Correlation between VEGF expression and angiogenesis in breast carcinoma.

OBJECTIVE: To analyze the role of vascular endothelial growth factor (VEGF) secreted by tumor cells in angiogenesis of breast carcinoma using image morphometry. STUDY DESIGN: Thirty-four cases of node-negative breast carcinoma were used in the study. There were 6 grade 1, 20 grade 2 and 8 grade 3 tumors. For each case, 2 consecutive sections from the same block were cut. Immunostaining for VEGF and CD31 was carried out, and areas of highest staining density were marked. Those marked "hot spots" for CD31 and VEGF for each case were subsequently compared morphometrically. The area and intensity of immunostaining on each slide were also scored. RESULTS: The total scores for VEGF and CD31 were 5.15 and 3.79, respectively. All 34 cases showed cytoplasmic positivity for VEGF within the tumor cells. The average number of hot spots for VEGF and CD31 were 2.41 and 2.47, respectively, and the average number of hot spots that matched between these 2 groups were 0.79. Statistical analysis using Pearson's coefficient of correlation showed no significant match between the hot spots for CD31 and VEGF. Also, there was no significant difference between the total scores of CD31 and VEGF. CONCLUSION: VEGF is expressed in most breast carcinomas. However, the lack of topographic correlation between microvessel density and VEGF expression supports the notion that multiple angiogenic factors may play a role along with VEGF in the angiogenic process.

Effective human defense against E. histolytica: high amoebicidal activity of lymphocytes and monocytes in amoebic liver abscess patients until 3 months follow-up.

Adherence of pathogenic Entamoeba histolytica trophozoites mediated by Gal/GalNAc lectin is a prerequisite for killing naïve T cells and monocytes but the activated T cells and monocyte derived macrophages (MDMs) not only resist the attack but can kill the parasite. In the present study, we have analysed the adherence and cytotoxicity of the immunecompetent cells from patients of amoebic liver abscess at the time of their diagnosis and after 3 months to elucidate the development of cell mediated cytotoxicity, a major mechanism of resistance to amoebic infection. The results show that CD3+ cells from amoebic liver abscess cases, when stimulated, in vitro, bound E. histolytica trophozoites with increased intensity and their viability was also increased. The activated lymphocytes (taken at 3 months post treatment) were also able to kill amoebae. MDMs bound amoebae with greater intensity than lymphocytes, until 3 months post infection. These MDMs were effective in killing approximately 40% amoebae which was significantly less than at the time of diagnosis but was very significant as compared to the controls. The data suggest that cell mediated cytotoxic responses are maximum until 1 month post treatment and are significantly reduced thereafter.