AKT plays a central role in tumorigenesis

By J. Testa, A. Bellacosa. Proceedings of the National Academy of Sciences of the United States of America, 2001

994 citations recorded by the source corpus.

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Citations in the corpus

Endocrine-responsive breast cancer and strategies for combating resistance (2002, background): “The expression and activity of all three AKT family members is increased in breast cancers, as well as other cancers, and often involves gene amplificatio”
The protein kinase Akt induces epithelial mesenchymal transition and promotes enhanced motility and invasiveness of squamous cell carcinoma lines. (2003, background): “The antiapoptotic function of AKT has been linked to inhibition of cytochrome c release from mitochondria, stimulation of glucose uptake and utilization, phosphorylation and inactivation of Bad and (pro)caspase 9, activation of nuclear factor ␬B, overexpression of Bcl-2 or Bcl-xL, and phosphorylatio”
Epithelial–mesenchymal transition in development and cancer: role of phosphatidylinositol 3′ kinase/AKT pathways (2005, background): “AKT is frequently activated in human epithelial cancer (Cheng et al., 1992, 1996; Bellacosa et al., 1995; Yuan et al., 2000; Brognard et al., 2001 and reviewed by Altomare and Testa, in this issue; Ringel et al., 2001; Sun et al., 2001; Testa and Bellacosa, 2001).”
Cytoplasmic relocalization and inhibition of the cyclin-dependent kinase inhibitor p27Kip1 by PKB/Akt-mediated phosphorylation in breast cancer (2002, background): “The serine/threonine protein kinase Akt (here termed 'Akt')/protein kinase B (PKB) plays a pivotal role in tumorigenesi”
MicroRNA expression profiling in human ovarian cancer: miR-214 induces cell survival and cisplatin resistance by targeting PTEN. (2008, background): “Because Akt is a major cell survival pathway and its activation plays a key role in multiple drug resistance, including cisplatin (20, 21), we next examined the effects of miR-214 on cell survival and cisplatin resistance.”
The oncogene HER2: its signaling and transforming functions and its role in human cancer pathogenesis (2007, background): “Readers are referred to a number of excellent recent reviews of this topic ((Testa and Bellacosa, 2001; Vivanco and Sawyers, 2002; Luo et al., 2003; Paez and Sellers, 2003) and the entire Oncogene vol. 24; issue 50 (11/14/2005)).”
Targeting PI3K/Akt/mTOR Signaling in Cancer (2014, background): “of other pro-apoptotic factors, such as Fas-ligand (FasL) (7, 8).”
Mitochondrial mutations in cancer (2006, background): “The Akt kinases, in turn, mediate the signals of a variety of oncogenes (Aoki et al., 1998; Testa and Bellacosa, 2001; Brazil et al., 2004; Yanagihara et al., 2005).”
Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake. (2002, background): “Akt has been shown to phosphorylate and inactivate several proapoptotic mediators such as BAD, caspase 9, and the Forkhead transcription factors (Datta et al., 1999; Testa and Bellacosa, 2001).”
Regulation and role of autophagy in mammalian cells. (2004, neutral): “3) (Di Cristofano & Pandolfi, 2000; Lawlor & Alessi, 2001; Testa & Bellacosa, 2001; Vogt, 2001; Weaver & Ward, 2001; Young & Povey, 1998).”
Perturbations of the AKT signaling pathway in human cancer (2005, background): “AKT also directly antagonizes the action of the cell cycle inhibitors p21WAF1 and p27Kip1 by phosphorylating a site located near the nuclear localization signal to induce cytoplasmic retention of these cell cycle inhibitors (reviewed in Testa and Bellacosa, 2001; Bellacosa et al., 2005).”
Activation of the PI3K/Akt pathway and chemotherapeutic resistance. (2002, background): “Inappropriate activation of the PI3K/Akt pathway has been associated with the development of diseases such as diabetes, autoimmunity, and cancer (Di Cristofano et al., 1999; Hill and Hemmings, 2002; Nicholson and Anderson, 2002; Testa and Bellacosa, 2001; Vivanco and Sawyers, 2002).”
Exploiting the PI3K/AKT Pathway for Cancer Drug Discovery (2005, background): “AKT2 is genomically amplified in pancreatic, breast and ovarian tumours, and AKT3 is overexpressed by an unknown mechanism in hormone-insensitive breast and prostate cancer”
Cell Cycle Inhibition by FoxO Forkhead Transcription Factors Involves Downregulation of Cyclin D (2002, background): “Importantly, constitutive activation of this pathway facilitates tumor formation both by supporting S-phase entry and by conferring resistance to apoptotic signals which normally restrict uncontrolled cell growth (7, 47).”