| Background and ObjectivePancreatic cancer has been a common disease. It is difficult to early diagnosis, so the resection rate is very low. It is also insensitive to radiochemotherapy. The prognosis is very poor with the average 5-year survival less than 5%. In order to improve the prognosis, it's necessary to pay more attention to the biologic feature of pancreatic cancer.It is the most two important steps of tumor metastasis that the tumor cells break through the barrier composed of extracellular matrix (ECM) and basal membrane (BM), and the angiogenesis of the tumor. Heparanase (HPR), a type of endogenous endoglucoronidase, can degrade glycosaminoglycan , one of the main components of the barrier, to destroy ECM and BM to facilitate the invasiveness and metastasis of the tumor cells. Moreover, HPR can also induce tumor angiogenesis. Until now, there is few study on HPR and pancreatic cancer.Vascular endothelial growth factor (vEGF) is the most important factor that facilitating vascular growth. It was paracrined and acts on vascular endothelial cells. vEGF can induce angiogenesis and increase permeability of capillaries.In order to evaluate their role in pancreatic cancer, and set up new effective therapy strategy, the expression of HPR and vEGF in pancreatic cancer were investigated by immunohistochemical method, the correlation between the expression of HPR/vEGF and tumor angiogenesis, clinical pathological agents and prognosis were also be investigated.Material and methodParaffin embedded tissues from 43 patients who had undergone radical resection ofpancreatic carcinoma at Department of General Surgery, Sir Run Run Shaw Hospital, for pancreatic adenocarcinoma between Jan 1997 and Sep 2003 were studied. 15 cases with normal pancreatic tissue from some benign diseases, such as common bile duct cyst and periampullary adenoma, were selected as control. Expression of HPR and vEGF were detected by immunohistochemical En-vision method with 1:100 dilution of HPR and 1:200 dilution of vEGF. Positive and negative controls were designed. The positive cell was defined brown-stained cell plasma. Samples were evaluated by microscopy and semiquantitavely analysed for HPR and vEGF expression. We followed up the postoperative survivals and whether the patients had relapse or metastasis during their survivals.Statistical analysis: independent t test, chi-square test, bivariate-correlation and Kaplan-Meier method by SPSS 10.0.Result1. HPR expressed positively at a rate of 79% in pancreatic cancer, versus expressed negatively in the control with significant difference (P<0.001). vEGF expressed positively at a rate of 83.7%, versus a rate of 13.3% in the control with significant difference (P<0.001). There was positive correlation between the expressions of HPR and vEGF (r=0.535).2. There is statistical difference (P<0.05) between the MVD of negative expression of HPR and median/high expression in PDA. There is also significant difference (P<0.01) between the MVD of negative expression of vEGF and median/high expression in PDA. The expression of these two marks correlated positively with MVD (r=0.387,0.536).3. The difference between expression of HPR in PDA and microscopic invasive behavior is significant (P<0.05). There was no difference between the expression of vEGF and clinical pathological agents. The expression of these two marks correlated positively with differentiation and microscopic invasive behavior of PDA, but the expression of vEGF correlated negatively with lymph nodes metastasis(r=-0.378).4. The average postoperative survival time was 26.29 + 7.87 months in PDA of HPR negative group, while it was only 15.62 + 2.47 months of HPR positive group, with significant difference (P<0.05). The expression of HPR correlated negatively with postoperative survivaltime (r= - 0.575). There was significant difference (P<0.001) and positive correlation (r=0.657) between expression of HPR and relapse or metastasis within median postoperat...
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