ABSTRACT
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]
Subject(s)
Humans , Male , Female , Polymorphism, Genetic/genetics , Smoking/genetics , Pulmonary Disease, Chronic Obstructive/geneticsABSTRACT
The aim of this study was to analyze changes in autotoxin [ATX] [both enzyme activity and gene expression], metalloproteinase-9 [MMP-9] and p53 antibodies [Abs] serum levels in breast cancer patients and to correlate their results with various clinical, pathological features of breast cancer. Sixty female breast cancer patients [42 with lymph node [LN] metastasis and 18 without LN metastasis] were included in this study and subjected to determination of ATX [both activity by colorimetric method and gene expression by RT-PCR] and both p53 Abs and MMP-9 by ELISA technique. Our results showed that there were statistically significant differences between breast cancer patients with and without LN metastasis in all the studied parameters except for p53 Abs. ATX [both activity and gene expression] and the serum levels of both MMP-9 and p53 Abs, were significantly different between different stages and grades of breast cancer patients with increasing activity and levels from stage I to IV and from grade I to III. Only ATX [both activity and expression] was significantly different between patients with tumor size less than or more than 5. There was a highly significant correlation between ATX activity and gene expression. The present study suggested that ATX activity, MMP-9 and p53Abs could serve as useful and convenient prognostic and detection markers of metastasizing breast cancer. Also, ATX activity may be used as an index for increased ATX gene expression