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Integrated Oncogenomic Profiling of Copy Numbers and Gene Expression in Lung Adenocarcinomas without EGFR Mutations

Yanzhuo Luo1,2, Bingjin Li3, Guangxin Zhang4

  • 1Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, 250021, China.

Journal of Cancer
|March 28, 2018
PubMed

Insights

Most lung adenocarcinoma patients lack EGFR mutations or ALK fusions. This study identifies genomic alterations in these patients, highlighting PTEN-PIK3CA and RB1-CCND1 pathways for potential targeted therapies.

Area of Science:

  • Oncology
  • Genomics
  • Molecular Biology

Background:

  • Targeted therapies for EGFR mutations and ALK fusions are standard for some lung adenocarcinoma (LUAD) patients.
  • Most LUAD patients lack these specific alterations, necessitating characterization of their oncogenetic landscape.

Purpose of the Study:

  • To assess genomic alterations in 23 key lung cancer genes in LUAD patients without EGFR mutations or ALK fusions.
  • To explore correlations between copy number and gene expression for therapeutic target identification.

Main Methods:

  • Integrated analysis of public genomic datasets.
  • Measurement of copy numbers for 23 cancer-associated genes in paired tumor and normal LUAD tissues.
  • Analysis of gene expression and copy number alterations.

Main Results:

  • Lower copy numbers of PTEN, RB1, HMGA2, and PTPRD observed in tumors versus normal tissues.
  • Reduced mRNA levels for PTEN and RB1, with copy number-expression correlation only for PTEN.
  • Identified correlations between EMSY/CCND1, EMSY/PIK3CA, CCND1/CDKN2A, and CCND1/PIK3CA.

Conclusions:

  • The PTEN-PIK3CA and RB1-CCND1 pathways are prioritized for developing therapeutic strategies in LUAD patients lacking EGFR mutations or ALK fusions.
  • Genomic profiling is crucial for identifying novel therapeutic targets in LUAD subtypes.
Keywords:
Genetic alterationLung adenocarcinomaOncogenomic profilingPTENRB1

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