Lung cancer is a very common malignancy with a low five-year survival rate. Artificial olfactory sensor (electronic nose) is a tool that recently has been studied as a probable optimal screening tool for early detection of lung cancer, but still no statistical method has been put forward as the preferable one. The aim of the study was to explore the use of logistic regression analysis (LRA) to analyse patients' exhaled breath samples with electronic nose in order to differentiate lung cancer patients (regardless of the stage of the cancer) from patients with other lung diseases and healthy individuals. Patients with histologically or cytologically verified, untreated lung cancer, patients with other lung diseases such as benign lung tumors, chronic obstructive pulmonary disease, asthma, pneumonia, etc, and healthy volunteers were enrolled in the study, in total 252 cancer patients and 223 patients without cancer. Breath sample collection and analysis were performed with Cyranose 320 sensor device and data further analysed using LRA. The LRA correctly differentiated lung cancer patients from no-cancer patients. The overall sensitivity in detecting patients having cancer was 95.8% for smokers and 96.2% for non-smokers and the overall specificity was 90.6% for non-smokers and 92.3% for smokers. Exhaled breath analysis by electronic nose using LRA is able to discriminate lung cancer patients from patients with other lung diseases and from healthy individuals.

Lung cancer is one of the most common malignancies and has a low 5-year survival rate. There are no cheap, simple and widely available screening methods for the early diagnostics of lung cancer. The aim of this study was to determine whether analysis of exhaled breath with an artificial olfactory sensor using support vector analysis can differentiate patients with lung cancer from healthy individuals and patients with other lung diseases, regardless of the stage of lung cancer and the most common comorbidities. Patients with histologically or cytologically verified lung cancer, healthy volunteers and patients with other lung diseases (e.g. chronic obstructive pulmonary disease (COPD), asthma, pneumonia, pulmonary embolism, benign lung tumors) were enrolled in the study. Breath sample collection and analysis with a Cyranose 320 sensor device was performed and data were further analyzed using a support vector machine (SVM). The SVM correctly differentiated between cancer patients and healthy volunteers in 98.8% of cases. The cancer versus non-cancer group patients (healthy volunteers and patients with other lung diseases) were classified correctly by SVM in 87.3% of cases. In the mixed diagnosis groups (only cancer, only COPD, cancer + COPD and control) all 79 out of 79 patients were predicted correctly in the cancer + COPD group, with the rate of correct prognosis in other patient groups being lower. Exhaled breath analysis by electronic nose using a SVM is able to discriminate patients with lung cancer from healthy subjects and mixed groups of patients with different lung diseases. It can also provide a certain level of discrimination between lung cancer patients, lung cancer patients with concomitant COPD, COPD alone and a healthy control group.

CD4+CD25+ FOXP3-positive T-regulatory cells have an important role in controlling immune and inflammatory reactions. The present authors hypothesise that these cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). The aim of the present study was to characterise the expression of FOXP3 in large and small airways of nonsmokers, smokers with normal lung function and COPD patients.A total of 19 nonsmokers, 20 smokers with normal lung function and 20 smokers with moderate COPD, undergoing lung resection for a solitary peripheral nonsmall cell carcinoma, were enrolled in the study. Immunohistochemical methods were used to evaluate FOXP3 expression in large and small airways.Smokers with normal lung function and COPD patients had increased numbers of FOXP3-positive cells in large airways compared with nonsmokers. A positive correlation was observed between FOXP3 expression in large airways and smoked pack-yrs. In small airways, COPD patients had decreased numbers of FOXP3-positive cells, compared with asymptomatic smokers and nonsmokers, that negatively correlated with airflow obstruction.To conclude, chronic obstructive pulmonary disease is characterised by upregulation of FOXP3-positive cells in large airways but a downregulation in small airways that correlated with airflow limitation. The results of the present study contribute to a better understanding of the pathogenesis of chronic obstructive pulmonary disease.

Background: Chronic obstructive pulmonary disease (COPD) is characterised by progressive and irreversible airway obstruction. Smoking causes persistent inflammation in lung tissue. However, differences in inflammatory responses between the large and small airways have not been systematically explored among smokers with and without COPD. Objectives: The aim of our research was to characterise the expression and localisation of NF-ĸBp65 and histone deacetylase 2 (HDAC2) as well as inflammatory cell (macrophages, lymphocytes, neutrophils) distribution in large and small airways, in nonsmokers and in smokers with and without COPD. Methods: Nineteen nonsmokers, 20 smokers with normal lung ventilation function and 20 smokers with moderate COPD, undergoing lung resection for a solitary peripheral carcinoma, were enrolled in the study. Immunohistochemical methods were used to evaluate NF-ĸBp65 and HDAC2 expression and identify inflammatory cells in airways. Results: COPD patients had increased NF-ĸBp65 expression compared to nonsmokers and smokers without COPD, in both large and small airways, which corresponded to increased numbers of macrophages, CD8+ T lymphocytes and neutrophils. COPD patients had more macrophages in large compared to small airways and more CD8+ T lymphocytes and neutrophils in small compared to large airways. HDAC2 expression was significantly downregulated in smokers with COPD in small compared to large airways. Conclusions: Our findings indicate a nonuniform distribution of inflammatory cells throughout the bronchial tree. However, in both smokers with and without COPD, similar patterns of inflammatory processes occur in both large and small airways. The difference between smokers with and without COPD is only quantitative.