Liver Transplantation for Hepatitis B Virus-related Hepatocellular Carcinoma in Hong Kong

Hepatocellular carcinoma(HCC)is the fifth most common cancer and the third most common cause of cancer-related deaths worldwide.Curative resection is frequently limited in Hong Kong by hepatitis B virus-related cirrhosis,and liver transplantation is the treatment of choice.Liver transplanta-tion has been shown to produce superior oncological benefits,when compared to hepatectomy for HCC.New developments in the context of patient selection criteria,modification of organ allocation,bridging therapy,salvage liver transplanta-tion and pharmaceutical breakthrough have improved the survival of HCC patients.In this article,we will share our experience in transplanting hepatitis B virus-related HCC patients in Hong Kong and discuss the recent progress in several areas of liver transplantation.

Incidental Collision Tumor of Hepatocellular Carcinoma and Neuroendocrine Carcinoma

The composite tumors of the liver are very rare,including the coexistence of HCC(hepatocellular carcinoma)with NEC(neuroendocrine carcinoma).The rare occurrence of these tumors necessitates more reported cases in order to fully understand their clinical characteristics,behaviors and treatments.Herein is described an incidental collision tumor of HCC-NEC,along with a review of the literature focusing on their clinicopathological findings and prognosis.The tumor presented here was found incidentally in the hepatectomy specimen of a 56-yearold man who had undergone liver transplantation for rapidly progressive liver failure because of alcoholic hepatitis and cirrhosis.Imaging and laboratory examinations did not demonstrate tumor-related findings.During macroscopic examination,two sharply defined and distinctive areas(1.7 cm and 0.6 cm dimension respectively)were detected among the cirrhotic nodules.The characteristic histopathological features and immunohistochemical findings allowed a diagnosis of HCCNEC to be made.There was no evidence of recurrence and metastasis after 10months following surgery.The present case and review revealed that these tumors are frequently found in older ages and males.Although serum markers are valuable in the discrimination of malignant tumors,their absence cannot completely rule out composite HCC-NEC.Diagnosis requires a comprehensive histopathological evaluation together with immunohistochemistry.The NEC component might influence the treatment strategy and eventually the outcome of the patient.In conclusion,the rare occurrence of HCC-NEC and the lack of diagnostic clinical signs and symptoms do not exclude their consideration in the differential diagnosis of liver tumors,especially in patients with the chronic liver disease.

Saikosaponin-b regulates the proliferation and apoptosis of HepG2 cells by targeting the MACC1/c-Met/Akt signaling pathway

OBJECTIVE Metastasis-associated in colon cancer-1(MACC1)is an oncogene that has been newly identified.It promotes tumor proliferation and invasion via the MET pathway.Our study investigated the effects of Saikosaponin-b(SS-b)on the proliferation and apoptosis of HepG2 cells and its regulation on MACC1/c-Met/Akt signaling pathway.METHODS HepG2 cells were treated with SS-b(10-800 g·L^(-1))for 48 h in vitro.The CCK-8 assay was used to assess cell proliferation,and cell apoptosis was determined by Hoechst33258 staining,AnnexinⅤ/PI staining and caspase 3 assay.RT-PCR was used to examine the expression of MACC1,c-MET and hepatocyte growth factor(HGF)mR NA.MACC1 protein was detected by Western blot and immunohistochemistry.The protein expressions of p-cMET,c-MET,p-AKT,AKT,p-BAD,BAD were measured by Western blot.RESULTS SS-b inhibited the growth of HepG2 cells in dose-dependent way and induced cell apoptosis significantly.HepG2 cells showed karyopyknosis,fragmentation and fluorescence highlight in SS-b treatment group.FCM results showed that apoptosis rate of HepG2 cells increased with SS-b concentration.The immunofluorescence results showed that the MACC1 expression decreased significantly in HepG2 cells treated with SS-b.The expression levels of MACC1,c-MET and HGF mR NA in HepG2 cells were significantly inhibited by SS-b.SS-b also significantly decreased the protein expressions of MACC1,p-c-MET and p-AKT while increased the expression of p-BAD and caspase 3 in HepG2 cells(P<0.05).CONCLUSION SS-b inhibited the proliferation and induced the apoptosis of HepG2 cells by targeting the MACC1/c-Met/Akt signaling pathway.