The Relationship Between Inflammatory Factor And Carcinoma Of Bladder

Along with the extension of mankind life period, cancer has become the mostimportant factor that affect mankind life period. Many results showed that there isan evident correlation between cancer and chronic inflammation and cancer is aneoplasm resulting from repeated damage and paraplasm. At present,"inflammation -cancer chain" is to become a hot investigate spot, so it is veryimportant to analyses the mechanism of cancer microenvironment in cancerdevelopment. The role of inflammation cell in the development of tumorous hasbeen identified. In the earlier period of tumorous development, inflammation cellsare a potent initiator through producing attraction circumstance, interfering genomestability and promoting angiogenesis. Inflammation cells together with theirchemotatic factor and cytokine influence the whole tumor organ by adjusting itsgrowth, transmigration and differentiation, therefore, Inflammation cells areessential component of tumor microenvironment. The activation of mononuclearphagocytic system is one of important character of chronic inflammation. Tumourassociation macrophage (TAMs) which is transformed from mononuclear cellinduced by chemokines of monocyte chemoattractant protein1 (MCP-1) is a majorinflammation infiltration cell constituent in neoplasma. TAMs have dual effects intumor neoplasm. On the one hand, they kills new cell directly and makesimmunomodulation role activated by interleukin-2, interferon andinterleukin-12.On the other hand, the tumor-association megalophages mayproduce angiogenic and lymphogenesis growth factor, cytokine and protease. Thesefactors are all tumor enhancement mediators. Macrophage colony-stimulatingfactor (M-CSF) is a cytokine which promote macrophagus proliferation,differentiation, and survival. Its function include stimulating granular leukocytesand mononuclear macrophage maturate, promoteing mature cells release inperipheral blood, hastening the function of megalophage and eosinophils,having aclose correlation with the megalophage infiltration in tumor tissue. MCP-1 mayattract monocyte assembling to inflammation position. Meanwhile, monocyte andmegalophage may be inducted to secrete MCP-1 under the stimulation of somevirus. Some tumour cells may also secrete MCP-1. Recent research indicated:MCP-1 may not only promote the region tissue to express of vascular endothelialgrowth factors(VEGF), but also induct angiogenesis. Salcedo et al reported MCP-1may chemotactic human endothelial cell and induct angiopoiesis on micromoleconcentration. The formations of neovascularity in tumor tissue not only take partin the inflammatory reaction, tissue remodeling, and regeneration, but promote thedevelopment of tumor. Urinary bladder carcinoma of which incidence rate account5﹪ of malignant tumor is the second malignant urinary system tumor, gettingworsen once recurrence. Urinary bladde carcinoma of which the preciseetiopathogenisis is still not clear has a correlation with many factors and itsdevelopment is poly-phase. Therefore, it is vital to investigate the etiopathogenisis,genesis, and development of urinary bladder carcinoma in the work of urinarysurgery. In this study, we approach the network mechanism of tumor-macrophage-inflammatory factor and its relationship with urinary bladder carcinoma.Megalophage is the core of the search;M-CSF, MCP-1 and VEGF are the object ofthe search.In our work, immunohistochemistry and immunohistochemistry double stainwere utilized to detect the expression of M-CSF , MCP-1and VEGF inCD68-marked megalophage. In addition, in-situ hybridization was used to detectthe mRNA expression. Our object is to identify whether megalophages are the mainsource cell of MCP-1 and VEGF, at the same time, investigate the dependability ofinfiltrive megalophage number, analyze the dependability of MCP-1,VEGFmRNA and protein in urinary bladder carcinoma tissue, study the relationship ofMCP-1,VEGF expression with clinical stage as well as pathology stage, reveal therelationship of tumor-megalophage-inflammatory factor with the genesis anddevelopment of urinary bladder carcinomaThe main results are given as follows.1. M-CSF expression positive cell rate and megalophage infiltration number:both indexes expressed more highly in urinary bladder carcinoma group than theydid in normal bladder mucosa( P<0.01)and both them had close correlation withclinic stage as well as pathology stage(metastatic>invasion>superficial;T4>T3>T2>T1). In addition, there was apparent positive correlation between the twoindexes.2. MCP-1and VEGF expression (including mRNA and protein) positive cellrate: both them expressed more highly in urinary bladder carcinoma group thanthey did in normal bladder mucosa( P<0.01)and both them had close correlationwith clinic stage as well as pathology stage. In addition, there was apparent positivecorrelation between the two indexes(r=0.728;P<0.05).3.the number of megalophage which express MCP-1and VEGF: superficial