| Objective: to explore if vasculogenic mimicry (VM) exists in hepatocelluar carcinoma (HCC) and further to investigate its potential mechanism, to explain the clinical significance of VM.Methods: to collect 99 HCC resection samples with complete clinical and prognostic data. Immunohistochemical staining of CD31, CD 105, Hepatocyte, VEGF and PAS special histochemical staining were conducted to explore if VM exist in HCC. immunohistochemical staining of MMP-2,MMP-9,VEGF to explore its mechanism. Their expression were evaluated according to a scoring method reported by Mattern et al.Results: The observed evidence of VM through histologic and immunohistochemical analysis of HCC: (i ) CD31and CD 105 did not stain the cells that outlined these pathologic solid tubular structures (VM) , which prove these cells are not endothelial cells. (ii )Hepatocyte stained the cells which outlined the vasculogenic-like tubular wall, which prove these cells are tumor cells of hepatocellular Carcinoma, (iii) the cells outlined these pathologic solid tubular structures (VM) stained by Hepatocyte can express VEGF protein, which suggest these tumor cells demonstrate an endothelial phenotype. (iv) there were multiple blood pooling without endothelial cells lining in these pathologic solid tubular structures (VM) which were present in blood cells instead of necrotic tumor cells in the central area of the tumor nests.12%(12 specimens)of the 99 specimens exhibited evidence of VM.Vasculogenic mimicry is not a rare pathologic feature in hepatocelluar carcinoma.The biologic behavior of VM and the prognostic role for the clinicalimaging of vasculogenic mimicry. ( i ) Edmondson pathologic grade of HCC and VM . 2.5%(1 specimen)exhibited VM of 40 HCC specimens which belong to Edmondson pathologic grade I —- II; 18.64%(11 specimens)exhibited VM of 59 HCC specimens which belong to Edmondson pathologic grade III ~ IV. to compare the grade I — II and grade El ~ IV ,The high differentiated HCC( grade EI~IV) exhibited more VM specimens than the low differentiated HCC (grade I ~ II )(P=0.036). (ii) TNM classification of 99 HCC specimens. The biological behavior of VM was assessed by evaluating TNM (tumor size, lymph node metastases, remote metastases) classification pathological at the operative state and comparing the VM and non-VM groups. The mean TNM classification stage of the VM group was not more advanced than that of the non-VM group (P=0.407). Though there was no difference in TNM classification between the 2 groups, we compare the hematogenous metastases ( lung, bone, peritoneum et al) between the 2 groups, the VM group had a higher rate of occurrence of hematogenous metastases(P=0.003 ). (iii) Survival analysis of VM and non-VM groups. Kaplan-Meier actuarial survival curves were used to comare the VM group(n=12)with the non-VM group(n=87).The VM group had 12-,24-and 36-month survival rates of 50,25 and 9%, respectively ,and the non-group had survival rates of 77,60 and 45%, respectively. The VM group has a lower 22-month survival rate than the non-VM group (P=0.00\).The primary investigation of the mechanism of VM in HCC by expression of VEGF , IMP-2, IMPS. (i) VEGF was mainly distributed in cytoplasm of the HCC cells, VEGF expressed intensively near the zones of necrosis. Furthermore we observed the faint expression of VEGF in hepatocye and ECM. 57.6% (57/99) HCC specimens expressed VEGF, The positive expression rate of VEGF of the VM group was 41.7(5/12), The positive expression rate of VEGF of the non-VM group was 59.8% (52/87). We select a scoring method reported by Mattern et al to... |
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