Profiles of Endoglin and Vascular Endothelial Growth Factor Based on Staging and Histological Grading of Colorectal Cancer and Their Relationship with Bevacizumab Therapy

Abstract

Objective The present study evaluated the profile of endoglin (CD105) and vascular endothelial growth factor (VEGF) based on staging and histopathological grading of colorectal cancer as well as their relationship with bevacizumab therapy. Methods A total of 88 cases of colorectal adenocarcinoma were included in the present study. The levels of VEGF and CD105 protein were evaluated with enzyme-linked immunosorbent assay (ELISA). Results There was a significant difference in the level of CD105 (p = 0.002) between metastases and non-metastases subjects, showing that CD105 was higher in metastases subjects (4.59 ng/ml). There was no significant difference in the level of VEGF based on the presence of metastasis (p = 0.625). There was a significant difference in the levels of CD105 (p = 0.038) and VEGF (p = 0.010) between the subjects who received chemotherapy and those who did not. The CD105 level was higher in the subjects who received chemotherapy (4.43 ng/ml); conversely, the level of VEGF was lower in subjects who received chemotherapy (543.65 pg/ml). There was a statistically significant difference in the levels of CD105 (p = 0.003) and VEGF (p = 0.002) between subjects who received bevacizumab therapy and subjects who did not. The levels of CD105 were higher in subjects who received bevacizumab therapy (5.11 ng/ml); in contrast, the level of VEGF was higher in subjects who did not receive bevacizumab therapy (645.92 pg/ml). There was a significant positive correlation between CD105 and VEGF in subjects who did not receive bevacizumab (p < 0.01). Conclusion The results of this study support a hypothesis of “escape mechanism” in the failure of anti-angiogenesis therapy (anti-VEGF).

Endoglin (CD105) and proliferation index in recurrent glioblastoma treated with anti-angiogenic therapy

“…There is also evidence from other cancers, such as colorectal cancer, that treatment with BEV therapy elevates the levels of CD105, in comparison to patients not treated with this drug. Therefore, CD105 could be an intrinsic or adaptive escape mechanism to anti-angiogenic therapy (BEV) ( 25 ). Interestingly, TRC105, a chimeric antibody targeting CD105, seems to enhance the effect of bevacizumab in vivo ( 26 ).…”