J Cancer 2018; 9(6):1096-1105. doi:10.7150/jca.23909 This issue
1. Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, 250021, China;
2. Department of Cardiac Surgery, The First Hospital Affiliated to Jiamusi University, Jiamusi, Heilongjiang, 154002, China;
3. Provincial Key Laboratory on Molecular and Chemical Genetic, Second Hospital of Jilin University, Changchun, 130041, Jilin, China;
4. Department of Thoracic Surgery, Second Hospital of Jilin University, Changchun, 130041, Jilin, China;
5. Department of Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning, 110003, China.
6. Department of Genetics, University of Alabama at Birmingham, Birmingham, Alabama, 35294, USA;
7. Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, Alabama, 35294, USA.
Targeted therapies based on EGFR mutations or on the ALK fusion oncogene have become the standard treatment for certain patients with lung adenocarcinoma (LUAD). However, most LUAD patients have no EGFR mutation or ALK fusion, and their oncogenetic alterations remain to be characterized. Here we conducted an integrated analysis of public datasets to assess the genomic alterations of 23 highly lung cancer-associated genes. The copy numbers of these genes were measured in ten micro-dissected, paired tumors and normal lung tissues of LUAD patients without EGFR mutations or ALK fusion. The copy numbers of PTEN, RB1, HMGA2, and PTPRD were lower in tumors compared with those for normal tissues. Although there were reduced mRNA levels of PTEN and RB1 in tumors, there was a correlation between copy number and expression only for PTEN. In addition, analysis of the copy number alterations of these 23 genes revealed correlations between EMSY/CCND1, EMSY/PIK3CA, CCND1/CDKN2A, and CCND1/PIK3CA. Our exploration of integrated copy number and gene expression analysis gives priority to the PTEN-PIK3CA and RB1-CCND1 pathways in developing therapeutic strategies for LUAD patients without EGFR mutations or ALK fusion.
Keywords: Lung adenocarcinoma, Oncogenomic profiling, Genetic alteration, PTEN, RB1