| Objective Through detecting the expression and analysing their relationship ofvascular endothelial growth factor-C (VEGF-C) and its upstream regulatorygene NF-K Bp65 and COX-2, vascular endothelial growth factor receptor-3(VEGFR-3), lymphatic endothelial specific markers D240, lymphangioma lamininin gastric cancer, to evaluate the molecular mechanisms of lymphangiogenesis andvarious gene products are how to synergies the functional organizational structur ofthe lymphangiogenesis in gastric cancer, and the features of "Tumor microlymph-vascular architecture phenotypy" (T-MLAP) and "Tumor microlymph-vasculararchitecture phenotypy heterogeneity" (T-MLAPH), and the relationship withT-MLAP and evolution, differentiation, metastasis and prognosis in gastric cancer,to provid a theoretical basis to determine the clinical treatment programs, inparticular, the choice of anti-angiongenesis treatment of lymphatic drug.Methods Immunohistochemical streptavidin-peroxidase method was performed indetecting the expression of VEGF-C, VEGFR-3, COX-2, NF-K B p65, D240 andlaminin protein gene products in 53 case with gastric cancer and 48 case withnormal gastric mucosa and analysising their relationship.Results1. The positive expression rate of VEGF-C, VEGFR-3, NF-K B p65 and COX-2gene product protein in gastric cancer was 89％(47/53),81％(43/53),87％(46/53) and 77％(41/53), significantly higher than that of the normalcomparison group, there was a significant difference (P＜0.05) and significantly(P＜0.01). The positive expression rate of these four indicators in gastric cancer with lymph node metastasis were higher than those without lymph nodemetastasis, the difference was statistically significant (P＜0.05), and those in theintestinal type gastric cancer was significantly higher than those of diffuse gastriccancer, the difference was statistically significant(P＜0.05 or P＜0.01).The resultof statistical correlation analysis shows that VEGF-C and VEGFR-3, COX-2 andVEGF-C, NF-κBp65 and VEGF-C, NF-κBp65 and COX-2 were significantlypositive correlation, the correlation coefficients were r=0.436 (P＜0.05), r=0.441(P＜0.01), r=0.329 (P＜0.05) and r=0.328 (P＜0.05).2. The expression of laminin in the stomach mucoss and submucoss of normalgastric tissue was strong positive and shows continuous linear coloring, theexpression of laminin in gastric cancer tissues lymphangiogenesis with lightcoloring, and shows incomplete, thin, debris or even the absence of defects.3. The lymphangiogenesis in gastric cancer form by the way of shooting frompreexisting lymphatic Netcom. Microlymphatic density has obvious heterogeneityin the volume and distribution: a. Tumor Infiltrating front MLD is 27.67, whichwas significantly higher than that of gastric cancer(12.66). The Formerlymphangiogenesis appears expansion, while the latter is often squeezed smallcords. B. There was significant difference between MLD of tumor infiltratingfront and that of the comparison group (P＜0.01). C. Lymphnodus group MLD(35.8) was significantly higher than diffuse gastric cancer MLD (23.78) (P＜0.01).And intestinal type with the lymph node metastasis of gastric cancer MLD(41.89) was significantly higher than those without lymph node metastasis ofMLD (22.13), the difference was significant (P＜0.01). And diffuse gastric cancerMLD has norelation with lymph node metastasis.Conclusion1.VEGF affects the vascular endothelial growth factor receptor VEGFR-3 of lymphatic endothelial cells through paracrine mechanism, leading to the formationof the gastric cancer lymphatic tissue.2. NF-κBp65 and COX-2 may promote gastric cancer lymphangiogenesis generation.by raising VEGF-C.3.The lymphangiogenesis of Gastric Cancer nascent T-MLAP. Differentiation ofdifferent tumor cells because of the volume of different VEGF secretion, thusinduced microlymph-vascular architecture phenotypy also marked heterogeneity,with tumor progressing, the heterogeneity of tumor cell was raised, T-MLAP willalso be showing diversity and differences, on the contrary, T-MLAPH also affectthe tumor invasive and prognosis, so we can speculate that lymphangiogenesisfactor, tumor cell secretion and micro-environmental factors 3D expressionprofile may play an important role in the formation mechanism of T-MLAPH.
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