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Genetic deregulation of the PIK3CA oncogene in oral cancer

Avaniyapuram Kannan Murugan1, Arasambattu Kannan Munirajan, Nobuo Tsuchida

  • 1Department of Molecular Cellular Oncology and Microbiology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549, Japan. amuruga1@jhmi.edu

Cancer Letters
|April 20, 2013
PubMed

Insights

Genetic alterations in the PIK3CA gene are common in oral cancer, driving phosphatidylinositol 3-kinase (PI3K)/Akt pathway activation. Targeting PIK3CA and its downstream effectors offers potential for personalized oral cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is frequently dysregulated in human cancers.
  • PI3K signaling involves catalytic (p110α) and regulatory (p85) subunits; p110α is encoded by the PIK3CA gene.
  • PIK3CA gene alterations are prevalent in various cancers, including oral cancer.

Purpose of the Study:

  • To review genetic alterations (mutations, amplifications) of the PIK3CA oncogene in oral cancer.
  • To discuss the association of PIK3CA mutations with oral cancer, including ethnicity and disease stage.
  • To highlight the therapeutic potential of targeting PIK3CA and its downstream signaling pathways (Akt, mTOR) for oral cancer treatment.

Main Methods:

  • Literature review and critical analysis of existing studies on PIK3CA in oral cancer.
  • Examination of genetic alterations, including mutations and amplifications.
  • Discussion of pathway activation, oncogenicity, and clinical associations.

Main Results:

  • PIK3CA gene is frequently altered in oral cancer, leading to constitutive PI3K/Akt pathway activation.
  • PIK3CA mutations exhibit mutual exclusivity with other pathway genes and vary in incidence across ethnicities.
  • PIK3CA deregulation is linked to oral cancer progression and disease stage.

Conclusions:

  • Targeting the genetically deregulated PIK3CA oncogene is crucial for oral cancer therapy.
  • Downstream effectors Akt and mTOR represent potential molecular targets for PIK3CA-driven oral carcinogenesis.
  • Understanding PIK3CA alterations can facilitate early diagnosis and personalized treatment strategies for oral cancer.
Keywords:
HNSCCHead and neckOncogenePI3K/Akt signalingPIK3CA mutation and amplification

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