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Establishment and Characterization of Small Bowel Neuroendocrine Tumor Spheroids
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PI(3)K-Akt-mTOR pathway as a potential therapeutic target in neuroendocrine tumors

Kathrin Zitzmann1, George Vlotides2, Burkhard Göke3

  • 1a Department of Internal Medicine II - Grosshadern, Ludwig-Maximilians- University of Munich, Marchioninistr. 15, 81377 Munich, Germany. kathrin.zitzmann@med.uni-muenchen.de.

Expert Review of Endocrinology & Metabolism
|February 16, 2019
PubMed

Insights

Hyperactive PI3K-Akt-mTOR signaling drives neuroendocrine tumor (NET) growth and survival. Targeting this pathway with novel kinase inhibitors shows promise for NET treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Constitutive activation of the PI3K-Akt-mTOR pathway is common in human cancers, including neuroendocrine tumors (NETs).
  • In gastroenteropancreatic NETs, this hyperactivation is linked to tumor-suppressor gene mutations (e.g., PTEN) and autocrine growth factor loops.
  • This signaling pathway promotes tumor cell proliferation and resistance to apoptosis.

Purpose of the Study:

  • To review the role of PI3K-Akt-mTOR signaling in NET pathogenesis.
  • To summarize current knowledge on therapeutic strategies targeting the PI3K-Akt-mTOR pathway in NETs.

Main Methods:

  • Literature review of studies on PI3K-Akt-mTOR signaling in NETs.
  • Analysis of molecular mechanisms driving pathway activation.
  • Evaluation of preclinical and clinical data on targeted therapies.

Main Results:

  • PI3K-Akt-mTOR pathway dysregulation is a key feature of NETs, contributing to uncontrolled cell growth.
  • Novel small-molecule inhibitors targeting kinases in this pathway have demonstrated significant anti-tumor effects.
  • Targeted therapies offer new avenues for managing NET disease.

Conclusions:

  • The PI3K-Akt-mTOR pathway is a critical therapeutic target in NETs.
  • Targeted inhibition of this pathway holds significant potential for improving patient outcomes in NET disease.
Keywords:
PI(3)K–Akt–mTOR signalingapoptosis resistancegrowth factorskinase inhibitorsneuroendocrine tumorproliferationreceptor tyrosine kinasetargeted therapy

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