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ObjectiveTo investigate the feasibility of extended hepatectomy for huge hepatic carcinoma.MethodsA retrospective analysis was made on the clinical data of 28 patients with huge hepatic carcinoma who underwent extended hepatectomy from December 2006 to June 2011.Twenty-two cases were Child-Pugh grade A,6 cases were Child-Pugh grade B,19 cases were indocyanine green retention at 15 minutes (ICGR15)≤10％,5 cases were 10％ ＜ ICGR15 ≤15％,4 cases were 15％ ＜ ICGR15 ≤20％.ResultsThe operative death rate was 7.1％ (2/28) with Child-Pugh grade B,15％ ＜ ICGR15 ≤20％ and liver resection volume 60％-70％.Postoperative complications were found on 15 cases,but all recovered after treatment.ConclusionExtended hepatectomy for huge hepatic carcinoma can be feasible in the patients with enough reserve of the liver function provided.
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Objective To evaluate the specificity of CD105 labeled microvessel density (MVD)and its clinical significance.Methods Formalin fixed,paraffin wax embedded specimens from 63 patients with hepatocellular carcinoma (HCC) were stained with anti-CD105 monoclonal antibody.A correlation was analyzed between the expression and distribution of MVD-CD105 in HCC/adjacent non-tumorous tissues and clinicopathological features.Results CD105 immunoreactivity was seen in all the specimens of HCC and adjacent non-tumorous tissues.Immunoreactivity intensity was higher in adjacent non-tumorous tissues than in HCC (χ2=9.184,P＜0.01).The mean scores of M VD-CD105 were also higher in adjacent non-tumorous tissues than in HCC.The levels of expression and distribution of MVD-CD105 in HCC were associated with tumor metastasis and TNM staging (P＜0.01).The levels of expression and distribution of MVD-CD105 in adjacent non-tumorous tissues were associated with TNM staging and 2-year survival rate (P＜0.01).Conclusions CD105 showed no specificity in labeling MVD of HCC specimens.The higher level of expression and distribution of MVD-CD105 in HCC was associated with local tumor metastasis and progression.CD105 cannot be used as a target for anti-angiogenesis therapy for HCC.
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Objective To investgate the expression and the clinical significance of survivin in the primary hepatocellular carcinoma (HCC). Methods S-P immunohistochemical staining was performed to detect the expression of survivin in 50 samples of HCC tissue and 20 of normal liver tissue. Results The positive rate of survivin expression in HCC was 66. 0% (33/50) , which was significantly higher than that in normol liver tissues (negative expression) (P<0. 001). The expression of survivin was correlated with intrahepatic dissemination and multiple masses (P = 0. 019, P=0. 030). The high survivin expression was associated with the survival time less than three years(P = 0. 018). Conclusion The survivin may play certain roles in the oncogenesis and progression of HCC. Detection of the survivin can supply certain evidence on prognosis of primary hepatocellular carcinoma.
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Objective:To study the expression of tenascin in hepatocellular carcinoma(HCC)and to investigate the roles of tenascin expression in microvessel angiogenesis,invasion,metastasis and prognosis of HCC.Methods:Formalin fixed,paraffin wax embedded specimens from 63 HCC patients were stained with an anti-tenascin monoclonal antibody,and the measurements were also done for paracancerous specimens from the same patients and specimens from 15 patients with liver cirrhosis and 10 normal liver.The correlation was analyzed between expression of tenascin and clinicopathological features as well as microvessel angiogenesis.Results:Tenascin immunoreactivity was observed in 65.1% samples of HCC,69.8% of paracarcinoma,20.0% of liver cirrhosis and negative of normal liver samples.Positivity and intensity of tenascin expressions in samples of HCC and paracarcinoma were higher than those in samples of cirrhotic and normal liver.Tenascin expression was correlated with Edmondson-Steiner grades,tumour numbers,capsule invasion,tumour metastasis and microvessel angiogenesis.Conclusion:The up-regulation of tenascin expression may play an important role in invasion and metastasis of HCC.