Immunohistochemical Expression of MMP2 , VEGF and D2-40 as Biological Markers of Local Invasion Potential , Angiogenesis and Lymphangiogenesis in Oral Squamous Cell Carcinoma and Verrucous Carcinoma
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Lymphangiogenesis
Verrucous carcinoma
MMP2
Objective To explore the expressions of VEGF-C and VEGF-D and the correlation with the metastasis through the lymphatic system in nasopharyngeal carcinoma.Method VEGF-C and VEGF-D were labeled by improved immunohistochemical method(S-P), and the relation between their expressions and biological characteristics of nasopharyngeal carcinoma was studied.Result Expressions of VEGF-C and VEGF-D were related to the tumor metastasis through the lymphatic nodes.Conclusion VEGF-C and VEGF-D can regulate the lymphangiogenesis of nasopharyngeal carcinoma and provide scientific theoretical arguments for the therapy of anti-lymphangiogenesis in nasopharyngeal carcinoma patients.
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Interplay between various lymphangiogenic factors in promoting lymphangiogenesis and lymphatic metastasis remains poorly understood. Here we show that FGF-2 and VEGF-C, two lymphangiogenic factors, collaboratively promote angiogenesis and lymphangiogenesis in the tumor microenvironment, leading to widespread pulmonary and lymph-node metastases. Coimplantation of dual factors in the mouse cornea resulted in additive angiogenesis and lymphangiogenesis. At the molecular level, we showed that FGFR-1 expressed in lymphatic endothelial cells is a crucial receptor that mediates the FGF-2-induced lymphangiogenesis. Intriguingly, the VEGFR-3-mediated signaling was required for the lymphatic tip cell formation in both FGF-2- and VEGF-C-induced lymphangiogenesis. Consequently, a VEGFR-3-specific neutralizing antibody markedly inhibited FGF-2-induced lymphangiogenesis. Thus, the VEGFR-3-induced lymphatic endothelial cell tip cell formation is a prerequisite for FGF-2-stimulated lymphangiogenesis. In the tumor microenvironment, the reciprocal interplay between FGF-2 and VEGF-C collaboratively stimulated tumor growth, angiogenesis, intratumoral lymphangiogenesis, and metastasis. Thus, intervention and targeting of the FGF-2- and VEGF-C-induced angiogenic and lymphangiogenic synergism could be potentially important approaches for cancer therapy and prevention of metastasis.
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<div>Abstract<p>Metastases are commonly found in the lymphatic system. The molecular mechanism of lymphatic metastasis is, however, poorly understood. Here we report that vascular endothelial growth factor (VEGF)-A stimulated lymphangiogenesis <i>in vivo</i> and that overexpression of VEGF-A in murine T241 fibrosarcomas induced the growth of peritumoral lymphatic vessels, which occasionally penetrated into the tumor tissue. As a result of peritumoral lymphangiogenesis, metastases in lymph nodes of mice were detected. VEGF-A–overexpressing tumors contained high numbers of infiltrating inflammatory cells such as macrophages, which are known to express VEGF receptor (VEGFR)-1. It seemed that in the mouse cornea, VEGF-A stimulated lymphangiogenesis through a VEGF-C/-D/VEGFR-3–independent pathway as a VEGFR-3 antagonist selectively inhibited VEGF-C–induced, but not VEGF-A–induced, lymphangiogenesis. Our data show that VEGF-A contributes to lymphatic mestastasis. Thus, blockage of VEGF-A–induced lymphangiogenesis may provide a novel approach for prevention and treatment of lymphatic metastasis.</p></div>
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Lymphangiogenesis
Lymphatic Endothelium
Podoplanin
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Purpose of review The purpose of the present review is to describe new antilymphangiogenic treatment strategies and recent findings on strain-dependency of corneal lymphangiogenesis and the interdependency between blood and lymphatic vessel growth. Recent findings Studies on mice have revealed that apart from haemangiogenesis, lymphangiogenesis can also differ markedly between several mouse strains under normal and inflammatory conditions. Although haemangiogenesis and lymphangiogenesis are closely interconnected in their spatial-temporal patterning, recent data suggest that they can also occur independently. Summary Understanding the coordinated regulation of blood and lymphatic vessel growth and genetic factors determining lymphangiogenesis in more detail could improve the development of specifically targeted antihaemangiogenic or antilymphangiogenic strategies.
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<div>Abstract<p>Metastases are commonly found in the lymphatic system. The molecular mechanism of lymphatic metastasis is, however, poorly understood. Here we report that vascular endothelial growth factor (VEGF)-A stimulated lymphangiogenesis <i>in vivo</i> and that overexpression of VEGF-A in murine T241 fibrosarcomas induced the growth of peritumoral lymphatic vessels, which occasionally penetrated into the tumor tissue. As a result of peritumoral lymphangiogenesis, metastases in lymph nodes of mice were detected. VEGF-A–overexpressing tumors contained high numbers of infiltrating inflammatory cells such as macrophages, which are known to express VEGF receptor (VEGFR)-1. It seemed that in the mouse cornea, VEGF-A stimulated lymphangiogenesis through a VEGF-C/-D/VEGFR-3–independent pathway as a VEGFR-3 antagonist selectively inhibited VEGF-C–induced, but not VEGF-A–induced, lymphangiogenesis. Our data show that VEGF-A contributes to lymphatic mestastasis. Thus, blockage of VEGF-A–induced lymphangiogenesis may provide a novel approach for prevention and treatment of lymphatic metastasis.</p></div>
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A bstract : A mouse model has been developed to study lymphangiogenesis dissociated from angiogenesis. bFGF implanted in a mouse cornea at a concentration below the threshold to induce angiogenesis potently induces lymphangiogenesis. This model has permitted a study of cellular and molecular mechanisms of lymphangiogenesis.
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