Detection of cyclooxygenase-2 [COX-2] expression in non-small cell lung carcinoma. An immunohistochemical and computerized image analysis study

Lung cancer is the leading cause of cancer death all over the world. Evidence is accumulating to suggest that cyclooxygenase-2 [COX-2] is involved the pathogenesis and progression of some types of lung cancer. COX-2 is one of the novel targets under evaluation for non-small cell lung carcinoma [NSCLC] therapy and chemoprevention. The aim of the present study was to detect COX-2 expression in non-small cell lung carcinoma [NSCLC] and to determine its correlation with various clinic pathological parameters. The expression of COX-2 was assessed in 30 patients with NSCLC using immunohistochemistry, followed by quantitative assessment of the immunostaining using computerized image analysis. The present work was conducted on 30 patients with NSCLC: squamous cell carcinoma [15 patients], adenocarcinoma [10 patients], and undifferentiated large cell carcinoma [5 patients]. Overall, 70% of studied NSCLC expressed COX-2. 60% of squamous cell carcinoma [SCC], 80% of adenocarcinoma [ADC] and 80% of undifferentiated large cell carcinoma [ULCC] showed positive immunostaining for COX-2. No significant correlation was found between tumor histological type and each of frequency and degree of COX-2 expression [p=0.569 and p=0.094 respectively]. Though the expression of COX-2 increased with tumor grade, the relation between COX2 expression [both the frequency and degree of expression] and tumor grade was not significant [p=0.778 and p=0.247 respectively for SCC, and p=0.641 and p=0.067 respectively for ADC]. A statistically significant difference was found between node positive and node negative cases as regards the degree of COX2 expression [p=0.05]. No significant relationship was found between COX-2 expression and age and sex of patients, smoking and tumor stage. COX-2 is frequently overexpressed in NSCLC especially in adenocarcinoma and undifferentiated large cell carcinoma. Expression was higher in node-positive tumors and tended to increase with tumor grade, suggesting that COX-2 might play a role in the pathogenesis and/or progression of these tumors. COX-2 appears to be a potentially promising target for therapy and chemoprevention of NSCLC

study of expression of matrix metalloproteinase-1 [MMP-1] and tissue inhibitor of metalloproteinase-1 [TIMP-1] in inflammatory bowel disease

Extracellular matrix [ECU] degradation and remodeling are major features of inflammatory bowel disease [IBD]. Matrix metalloproteinase-1 [MMP-1] is an important enzyme in ECM degradation. Its activity is controlled by tissue inhibitor ofmetalloproteinase-1 [TIMP-1]. To study the expression of MMP-1 and TIMP-1 in intestinal biopsies of patients with IBD and to determine its correlation with the endoscopic and histological scores of inflammation. Immunohistochemistry was used to study the expression of MMP-1 and TIMP-1 in 30 patients with IBD [16 patients with ulcerative colitis [UC] and 14 patients with Crohn's disease [CD]]. In addition, a control group of 10 non inflamed intestinal biopsies from these patients was studied. A semi-quantitative [ordered] method based on both the degree of staining and the percentage of positive cells was used to score immunohistochemical results. 76.67% and 90% of the studied cases of IBD showed positive staining for MMP-1 and TIMP-1 respectively. The mean staining scores of both MMP-1 and TIMP-1 were significantly higher in IBD [3.27 +/- 2 and 3.6 +/- L61 respectively] than control [0.8+0.92 and 1.9+ and .88 respectively] [p=0.001 and p-0.004 respectively]. A significant correlation was found between MMP-1 and TIMP-1 expression [p<0.001]. The expression of both MMP-1 and TIMP-1 was higher in UC [3.38 +/- 1.93 and 3.63 +/- 1.71 respectively] than CD [3.14+2.14 and 3.57 +/- 1.56 respectively], yet the difference was not significant [p=0.8 and p=0.9 respectively]. A significant correlation was detected between both MMP-1 and TIMP-1 expression and each of histological score [p<0.001] and endoscopic score [p < 0.001] of inflammation. MMP-1 and TIMP-1 are overexpressed in the affected mucosa of IBD and their expression correlates with the endoscopic and histological scores of inflammation. Thus, MMP-1 and TIMP-1 are likely to play a major role in the process of tissue destruction and remodeling in IBD. MMP-1 inhibitor therapy may prove useful in modulation of mucosal inflammation and promotion of healing in IBD

Study of some micronutrients in patients with helicobacter pylori infection

Helicobacter pylon [HP] plays a fundamental role in gastric inflammation and gastric adenocarcinoma. A number of studies have suggested that HP infection may affect the homeostasis of different important micronutrients. Is to study iron, copper, selenium, vitamins A, E, and C in serum and gastric biopsies in patients with HP infection to clarify the effect of HP infection on the homeostasis of these micronutrients. This work included 35 patients, classified into two groups: group I consisted of 25 patients positive for HP as detected by rapid urease test, while group II consisted of 10 patients negative for HP. All patients had undergone esophagogastroduodenoscopy. Multiple antral biopsies were taken for rapid urease test, PCR for urease and Cag genes, and for histopathological examination. Trace elements were studied in serum as well as in gastric biopsies. Results showed that serum iron and serum ascorbic acid were significantly lower in group I than in group II [62. 5 +/- 10.5 versus 78.5 +/- 19.68 u micro/dl] [p=0.045] and [32.5 +/- 4.25 versus 115.5 +/- 29.8 mg/I] [p=0.0001] respectively. In gastric biopsies it was found thai copper, vitamin A and vitamin C were significantly lower in groupl than in group II [20.8 +/- 4.21 versus 28.6 +/- 7.98miicro g/mg [p=0.0098], 170. 6 +/- 2 and 6 versus 189.6+50.1 ug/gm [p=0.042], 422.6 +/- 49.8 versus 552.6 +/- 68.2 mg/gm] [p=0.01] respectively. Only tissue selenium was higher in group 1 than in group 11[20.3 +/- 3.98 versus 14.65 +/- 2.98 micro g/gm] [p=0.01]. HP infection is associated with disturbed metabolism of iron, copper, selenium, vitamin A and vitamin C. Moreover, the progression of HP pathological outcome from superficial gastritis to chronic atrophic gastritis is associated with disturbed homeostasis of some micronutrients, most notably vitamin C and selenium. This disturbance is more pronounced in patients with Cag positive strains than in Cag negative strains of HP

Immunohistochemical expression of survivin and Bcl-2 in prostatic adenocarcinoma

The present work was carried out to detect the expression of survivin and Bcl-2 in twenty cases of prostatic adenocarcinoma, and to determine its correlation with the different clinicopathologic parameters including age of the patient, serum prostate -specific antigen [PSA] level, clinical stage and Gleason score. Positive staining for both survivin and Bcl-2 was seen as brown cytoplasmic staining. A semiquantitative method based on both intensity and distribution of staining was used to score immunohistochemical positivity. 75% and 35% of the studied cases of prostatic adenocarcinoma showed positive staining for survivin and Bcl-2 respectively. 20% of cases showed concomitant expression of both survivin and Bcl-2. Expression of survivin alone was detected in 55% of cases, while 15% of cases expressed Bcl-2 only. No correlation was found between survivin and Bcl-2 expression [p=0.176]. A significant association was detected between survivin expression and the Gleason score of prostatic adenocarcinoma, where p=0.004. Another significant correlation was found between Bcl-2 expression and the tumor stage [p=0.007]. Overexpression of survivin and Bcl-2 in prostatic adenocarcinoma indicate their possible role in tumorigenicity and/or tumor progression. A definite correlation was found between survivin expression and the Gleason score of prostatic adenocarcinoma. In addition,a significant correlation was detected between Bcl-2 expression and tumor stage. Survivin and Bcl-2 may serve as targets for apoptosis-based therapy of prostatic adenocarcinoma