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Targeting the PI3K/AKT/mTOR pathway: potential for lung cancer treatment

Haiying Cheng1, Marina Shcherba1, Gopichand Pendurti1

  • 1Montefiore Medical Center/Albert Einstein College of Medicine, Department of Oncology, 111 East 210th Street, NY 10467, USA.

Lung Cancer Management
|October 25, 2014
PubMed

Insights

The PI3K/AKT/mTOR pathway is often activated in non-small-cell lung cancer, driving cancer growth and drug resistance. This review covers pathway issues, new targeted drugs, and biomarkers for patient selection.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • The phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway is frequently dysregulated in non-small-cell lung cancer (NSCLC).
  • This pathway activation promotes tumor development and contributes to resistance against epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs).

Purpose of the Study:

  • To review the role of PI3K/AKT/mTOR pathway dysregulation in NSCLC.
  • To discuss novel targeted agents and potential predictive biomarkers for PI3K/AKT/mTOR pathway inhibition in lung cancer.

Main Methods:

  • Literature review of preclinical and clinical studies.
  • Analysis of pathway components, targeted therapies, and biomarker research in NSCLC.

Main Results:

  • The PI3K/AKT/mTOR pathway is a key driver of oncogenesis and acquired resistance in NSCLC.
  • Several targeted agents inhibiting pathway components are under investigation, but their clinical efficacy requires further definition.

Conclusions:

  • Targeting the PI3K/AKT/mTOR pathway presents a promising therapeutic strategy for NSCLC.
  • Identifying predictive biomarkers is crucial for patient selection and optimizing treatment outcomes with these novel agents.

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