Abstract 307P
Background
Several epidemiological and experimental studies suggest that the etiology of many chronic illnesses is caused by the joint effect between genetics and the environment. Smoking tobacco is the major hazard feature for lung cancer in Indian subcontinent especially men, compare to woman where, other important risk factors i.e., exposure to agents and level of pollutions are responsible. So, the aim of the study is to compare the expression level of transcript-based biomarkers IDH1, CEA, Cyfra21-1, and TPA in NSCLC fifty tumor tissue stage IIIa patients compared to control benign tissues of smokers and non-smokers cases living in areas with air quality categorized as poor (AQI 201–300) or moderate (AQI 101–200).
Methods
Total RNA was isolated from 50 to 100 mg of surgical removed lung tissue. RNA samples showing clear separation of the 28S and 18S bands in a 1% denaturing gel and A260/A280 absorption ratios greater than 1.8 were further analyzed. First strand cDNA was synthesized from total RNA. Primers Sequences of the Transcripts IDH1, TPA, CEA, Cyfra21-1 and β-actin using were designed for expression study. The expression data was normalized and log transformed prior to theanalysis. The aim of the analysis was to identify differentially expressed genes between groups (e.g. smoker vs. non-smoker etc.).
Results
The study inferred that the level of expression of the transcripts IDH1, CEA, TPA and Cyfra21-1, in smokers were observed significantly up-regulated in tumor tissues compared to control benign tissues,the fold change increase of IDH1 and CEA was highest in CS-poor/moderate AQI, followed by non-smokers-poor AQI and non-smokers moderate AQI. This indicates the aggressiveness and poor prognosis in CS living in either poor or moderate AQI areas. The level of Cyfra21-1 was lower in in the CS groups in comparison to non-smokers in the poor AQI area. This suggest higher Lung cancer in non-smokers living areas with poor AQI.
Conclusions
Hence, we conclude that poor air quality can be as injurious for lung cancers as chronic smoking, the geneto-environmantal study can be helpful for a strong message to society toward the use of tobacco and pollution levels.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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