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Nat. Rev. Clin. Oncol. doi: /nrclinonc

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Presentation on theme: "Nat. Rev. Clin. Oncol. doi: /nrclinonc"— Presentation transcript:

1 Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2016.85
Figure 3 Points of interaction between the PI3K/AKT/mTOR and RAS/RAF/MEK/MAPK pathways Figure 3 | Points of interaction between the PI3K/AKT/mTOR and RAS/RAF/MEK/MAPK pathways. The PI3K/AKT/mTOR signalling cascade is central to the growth-regulatory pathway that is activated not only in pancreatic neuroendocrine neoplasms (NEN), but also in other NENs. Signalling through the mTOR pathway regulates cell growth and proliferation, cellular metabolism, and angiogenesis — processes that are essential for tumorigenesis. The mitogen-activated protein kinase (MAPK) pathway is also critical for cell growth and proliferation, and is frequently upregulated in cancer. Extensive crosstalk exists between the mTOR and MAPK pathways; both pathways can be activated by the same receptor tyrosine kinases, dependent on the triggering ligand, and the pathways intersect at multiple points to regulate and coordinate signalling flux. Nodes in these pathways that are key therapeutic targets in NENs include receptor tyrosine kinases that can be targeted with monoclonal antibodies and multikinase inhibitors, and mTOR, which can be targeted with rapalogs. Expression of PTEN is often lost through genetic aberrations of PTEN. Kidd, M. et. al. (2016) Towards a new classification of gastroenteropancreatic neuroendocrine neoplasms Nat. Rev. Clin. Oncol. doi: /nrclinonc

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