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PTEN and PI3K/AKT in non-small-cell lung cancer

Cristina Pérez-Ramírez1,2, Marisa Cañadas-Garre1, Miguel Ángel Molina3

  • 1Pharmacogenetics Unit. UGC Provincial de Farmacia de Granada. Instituto de Investigación Biosanitaria de Granada. Complejo Hospitalario Universitario de Granada. Avda. Fuerzas Armadas, 2. 18014 Granada, Spain.

Pharmacogenomics
|November 12, 2015
PubMed

Insights

Non-small-cell lung cancer (NSCLC) patients with PTEN inactivation show resistance to EGFR-tyrosine kinase inhibitor therapy. This review explores PTEN/PI3K/AKT pathway alterations linked to NSCLC tumorigenesis and treatment resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Non-small-cell lung cancer (NSCLC) is a leading global cause of cancer mortality.
  • Activating EGFR mutations improve outcomes for NSCLC patients treated with tyrosine kinase inhibitors.
  • The PTEN/PI3K/AKT pathway is crucial for cellular functions and implicated in cancer development.

Purpose of the Study:

  • To review PTEN/PI3K/AKT pathway alterations in NSCLC.
  • To discuss how these alterations contribute to tumorigenesis.
  • To examine the role of this pathway in resistance to EGFR-tyrosine kinase inhibitors.

Main Methods:

  • Literature review of studies on NSCLC, EGFR mutations, and the PTEN/PI3K/AKT pathway.
  • Analysis of molecular mechanisms underlying pathway alterations and their functional consequences.
  • Synthesis of current knowledge on PTEN inactivation and treatment resistance.

Main Results:

  • PTEN inactivation is a key alteration in the PTEN/PI3K/AKT pathway in NSCLC.
  • Alterations in this pathway are associated with resistance to EGFR-tyrosine kinase inhibitor therapy.
  • These alterations impact cell growth, survival, and invasion, promoting tumorigenesis.

Conclusions:

  • The PTEN/PI3K/AKT pathway plays a significant role in NSCLC development and progression.
  • Understanding PTEN/PI3K/AKT alterations is critical for overcoming resistance to targeted therapies.
  • Targeting this pathway may offer new therapeutic strategies for NSCLC patients.
Keywords:
EGFRNSCLCPI3KPTENTKIpharmacogeneticsresistance

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