Expression of Endoglin and Vascular Endothelial Growth Factor as Prognostic Markers in Experimental Colorectal Cancer.

BACKGROUND/AIM: Endoglin (CD105) is a receptor for the transforming growth factor-beta 1 (TGFß1) with crucial role in vascular development and angiogenesis. Additionally, vascular endothelial growth factor (VEGF) overexpression has been associated with advanced stage and poor survival for several cancer types. These molecules have been shown to be useful markers for identifying proliferating endothelium involved in tumor angiogenesis, especially in patients with cancer at risk of developing metastases. The aim of this study was to evaluate the relationship between VEGF and endoglin expression in an experimental model of colorectal cancer, as well as to investigate the effect of cyclooxygenase-2 (COX2) inhibitors on tumor development incidence. MATERIALS AND METHODS: Colon cancer was induced with 1,2-dimethylhydrazine dihydrochloride (DMH). Celecoxib and diclofenac treatment was started simultaneously with DMH induction. Endoglin protein expression was performed using western blot analysis. VEGF plasma concentrations were measured by enzyme-linked immunosorbent assay. RESULTS: In histopathological evaluations, no pathological change was observed in control rats, while adenocarcinoma (62.5%), dysplasia (31.25%) and inflammation (6.25%) were detected in the group given DMH. In treatment groups, a marked decrease was observed in adenocarcinoma rate. Expression of endoglin protein was significantly elevated in the DMH group compared to controls (p<0.001). No statistically significant difference was noted between treatment groups and DMH group regarding endoglin expression but a decrease was detected in the celecoxib-treated groups. CONCLUSION: It was confirmed by histopathology and western blotting that COX2 inhibitors, particularly celecoxib, decrease the rate of disease and slow-down progression of existing CRC. These data show that endoglin expression may have an important role in tumor angiogenesis and predict of tumor invasion.

Efficacies of vitamin D and omega-3 polyunsaturated fatty acids on experimental endometriosis.

OBJECTIVE: The aim of this study was to investigate the effects of 1,25-dihydroxyvitamin-D3 (vitamin D) and omega-3 polyunsaturated fatty acids (omega-3 PUFA) on experimentally induced endometriosis in a rat model. MATERIALS AND METHODS: A prospective, single-blind, randomized, controlled experimental study was performed on 30 Wistar female rats. Endometriosis was surgically induced by implanting endometrial tissue on the abdominal peritoneum. Four weeks later, a second laparotomy was performed to assess pre-treatment implant volumes and cytokine levels. The rats were randomized into three groups: vitamin D group (42 µg/kg/day), omega-3 PUFA group (450 mg/kg/day), and control group (saline 0.1 mL/rat/day). These treatments were administered for 4 weeks. At the end of treatment, a third laparotomy was performed for the assessment of cytokine levels, implant volumes (post-treatment) and implants were totally excised for histopathologic examination. Pre- and post-treatment volumes, cytokine levels within the groups, as well as stromal and glandular tissues between the groups were compared. RESULTS: The mean post-treatment volume was statistically significantly reduced in the omega-3 PUFA group (p=0.02) and the level of the interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF) in the peritoneal fluid were significantly decreased at the end of treatment in the omega-3 PUFA group (p=0.02, p=0.03, and p=0.03, respectively). In the vitamin D group, only IL-6 levels were significantly decreased. In the histopathologic examination, the glandular tissue and stromal tissue scores of the implants were significant lower in the omega-3 PUFA group (p=0.03 and p=0.02). CONCLUSION: Omega-3 PUFA caused significant regression of endometriotic implants. Vitamin D has not been as effective as omega-3 PUFA on endometriosis.