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PIK3CA Mutation Analysis in Iranian Patients with Gastric Cancer

Mostafa Iranpour1, Mahyar Nourian1, Sana Saffari2

  • 1AJA Cancer Epidemiology Research and Treatment Center (AJA-CERTC), AJA University of Medical Sciences, Tehran, Iran.

Iranian Biomedical Journal
|April 30, 2018
PubMed
Abstract

Insights

Eleven percent of gastric cancer patients harbor PIK3CA mutations, linked to lymphatic invasion but not survival. Further research is needed to identify patients eligible for PI3K/AKT/mTOR pathway targeted therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Aberrant activation of the PI3K/AKT/mTOR pathway is crucial in gastric cancer progression.
  • Targeted therapies like AZD5363 show selective efficacy in PIK3CA-mutant gastric cancer.
  • Assessing PIK3CA mutations is essential for personalized treatment strategies.

Purpose of the Study:

  • To evaluate the frequency of PIK3CA mutations in gastric cancer patients.
  • To investigate the association between PIK3CA mutations and clinicopathological features, including lymphatic invasion.
  • To determine the impact of PIK3CA mutations on overall survival.

Main Methods:

  • Analysis of 100 gastric cancer patients who underwent surgical resection.
  • Evaluation of PIK3CA mutations in codon 1047 using tetra-primer ARMS-PCR and direct sequencing.
  • Kaplan-Meier analysis for overall survival assessment.

Main Results:

  • PIK3CA mutations (p.H1047R and p.H1047L) were detected in 11% of patients.
  • A significant association was observed between PIK3CA mutations and lymphatic invasion.
  • No significant difference in overall survival was found between mutated and non-mutated groups.

Conclusions:

  • Gain-of-function mutations in PIK3CA exon 20 occur in 11% of gastric cancer patients.
  • Further investigation into other PIK3CA regions is warranted to identify more patients for targeted therapy.
  • These findings highlight the importance of molecular profiling for guiding gastric cancer treatment.
Keywords:
MutationPhosphatidylinositol-3 kinasesSomach neoplasms

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