Growing body of evidence suggests that molecular markers are an important prognostic marker for non-small lung cancer (NSCLC). Using targeted therapy based on these markers leads to improved outcomes in lung adenocarcinoma. However, progress of targeted therapy in squamous lung cancer is still modest. p16(ink) protein acts as tumor suppressor and vascular endothelial growth factor (VEGF) promotes tumor angiogenesis. Purpose of this study was to evaluate the difference in p16(ink4) and VEGF expression between squamous and adenocarcinoma of the lung; to evaluate the relationship of p16(ink4) and VEGF expression to survival outcomes in NSCLC patients, and the difference of their prognostic values between squamous and adenocarcinoma subtypes. 100 NSCLC patients (50 squamous and 50 adenocarcinoma) and 80 healthy individuals were included. p16(ink4) and VEGF proteins were immunohistochemicaly detected on formalin-fixed tissues. One- and 2-year progression-free survival (PFS) and overall survival (OS) were observed. p16(ink4) expression was significantly lower in squamous type compared to adenocarcinoma. In both squamous and adenocarcinoma, high VEGF expression correlated with worse 1-year PFS and OS, but only with worse 2-year PFS. Low p16(ink4) expression correlated with worse 1- and 2-year PFS, as well as OS, in both NSCLC subtypes. In squamous lung cancer p16(ink4) expression was an independent negative prognostic marker. Our study confirms the difference of p16(ink4) protein expression in squamous and adenocarcinoma of the lung. Besides anti-VEGF therapy, the regulation of p16(ink4) expression could have a therapeutic potential in NSCLC, especially in squamous lung cancer.

Background Recommended by Resolution of Immunotherapy, issued by EAACI, Specific immunotherapy (SIT) was established as a mainstream method of treating allergic diseases. SIT produces long term challenges. SIT team should be aware that at first injection of allergen, the immunotherapy may cause a long lasting reaction. Anaphylaxis during SIT is very rare, but it is possible. We’ve experienced anaphylaxis after four year of SIT, against ragweed allergen.

Molecular regulatory mechanisms of lung cancer initiation and progression are poorly understood. Role of micro RNA (miRNA) 19a in lung cancer is still controversial, as well. Treatments of non-small-cell lung cancer (NSCLC), particularly of the squamous subtype are limited. However increasing evidence point many molecular markers as potential prognostic and therapeutic tools. Purpose of this study was to evaluate differences in miR-19a, as well as miR-126 and let-7b expression profiles between NSCLC tumor tissue and healthy lung tissue. Also, the purpose was to evaluate the relationship of miR-19a, miR-126 and let-7b expression to survival outcomes in NSCLC patients but to evaluate the differences of their prognostic values between squamous and adenocarcinoma subtypes. 50 non-small lung cancer patients (32 squamous and 18 adenocarcinoma) and 45 healthy individuals were included. miRNA expression was detected by quantitative real-time polymerase chain reaction. Microvascular density was immunohistochemicaly quantified by factor VIII-related antigen. One- and two-years survival outcomes were observed. Expression of anti-angiogenic miR-19a, miR-126 and let-7b were significantly lower in tumour tissue compared to control lung tissue. Low miRNAs expression correlated with worse progression-free survival in both squamous and adenocarcinoma of the lung. Poor overall survivals were associated with low miRNAs expression only in the squamous lung cancer. Besides miR-126 and let-7b, our observations confirm also anti-angiogenic role of miR-19a in NSCLC patients and suggest the potential new target therapy in squamous lung cancer.

BACKGROUND: Pulmonary embolism (PE) is many times life treating disease, and the diagnosis should be achieved as soon as possible. Presence of fever may be or not present at the start of PE. Haemoculture should be performed any time if PE is linked with fever. It is very important to check out any symptom and sign of PE. D-dimmer may only exclude the diagnosis, but for this purpose it is very important. AIM: To analyze the most important predictors for clinical course and outcome of septic or no septic PE: METHODS: Patients with PE treated in Department of Pulmology in General Hospital Tesanj. PE was considered if Geneve score was five points or more. For any patient CT scan of the chest, chest X-ray at admission, and 4th, 7th and 14th day of hospitalization. Lactat-dechidrogenase, Creatin-kinase, CRP, D-dimmer, ECG and blood gas analyzes were performed, so. RESULTS: During one year of follow up 36 patients were considered for PE, according to Geneve score, among them 11 with septic embolie. In patients with no septic PE no changes on control Chest X-ray were seen, but in any of septic ones X-ray appearance showed progression. Other parameters were nearly the same, with moderate higher level of CRP in PE. The gold standard for diagnosis of PE rest double scintigrafic imaging of the lung, with ventilation and perfusion phase. D-dimmer is very useful parameter to exclude if PE is not occurred. CONCLUSION: The most important parameter to distinguish septic or no septic PE was dynamic changes of chest X-ray appearance with substantial more progression in septic than in non septic ones.

Objective: The primary goal of this study was to determine the difference of abundance of CD4+, CD8+ and CD56+ bronchoalveolar fluid’s lymphocytes and their subpopulations between cancerous lung and healthy lung from the same patient. Methods: Mini-bronchoalveolar lavage was taken from 55 patients from lung with cancer and healthy lung. After laboratory processing and addition of CD4, CD8, CD27, CD28 and CD56 antibody, the material was analyzed by flow cytometer. Results from lung with cancer were compared to the ones from the healthy lung. The examined patients were the test and the control group at the same time. Results: CD27+28+ forms of CD4+ and CD8+ lymphocytes are more activated in the cancerous lung compared to healthy lung, while the CD27-28- forms are less activated in diseased lung. CD4+ forms of CD56+ lymphocytes are more activated in cancerous lung compared to the health lung, while the CD8+ forms are less activated in diseased lung. Conclusion: Immature helper and cytotoxic T lymphocyte response, as well as regulatory NK and NKT cell response are more activated in cancerous lung compared to the health lung of the same patient.