Diagnosis Of Non-smoking Peripheral Lung Adenocarcinoma By Bronchial Epithelial Cell Genomic DNA Copy Number Variation

Diagnosis of Non-smoking Peripheral Lung Adenocarcinoma by Bronchial Epithelial Cell Genomic DNA Copy Number VariationLung Adenocarcinomas incidence are increasing。Peripheral lung Adenocarcinoma (PLAd) is difficult pclinically。Effective and easy means to differentiate PLAd is not always available. Field cancerization exists in airway epithelial cells, and a series of molecular changes in the airway epithelial cells showed useful in the differential diagnosis of lung cancer. Such researches in non-smoking lung cancer patients are rare. In this study, array comparative genomic hybridization (Array-CGH) was performed on the bronchial epitherial cells of non-smoking patients with peripheral lung adenocarcinoma (NSPLAd) and patients with benign peripheral disease (PBPD),to identify the DNA copy number variation(CNV) profiles that specially related with NSPLAd and PBPD patients, respectively. From these, a set of gain or loss genes/regions could be identified to distinguish the two disease.The 32 bronchial epithelial cells (including the contralateral bronchial epithelial cells-1s and ipsilateral primary bronchial epithelial cell-2s) derived from 16patients (11 NSPLAd and 5 PBPD)were screened by Agilent Human Genomic CGH 44B array.With analyses by Agilent CGH Analytics 4.0 and GeneSpring GX 11.0.1, the genome-wide CNV profiles of bronchial epithelial cells were obtained.11 NSPLAds showed good accordance in regions of CNV. There were 15 copy number alterations with a frequency of more than 45% in 1s and 10 copy number alterations with a frequency of more than 50% in the NSPLAd. NSPLAd patients showed a much larger scale, much higher frequence in CNV. than PBPD. Bioinformatical analysis was performed with the array CGH data of the 32cases, and 34 genes that could differentiate NSPLAd from PBPD were screened out.In conclusion, data obtained from a reliable array CGH analysis indicated that there were a series of differences in the genome-wide CNV profiles in the bronchial epithelial cells of the NSPLAd from PBPD. It was promised to build up a molecular model to distinguish NSPLAd from PBPD with bronchial epithelial cells, by further invegestion with an enlarged sample size.