utility of survivin mRNA as a diagnostic biomarker in lung cancer with malignant pleural effusion

The sensitivity of conventional cytology for the detection of malignant cells in pleural effusion is insufficient. Since survivin is frequently overexpressed in lung cancer, it might play a role in oncogenesis and progression of the tumor. To evaluate diagnostic value of survivin mRNA expression in lung cancer with pleural effusion. Sixty-five pleural fluid specimens were collected from lung cancer patients [group I]. Twenty benign pleural fluid specimens were also collected [group II], considered to be control group, and this group was classified into transudate and exudate according to Light's criteria. Real time Polymerase chain reaction [RT-PCR] was performed to detect the survivin mRNA expression in the pleural fluid specimens. The sensitivity, specificity and accuracy were calculated by using receiver operating characteristic [ROC] analysis. Sixty-five pleural fluid specimens from lung cancer patients were tested by RT-PCR, only 30/65 [46%] had positive cytology. The positive rate of survivin mRNA expression in maligant pleural effusion [63/65; 95.38%] was much higher than that in the pleural effusion with benign disease [4/20; 20%, P < 0.01]. Twenty-seven cancer patients were negative for cytology and 24/27 were positive for survivin mRNA expression. The sensitivity, specificity and accuracy of survivin were 89.5%, 50%, 73.1% for diagnosing malignant pleural effusion. The detection of survivin by RT-PCR seems to be a promising assay to diagnose malignant pleural effusions, using the appropriate cut-off point, survivin mRNA has a significant role in differentiating benign from malignant pleural effusion

level of bronchoalveolar lavage fluid prostaglandine E2; is it diagnostic of bronchogenic carcinoma?

Lung cancer is the leading cause of cancer-related mortality in the United States. Cigarette smoking is the number one risk factor for lung cancer. It causes about 90% of lung cancers [14]. Evaluation of bronchoalveolar lavage level of PGE2 in patients with primary bronchogenic carcinoma. The study was conducted on forty subjects; including twenty patients with bronchogenic carcinoma, ten patients with non-malignant lesions, and ten healthy control subjects. All subjects were submitted to fiberoptic bronchoscopy with bronchoalveolar lavage was done and examined for prostaglandin E2. The PGE2 level was significantly higher in BALF of group III [malignant group] compared to group I and II, with no significant difference between group I and group II. The cut- off value of PGE2 was 45.63 pg/ml with minimal overlap between malignant and benign lesions. Bronchoalveolar lavage level of PGE2 was significantly increased in patients with bronchogenic carcinoma

Effect of a disintegrin and metalloprotease 33 [ADAMSS] gene polymorphisms and smoking in COPD

COPD is characterized by air flow limitation that is not fully reversed and associated with an influx of neutrophils, macrophages and CD8 T lymphocytes in the airways. The disease is characterized by airflow limitation and is associated with an abnormal inflammatory response of the lungs in response to noxious particles or gases and associated with systemic manifestation. Sixty consecutive patients with COPD and 40 normal healthy individuals were included. All cases and controls were subjected to detection of 2 polymorphic loci [S1 AND Q1] of ADAM33 by PCR-RFLP technique. The percentage of S1 and Q1 AA genotype and A allele were significantly increased in control than in COPD patients while there was significant increase in S1 and Q1 GG genotype and G allele in COPD patients than in control [p < 0.001]. No significant difference was found between smoker and non-smoker among the two studied groups in genotype and alleles distribution of ADAM33 SNPs S1 and Q1 p > 0.05, whereas there was significant increase in ADAM33 S1 G allele and Q1 G allele in smoker and non-smoker in COPD patients as compared to their corresponding fellows in control group [p < 0.05]. As regard to Pulmonary function test there was significant decrease in% of FEV1 in COPD patients as compared to control group for both smokers and non-smokers [p < 0.001]. Within both control and COPD groups smokers had significant decrease in FEV1% as compared to non-smokers [p < 0.001]. There was a significant decrease in FEV1% among all genotypes in smoker as compared to non-smoker COPD patients [p < 0.001], the most prominent decrease was found in smoker GG genotype for both ADAM33 S1 and Q1 in COPD patients. In conclusion, we found that polymorphisms in the SNPs [Q1 and S1] of ADAM33 gene are associated with COPD in the general population. In addition, smoker patients with GG genotype in [S1 and Q1] ADAM33 will have more pronounced decline in the pulmonary function test [FEV1]