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

Department of Pathology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.
Modern Pathology (Impact Factor: 6.36). 02/2004; 17(2):197-203. DOI: 10.1038/modpathol.3800034
Source: PubMed

ABSTRACT Endoglin (CD105) has been shown to be a more useful marker to identify proliferating endothelium involved in tumor angiogenesis than panendothelial markers such as CD31. We investigated endoglin and vascular endothelial growth factor expression as possible prognostic markers in colorectal cancer. Surgical specimens from 150 patients with resected colorectal carcinomas were immunostained for endoglin, CD31 and vascular endothelial growth factor. Colorectal carcinoma cases consisted of 50 cases without lymph node metastases, 50 cases with only lymph node metastases and 50 cases with liver metastases (38 cases also had positive lymph nodes). Positively stained microvessels were counted in densely vascular foci (hot spots) at x 400 fields in each specimen. For vascular endothelial growth factor, intensity of staining was scored on a three-tiered scale. Results were correlated with other prognostic parameters. Endoglin demonstrated significantly more proliferating neoplastic microvessels than CD31 (31+/-10 vs 19+/-8/0.15 mm2 field, P<0.001). Low vascular endothelial growth factor expression within tumor cells was seen in 49 (33%) and high expression in 101 cases (67%). There was a positive correlation of endoglin, CD31 counts and vascular endothelial growth factor overexpression with the presence of angiolymphatic invasion and lymph node metastases (P<0.05). Only endoglin counts correlated significantly with liver metastases and positive vascular pedicle lymph nodes (P<0.05), while vascular endothelial growth factor showed significant correlation with the depth of invasion (P<0.01). Endoglin, by staining higher numbers of the proliferating vessels in colon carcinoma, is a more specific and sensitive marker for tumor angiogenesis than the commonly used panendothelial markers. Endoglin staining also showed prognostic significance with positive correlation with angiolymphatic invasion and metastases to lymph nodes and liver.

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    ABSTRACT: Objectives: Intercellular adhesion mediated by claudin and cadherin/catenin complex is a prerequisite of epithelial integrity and differentiation and has been suggested to be frequently disturbed in cancers. Endoglin (CD105) has been shown to be a more useful marker to identify proliferating endothelium involved in angiogenesis than pan-endothelial markers such as CD31. The aim of this study was to assess the relationship between these markers and clinicopathological features of colorectal carcinomas. Materials and Methods: Surgical specimens from 69 patients with colorectal cancer were immunostained for claudin-1, E-cadherin, β-catenin, endoglin and CD31. Results: Forty-six (66.7%), 67 (97.1%), and 67 (97.1%) of the tumors, expressed immunostaining for claudin-1, E-cadherin and β-catenin, respectively. A significant association was seen between claudin-1 and E-cadherin expression (p=0.002), as well with β-catenin (p=0.009). High β-catenin expression appeared to reduce the risk of poor outcome. Endoglin vessel expression was correlated significantly with vessel invasion (p<0.0001), lymph node metastases (p=0.039), liver metastases (p<0.0001) and recurrence of the disease (p<0.010). Endoglin tumor cell expression was associated with E-cadherin and β-catenin expression (p=0.001 and p=0.068), but not with claudin-1 expression (p=0.299). Conclusions: Loss of the expression of claudin-1, E-cadherin/β-catenin downregulation, and high CD105-MVD counts may play a significant role in the high incidence of angiolymphatic invasion, metastases and prognosis in colorectal-cancer patients, but further studies are needed to clearly define their role in colorectal carcinoma.
    01/2014; 2:135-144.
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    ABSTRACT: Polymorphisms in angiogenesis-related genes and metabolic syndrome (MetS) risk factors play important roles in cancer development. Moreover, recent studies have reported associations between a number of 3[prime]-UTR polymorphisms and a variety of cancers. The aim of this study was to investigate the associations of three VEGF 3[prime]-UTR polymorphisms (1451C > T [rs3025040], 1612G > A [rs10434], and 1725G > A [rs3025053]) and MS with colorectal cancer (CRC) susceptibility in Koreans. A total of 850 participants (450 CRC patients and 400 controls) were enrolled in the study. The genotyping of VEGF polymorphisms was performed by TaqMan allelic discrimination assays. Cancer risks of genetic variations and gene-environment interactions were assessed by adjusted odds ratios (AORs) and 95% confidence intervals (CIs) of multivariate logistic regression analyses. VEGF 1451C > T was significantly associated with rectal cancer risk (Dominant model; AOR =1.58; 95% CI =1.09 - 2.28; p =0.015) whereas VEGF 1725G > A correlated with MetS risk (Dominant model; AOR =1.61; 95% CI =1.06 - 2.46; p =0.026). Of the gene-environment combined effects, the interaction of VEGF 1451C > T and MetS contributed to increased RC risk (AOR =3.15; 95% CI =1.74 - 5.70; p < .001) whereas the combination of VEGF 1725G > A and MetS was involved with elevated CC risk (AOR =2.68; 95% CI =1.30 - 1.55; p =0.008). Our results implicate that VEGF 1451C > T and 1725G > A may predispose to CRC susceptibility and the genetic contributions may be varied with the presence of MetS.
    BMC Cancer 11/2014; 14(1):881. DOI:10.1186/1471-2407-14-881 · 3.32 Impact Factor
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    ABSTRACT: To assess the expression of Endoglin (CD-105) and Microvessel Density in clinically normal oral mucosa of non-tobacco and tobacco habituated patients & also histopathologically confirmed cases of oral squamous cell carcinoma (OSCC) patients.


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