “Genetic amplification of AKT2 is prominently observed [270,274,275].”
• Fibroblast growth factor signalling: from development to cancer (2010, background): “A separate complex involving GRB2-associated binding protein 1 ( GAB1 ) recruits a complex, which includes PI3K, and this activates an AKT-dependent anti-apoptotic pathwa”
• Anoikis molecular pathways and its role in cancer progression. (2013, background): “Akt is essential to regulate several cellular functions such as cell survival and cell growth, and its aberrant or constitutive activation strongly contributes to sustain cancer growth [2,40,166,184,198].”
• PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer (2023, background): “In cancer cells, mutations [23] and/or gene amplifications in AKT [116], or mutations upstream genes in the PAM pathway, especially PI3K genes [15] and PTEN [148], can potentially result in AKT-induced overactivation of mTORC1, leading to increased cell survival, growth, proliferation, and metabolis”
• PHLPP and a second isoform, PHLPP2, differentially attenuate the amplitude of Akt signaling by regulating distinct Akt isoforms. (2007, background): “…bind receptors that activate the lipid kinase phosphatidylinositol 3-kinase (PI3K), resulting in production of 3 0 -phosphoinositide lipid second messengers, most notably phosphatidylinositol- 3,4,5-trisphosphate (PtdIns P3) (Altomare and Testa, 2005; Datta et al., 1999; Vivanco and Sawyers, 2002).”