scholarly journals LUNG INFLAMMATION, EMPHYSEMA, AND LUNG CANCER DEVELOPMENT IN A/J MICE IN RESPONSE TO CHRONIC EXPOSURE TO AEROSOL FROM A HEATED TOBACCO PRODUCT AND CIGARETTE SMOKE

Respirology ◽  
2018 ◽  
Vol 23 ◽  
pp. 41-41
Keyword(s):  
Lung Cancer ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Chronic Exposure ◽  
Tobacco Product ◽  
Cancer Development

scholarly journals Chronic exposure to cigarette smoke leads to activation of p21 (RAC1)-activated kinase 6 (PAK6) in non-small cell lung cancer cells

Oncotarget ◽  
2016 ◽  
Vol 7 (38) ◽  
pp. 61229-61245 ◽  
Author(s):  
Remya Raja ◽  
Nandini A. Sahasrabuddhe ◽  
Aneesha Radhakrishnan ◽  
Nazia Syed ◽  
Hitendra S. Solanki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cigarette Smoke ◽  
Cell Lung Cancer ◽  
Chronic Exposure ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung

scholarly journals Urinary Levels of Cigarette Smoke Constituent Metabolites Are Prospectively Associated with Lung Cancer Development in Smokers

2011 ◽  
Vol 71 (21) ◽  
pp. 6749-6757 ◽  
Author(s):  
Jian-Min Yuan ◽  
Yu-Tang Gao ◽  
Sharon E. Murphy ◽  
Steven G. Carmella ◽  
Renwei Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cigarette Smoke ◽  
Cancer Development ◽  
Urinary Levels

scholarly journals Exposures to 2,4-Dichlorophenoxyacetic acid with or without endotoxin upregulate small cell lung cancer pathway

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Geetika Kaur ◽  
B. V. Sunil Kumar ◽  
Baljit Singh ◽  
R. S. Sethi
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Lung Inflammation ◽  
Low Dose ◽  
Small Cell ◽  
Dichlorophenoxyacetic Acid ◽  
Small Cell Lung ◽  
Qrt Pcr ◽  
Histological Score ◽  
2,4 Dichlorophenoxyacetic Acid

Abstract Background Pesticide residues in food and environment along with airborne contaminants such as endotoxins pose health risk. Although herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) has been associated with increased risk of lung cancers such as small cell lung cancer (SCLC) among agricultural workers, there are no data on the SCLC signaling pathway upon 2,4-D exposure without LPS or in combination with endotoxin. Methods We exposed Swiss albino mice (N = 48) orally to high (9.58 mg kg− 1) and low (5.12 mg kg− 1) dosages of 2,4-D dissolved in corn oil for 90 days followed by E. coli lipopolysaccharide (LPS) or normal saline solution (80 μl/animal). Lung samples and broncho-alveolar fluid (BALF) were subjected to Total histological score (THS) and total leucocyte count (TLC) and differential leucocytes count (DLC) analyses, respectively. We used microarray and bioinformatics tools for transcriptomic analyses and differentially expressed genes were analyzed to predict the top canonical pathways followed by validation of selected genes by qRT-PCR and immunohistochemistry. Results Total histological score (THS) along with BALF analyses showed lung inflammation following long term dietary exposure to high or low doses of 2,4-D individually or in combination with LPS. Microarray analysis revealed exposure to high dose of 2,4-D without or with LPS upregulated 2178 and 2142 and downregulated 1965 and 1719 genes, respectively (p < 0.05; minimum cut off 1.5 log fold change). The low dose without or with LPS upregulated 2133 and 2054 and downregulated 1838 and 1625 genes, respectively. Bioinformatics analysis showed SCLC as topmost dysregulated pathway along with differential expression of Itgb1, NF-κB1, p53, Cdk6 and Apaf1. Immunohistological and quantitative real time PCR (qRT-PCR) analyses also supported the transcriptomic data. Conclusions Taken together, the data show exposures to high and low dose of 2,4-D with/without LPS induced lung inflammation and altered pulmonary transcriptome profile with the involvement of the SCLC pathway. The data from the study provide the insights of the potential damage on lungs caused by 2,4-D and help to better understand the mechanism of this complex relation.

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