Angiogenesis factors in esophageal tumors of various histogenesis.

Abstract

87 Background: Study of biological nature of tumors can provide important information on the malignant process course and contribute to the drug therapy development. The purpose of the study was to analyze levels of some growth factors in tissues of malignant esophageal tumors of various histogenesis. Methods: Levels of VEGF-А and its receptor sVEGF-R1, VEGF-С and its receptor sVEGF-R2, EGF, IFR-1, IFR-2 and TGF-β1 were studied by the ELISA using standard test-systems in tissue samples obtained from 39 patients: 27 – esophageal squamous cell carcinoma (ESCC), 12 – esophageal adenocarcinoma (EA). All patients had stage II disease (G2, pTNM). Results: Development of the pathogenic vascularization mechanism in ESCC and EA tissues was found to have both similar and different characteristics associated with the expression of growth factors. Similarities included activation of VEGF-А, VEGF-С, VEGF-R1, VEGF-R3, TGF-β1 and EGF in tissues of malignant tumors despite their histogenesis, while differences involved IGF-I and IGF-II content. A strong positive correlation between levels of VEGF-А and IGF-1 (r = 76; p < 0.01), but not IGF-II, was registered in EA tissues only, while in ESCC we found the negative correlation between VEGF-А and IGF-1(r = - 81; p < 0.01) and VEGF-А and IGF-2 (r = -79; p < 0.01). The same was observed for VEGF-С: a strong positive correlation with IGF-1(r = 79; p < 0.01), but not with IGF-II in EA, and a strong negative correlation with IGF-1(r = - 83; p < 0.01) and IGF-2 (r = -87; p < 0.01) in ESCC. EGF appears to be the only VEGF-А and VEGF-С inductor in ESCC, as a strong correlation with it was noted: r = 75 (p < 0.01) and r = 77 (p < 0.01) respectively, while activators of angio- and lymphogenesis factors in EA were presented by IGF-1 and EGF (r = 76 at p < 0.01 and r = 79 at p < 0.01 with VEGF-А and VEGF-С, respectively). Conclusions: Apparently, the two histological types of esophageal cancer are two different diseases with their own pathogenesis, prognosis and therefore approach to the targeted therapy.