Original Article
EXPRESSION OF VEGF RECEPTOR KDR IN DIFFERENT ORIGINATED CARCINOMAS
Abstract
Objective: To detect the expression of KDR in different originated carcinomas and to explore its expressed ways and the relationship with tumor progression.
Methods: KDR cDNA (V-VII domains) fragment was cloned from human umbilical vein with RTPCR and was expressed in Ecoli-Jml09. The fusion protein of GST-KDR was used for immunizing Balb/c mice to prepare monoclonal antibodies against KDR. The different tumor tissues and related normal tissues were examined with KDR McAb by S-P immunohistochemistry.
Results: the rate and intensification of KDR expression among different originated cancers are very different, bladder cancers from transmigrated epidermis are 100% positive and highest intensification. The expression of KDR in breast cancer and intestinal cancer lie in the second-rate, the weakest expression of KDR is in lung squamous carcinoma. Moreover, expression of KDR in tumor tissues lie both in endothelial cells (EC) of tumor blood vessels and tumor cells.
Conclusion: VEGF may be not only the para-secretory factor making EC proliferation but also auto-secretory factor stimulating the proliferation of tumor cells to benefit the growth and metastasis of malignant tumors. The different expression of KDR in different originated carcinomas may relate with malignant degree of tumor.
Methods: KDR cDNA (V-VII domains) fragment was cloned from human umbilical vein with RTPCR and was expressed in Ecoli-Jml09. The fusion protein of GST-KDR was used for immunizing Balb/c mice to prepare monoclonal antibodies against KDR. The different tumor tissues and related normal tissues were examined with KDR McAb by S-P immunohistochemistry.
Results: the rate and intensification of KDR expression among different originated cancers are very different, bladder cancers from transmigrated epidermis are 100% positive and highest intensification. The expression of KDR in breast cancer and intestinal cancer lie in the second-rate, the weakest expression of KDR is in lung squamous carcinoma. Moreover, expression of KDR in tumor tissues lie both in endothelial cells (EC) of tumor blood vessels and tumor cells.
Conclusion: VEGF may be not only the para-secretory factor making EC proliferation but also auto-secretory factor stimulating the proliferation of tumor cells to benefit the growth and metastasis of malignant tumors. The different expression of KDR in different originated carcinomas may relate with malignant degree of tumor.
