Endoglin (CD105) Expression in Endometrial Carcinoma

Abstract

Tumor angiogenesis plays an important role in tumor growth and metastasis. We evaluated endoglin (CD105) as an endothelial marker of angiogenesis in endometrial carcinoma (EC) and its prognostic significance. Fifty-five cases of EC, 10 cases of complex endometrial hyperplasia with atypia (CHA), and 10 cases of simple hyperplasia (SH) were immunohistochemically stained for endoglin, CD31, and vascular endothelial growth factor (VEGF). Positively stained microvessels (MV) were counted in densely vascular foci (hot spots) in a 400x field in each specimen. For VEGF, intensity of staining was scored on three-tiered scale. Results were correlated with other prognostic parameters using appropriate statistics. Endoglin staining demonstrated significantly more MV than did CD31 (mean 30.8 +/- 10.95 vs. 13.38 +/- 7.53, p < 0.001). There was a positive correlation of both endoglin and CD31 MV counts with tumor differentiation (p < 0.05) and the depth of invasion (p < 0.01). However, only endoglin counts correlated significantly with the presence of angiolymphatic invasion (p < 0.01), lymph nodes metastases (p < 0.01), and tumor stage (p < 0.001). VEGF expression in EC had a significant correlation with angiolymphatic invasion (p < 0.01) and lymph node status (p < 0.05) but not with other prognostic parameters. Endoglin and VEGF showed significant differences between CHA and SH (p < 0.001). Our study showed that endoglin, by staining the proliferating MV in EC, is a more specific and sensitive marker for tumor angiogenesis than is the commonly used pan-endothelial marker, CD31. Endoglin staining also had prognostic significance, with positive correlation with angiolymphatic invasion, lymph node metastases, and tumor stage.

Abnormal expression of Endoglin and its receptor complex (TGF-β1 and TGF-β receptor II) as early angiogenic switch indicator in premalignant lesions of the colon mucosa

“…As expected, we found overexpression of Endoglin protein in the endothelium of colon carcinoma tissue, positively correlated with disease progression. These results are in agreement with studies showing that the CD105 + -MVD value is a prognostic marker in colon carcinoma (41,(48)(49)(50), as well as in prostate (51), breast (52,53), kidney (54), esophageal (55,56), head and neck (57,58), uterus (59) and non-small cell lung cancers (60).…”

Endoglin (CD105) and vascular endothelial growth factor as prognostic markers in colorectal cancer

“…Endoglin stained small vessels with high sensitivity in or around the tumor, but the blood vessels in nonneoplastic tissue did not or only weakly stained with endoglin. This is in agreement with previous studies where endoglin was expressed mainly in proliferating blood vessels, while CD34 or CD31 stained all the blood vessels, 21,22,24,31 suggesting that endoglin is preferentially expressed in vessels undergoing neoangiogenesis. Endoglin is very selective for the blood vessel endothelium and reacts specifically with endothelial cells without significant staining of inflammatory or stromal cells within the neoplasm.…”

“…The endoglin antibody binds preferentially to the activated endothelial cells that participate in tumor angiogenesis, 22 but expression is weak/or negative in vascular endothelium of normal tissues. 23,24 Recently, several studies have examined endoglin expression in cancers of the endometrium, cervix and breast, 21,22,24 and found endoglin as a more specific and sensitive microvessel marker than other commonly used panendothelial antibodies.…”

Significant Expression of Endoglin (CD105), TGF&beta;-1 and TGF&beta; R-2 in the Atherosclerotic Aorta: An Immunohistological Study

“…Endoglin can bind TGF -1 and TGF -3 with high affinity and appears to do so only in the presence of TGF R-2 2,3) . So far, the role of endoglin in angiogenesis has been studied primarily in tumor endothelial cells of various organs [4][5][6][7][8] . A marked increase in the expression of endoglin has been demonstrated on the surface of vascular endothelial cells 9) .…”