Cigarette smoke and increased COX-2 and survivin levels in exhaled breath condensate of lung cancer patients: how hot is the link?
One of the most current intriguing hypotheses on lung cancerogenesis envisages a role for inflammation as a possible trigger of both epithelial-mesenchymal transition and cancer development. Cigarette smoke has been suggested to be the main factor underlying the inflammation of the airways described in lung cancer patients. Cycloxygenase and survivin, a COX-2 dependent factor of apoptosis resistance, seem to play a key role in this regard.


OBJECTIVE
The aim of this study was to study COX-2 and survivin in the airways of lung cancer patients and in those of a group of smokers in a view to increasing our understanding of the link between smoking, airway inflammation and lung cancer.


METHODS
70 NSCLC patients (28 smokers, 26 ex-smokers and 16 non-smokers) and 30 healthy subjects (20 smokers and 10 non-smokers) were enrolled in the study. Both COX-2 and survivin concentrations were measured in the exhaled breath condensates of all the subjects under study using EIA kits.


RESULTS
Higher levels of exhaled survivin and COX-2 were found in NSCLC patients compared to healthy smokers and non-smokers. These levels were observed to be significantly elevated in smokers (patients with lung cancer and healthy) and ex-smokers compared to non-smokers and exhibited a positive correlation with the number of cigarettes smoked expressed as pack/year. A correlation was also found between exhaled COX-2 and survivin and the progression of cancer.


CONCLUSIONS
We support the hypothesis that cigarette smoke be strongly connected to the inflammation of the airways observed in lung cancer patients. On the basis of the results obtained the use of exhaled breath condensate COX-2 and survivin levels could be suggested as two potential markers within an early non-invasive screening of populations of smokers at risk of lung cancer.
Carpagnano
Giovanna E
GE
Institute of Respiratory Disease, Department of Medical and Occupational Sciences, University of Foggia, Foggia, Italy. ge.carpagnano@unifg.it
Spanevello
Antonio
A
Palladino
Grazia P
GP
Gramiccioni
Claudia
C
Ruggieri
Cinzia
C
Carpagnano
Francesco
F
Foschino Barbaro
Maria P
MP
D000368:Aged; D014408:Biomarkers, Tumor / Q000032:analysis / Q000378:metabolism*; D001944:Breath Tests; D002289:Carcinoma, Non-Small-Cell Lung / Q000175:diagnosis / Q000209:etiology*; D002471:Cell Transformation, Neoplastic / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000032:analysis / Q000378:metabolism*; D045853:Exhalation; D005260:Female; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins; D008175:Lung Neoplasms / Q000175:diagnosis / Q000209:etiology*; D008297:Male; D008869:Microtubule-Associated Proteins / Q000032:analysis / Q000378:metabolism*; D008875:Middle Aged; D011014:Pneumonia / Q000139:chemically induced* / Q000150:complications / Q000378:metabolism; D012907:Smoking / Q000009:adverse effects*; D000077022:Survivin
C107489:BIRC5 protein, human; D014408:Biomarkers, Tumor; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins; D000077022:Survivin; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human