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PubMed2003

Investigation of associating factors in exacerbation of liver damage after chemotherapy in patients with HBV-related HCC.

BACKGROUND/AIMS: Flare-up of hepatitis due to the reactivation of hepatitis B virus (HBV) is a well-known complication in patients with malignant disease who receive chemotherapy. Despite the widespread use of chemotherapy for patients with HBV-related hepatocellular carcinoma (HCC), there is little corresponding data on exacerbation of liver damage in these patients. In the present study, we investigated the associating factors in exacerbation of liver damage in patients with HBV-related HCC who were undergoing trans-hepatic arterial infusion chemotherapy (THAIC). PATIENTS AND METHODS: Thirty-three patients who received THAIC for HCC were investigated. All patients were hepatitis B surface antigen positive. Hepatitis e antigen and antibody were generally tested at baseline and within 1 month of final chemotherapy. Serum alanine aminotransferase, asparate aminotransferase, albumin, total bilirubin, and prothrombin time were estimated once a week or every 2 weeks. HBV-DNA levels were measured at baseline and once a month. Mutation in the regions of precore and core promoter in HBV DNA was generally estimated at baseline and within 1 month of final chemotherapy. RESULTS: Eight patients with hepatitis Be antigen positive and hepatitis Be antibody negative at baseline were found to have exacerbation of liver damage during or after chemotherapy. Of these, three patients died of progressive liver failure. There was no association between exacerbation of liver damage and age, sex, hepatic reserve function, HBV-DNA levels, precore and core promoter sequencing, therapeutic regimen, or tumor stage. The only associating factor was HBeAg positivity. CONCLUSIONS: These results suggest that hepatitis B e antigen positivity is a significant associating factor in exacerbation of liver damage during or after chemotherapy in patients with HBV-related HCC.

Journal Article↗
PubMed2000

Inhibition of cell proliferation in HCC-9204 hepatoma cells by a c-myc specific ribozyme.

A ribozyme (RZ) gene targeting c-myc mRNA was synthesized and cloned. Cleavage reaction showed that cleavage of the RZ was efficient and specific. The RZ gene-containing retrovirus vector pDOR-RZ was transfected into HCC-9204 hepatoma cells, which constitutively express high levels of c-myc using Lipofectamine. Positively transfected cells were selected using G418. In situ hybridization showed that both pDOR-RZ and pDOR vectors had been integrated into the chromosome of HCC-9204 cells. Dot blot hybridization indicated that expression of the RZ was only evident in pDOR-RZ-transfected HCC-9204 cells. Avidin-biotin complex enzyme-linked immunosorbent assay showed that c-myc expression was down-regulated. Chromatin aggregation into compact masses, cytoplasmic vacuole degeneration, and blurring of cytoplasm structure were observed by transmission electron microscopy in HCC-9204-RZ cells. These results suggest that the use of a c-myc mRNA cleaving enzyme could be most effective in tumor cells that are highly proliferative and constitutively express high levels of c-myc.

Carcinoma, Hepatocellular↗
PubMed2003

Diagnosis of hepatocellular carcinoma (HCC) in a high-risk patient by using transgastric EUS-guided fine-needle biopsy (EUS-FNA).

Hepatocellular carcinoma (HCC) is the most common primary malignancy arising within the liver and most often affects individuals with chronic hepatitis and/or liver cirrhosis. Patients often present at an advanced stage of disease or with poor liver function, thus limiting treatment options and resulting in a poor prognosis of the disease. Therefore, an early tissue-based diagnosis of HCC is necessary to direct further work-up and treatment. We present the case of a 70-year-old man with alcoholic cirrhosis at stage Child C, in whom a tumor nodule was found incidentally within the left lobe of the liver. Percutaneous biopsy was deemed too dangerous because a deteriorated liver function with coagulopathy was present, and a significant amount of ascites surrounded the small cirrhotic liver. To obtain a conclusive diagnosis, we performed transgastric fine-needle biopsy of the tumor under direct endosonographic guidance (EUS-FNA) without complications. Cytologic examination confirmed the presence of a well differentiated HCC. Based on this finding, super-selective CT-guided angiography and chemoembolization were subsequently performed without complications and the patient remained free of tumor relapse for the 8 months of surveillance. We conclude that EUS-guided fine-needle biopsy and cytologic examination represent a reliable alternative for tissue sampling in HCC, particularly in selected high-risk patients such as those with poor liver function and coagulation disorders; this should be assessed in prospective clinical trials.

Aged↗
PubMed2005

[TACE: therapy of the HCC before liver transplantation--experiences].

PURPOSE: Analysis of the course of disease in patients with histologically proven HCC before and after orthotopic liver transplantation (LTx) who received transarterial chemoembolization (TACE). MATERIAL AND METHODS: Thirty-five of a total collective of 363 patients with histologically proven HCC underwent LTx. Before LTx, all patients were treated with sequential TACE. According to treatment pattern, TACE should be performed every 6 weeks, using a suspension consisting of max. 10 mg Mitomycin C as well as 10 - 30 ml iodized oil (Lipiodol). Patients were classified according to the Milano criteria. Criteria were called exceeded if the tumor size was > 5 cm and/or > 3 tumors larger than 3 cm were found. Therapy success and liver function were examined by means of spiral CT and laboratory controls. Investigation parameters included the number of tumor knots as well as the maximum tumor size. Additionally, the Lipiodol accumulation, the patency of the portal vein and the occurrence of complications were checked. RESULTS: Altogether, 184 TACE procedures were accomplished (5.3 +/- 3.3, range 1 - 14). The waiting period up to the transplantation amounted to 366 +/- 255 days (range 44 - 1137). The average number of tumor knots for each patient was 3.1 +/- 2.2 before and 2.9 +/- 2.2 after TACE (p = 0.887). The average tumor size was 4.2 +/- 2.5 before and 2.8 +/- 1.4 after TACE. The Milano criteria to LTx crossed 17/35 patients. Patients with exceeded Milan criteria showed a highly significant size reduction of the tumor after TACE (p = 0.001); in 9/17 cases the transplantation criteria were secondarily fulfilled through downstaging. A successful LTx was accomplished in 35/35 cases. Follow up after LTx was 769 +/- 509 days. The tumor recurrence in patients with exceeded vs. fulfilled transplantation criteria was 11.1 % vs. 11.8 % (p = 0.99). The recurrence free survival was 93.3 %, 82.5 % and 82.5 % at 1, 3 and 5 years, respectively. There were no relevant differences between patients with exceeded vs. fulfilled transplantation criteria (p = 0.99). CONCLUSION: The sequential TACE is an effective method for the therapy of the HCC before LTx in selected patients. A relevant downsizing could be achieved by TACE in patients with advanced HCC. Patients with larger tumors showed a significantly stronger size reduction after TACE. The recurrence rate and the survival rate for patients with advanced or small tumors do not differ.

Adult↗
PubMed2006

Past HBV viral load as predictor of mortality and morbidity from HCC and chronic liver disease in a prospective study.

BACKGROUND AND AIMS: In a prospective cohort study with 11 yr of follow-up, we assessed the relationship between past hepatitis B virus (HBV) viral load and mortality. Surviving cohort members were evaluated for current liver disease. METHODS: We measured HBV viral load by real-time polymerase chain reaction on stored samples from cohort entry (1992-1993) in 2,763 hepatitis B surface antigen (HBsAg)-positive adults. Major end points were death from hepatocellular carcinoma (HCC) or chronic liver disease (CLD). There were 447 deaths. In the 1,683 survivors, we assessed severity of liver disease on a return visit in 2003. Viral load was divided into three categories: undetected (<1.6 x 10(3) copies/mL); low titer (<10(5) copies/mL); and high titer (> or =10(5) copies/mL). RESULTS: For HCC, there was a significant increase in mortality across viral load categories (p(trend) < 0.001). Compared to the HBV undetected category, the relative risk (RR) for HCC mortality in the low viral load group was 1.7 (95% confidence interval [CI] 0.5-5.7) and 11.2 (3.6-35.0) in the high viral load group. For CLD mortality, the RRs were 1.5 (0.2-12.1) and 15.2 (2.1-109.8), respectively (p(trend) < 0.001). The RR associated with high viral load did not change with increased follow-up time. In surviving cohort members evaluated for liver disease in 2003, there was also a significant association of viral load with disease severity. CONCLUSION: In this prospective study, viral load is associated with increased mortality from HCC and CLD in HBV-infected subjects. Viral load may be a useful prognostic tool in HBV infection, and interventions aimed at its reduction should be explored.

Adult↗
PubMed2004

BJ-HCC-20, a potential novel cancer-testis antigen.

In an effort to identify novel Cancer-Testis genes, we analyzed the sequence in the q26-28 region of human X chromosome by several on-line tools. The candidate sequences were then confirmed by experiments. We have obtained a novel Cancer-Testis gene, BJ-HCC-20. In vivo, it was found to have two isoforms. In samples of liver, colon, gastric and lung cancer tested, the expression frequency of BJ-HCC-20 is 25%, 17%, 21% and 15%, respectively. Full-length cDNAs of both BJ-HCC-20 isoforms were isolated and their gene structures and promoter regions were characterized. BJ-HCC-20 might have implications in theoretical and practical tumor biology.

Antigens, Neoplasm↗
PubMed2007

Development of hepatocellular carcinoma (HCC) in a patient 17 years after recovery from chronic hepatitis B and seroconversion to anti-HBs.

A 63-year-old man was admitted to hospital in 2003 for treatment of a hepatocellular carcinoma (HCC). He was negative for HBs antigen (HBsAg) and anti-HCV antibody, and positive for anti-HBs. He had a past history of chronic hepatitis B. In 1986, HBsAg had become negative with the development of anti-HBs. In 2003, an HCC was detected and liver resection was carried out. Histological examination revealed moderately differentiated HCC and slightly fibrotic liver. It is suggested that a diagnosis of HCC, combined with negativity for HBsAg and anti-HCV antibody, may include cases of past recovery from chronic hepatitis B, such as this case.

Antibodies, Viral↗
PubMed2004

Rising plasma nociceptin level during development of HCC: a case report.

AIM: Although liver cirrhosis is a predisposing factor for hepatocellular carcinoma (HCC), relatively few reports are available on HCC in primary biliary cirrhosis. High plasma nociceptin (N/OFQ) level has been shown in Wilson disease and in patients with acute and chronic pain. METHODS: We report a follow-up case of HCC, which developed in a patient with primary biliary cirrhosis. The tumor appeared 18 years after the diagnosis of PBC and led to death within two years. Alfa fetoprotein and serum nociceptin levels were monitored before and during the development of HCC. Nociceptin content was also measured in the tumor tissue. RESULTS: The importance and the curiosity of the presented case was the novel finding of the progressive elevation of plasma nociceptin level up to 17-fold (172 pg/mL) above the baseline (9.2+/-1.8 pg/mL), parallel with the elevation of alpha fetoprotein (from 13 ng/mL up to 3 480 ng/mL) during tumor development. Nociceptin content was more than 15-fold higher in the neoplastic tissue (0.16 pg/mg) than that in the tumor-free liver tissue samples (0.01 pg/mg) taken during the autopsy. CONCLUSION: Results are in concordance with our previous observation that a very high plasma nociceptin level may be considered as an indicator for hepatocellular carcinoma.

Biomarkers, Tumor↗
PubMed2005

Prediction of HLA-A2-restricted CTL epitope specific to HCC by SYFPEITHI combined with polynomial method.

AIM: To predict the HLA-A2-restricted CTL epitopes of tumor antigens associated with hepatocellular carcinoma (HCC). METHODS: MAGE-1, MAGE-3, MAGE-8, P53 and AFP were selected as objective antigens in this study for the close association with HCC. The HLA-A*0201 restricted CTL epitopes of objective tumor antigens were predicted by SYFPEITHI prediction method combined with the polynomial quantitative motifs method. The threshold of polynomial scores was set to -24. RESULTS: The SYFPEITHI prediction values of all possible nonamers of a given protein sequence were added together and the ten high-scoring peptides of each protein were chosen for further analysis in primary prediction. Thirty-five candidates of CTL epitopes (nonamers) derived from the primary prediction results were selected by analyzing with the polynomial method and compared with reported CTL epitopes. CONCLUSION: The combination of SYFPEITHI prediction method and polynomial method can improve the prediction efficiency and accuracy. These nonamers may be useful in the design of therapeutic peptide vaccine for HCC and as immunotherapeutic strategies against HCC after identified by immunology experiment.

Amino Acid Sequence↗
PubMed1999

Gene expression of hepatocyte growth factor and its receptor in HCC and nontumorous liver tissues.

AIM:To study the changes of gene expression of hepatocyte growth factor (HGF) and hepatocyte growth factor receptor (HGFr) in hepatocellular carcinoma (HCC) tissue and nontumorous liver tissue and the relationship between these changes and the biological behavior of the tumor.METHODS:Gene expression of HGF and HGFr in 26 cases of HCC tissue and their adjacent nontumorous liver tissues was determined with digoxigenin labeled DNA probes.RESULTS:Positive expression of HGF in HCC tissue was similar to that in the adjacent nontumorous liver tissue, but positive rate of HGF expression was lower than HGFr gene expression. However, HGFr expression was higher in the metastatic cases than in those without metastasis. It was found that HGFr was overexpressed in HCC tissue as well as in the adjacent nontumorous liver tissue.CONCLUSION:There seems to be a close relationship between overexpression of HGFr gene and tumor metastasis, and the HGF and HGFr system plays an important role in regulating tumor growth and metastasis.

Journal Article↗
PubMed2000

Overexpression of p27(KIP1) induced cell cycle arrest in G(1) phase and subsequent apoptosis in HCC-9204 cell line.

AIM:We have previously reported that inducible over-expression of Bak may prolong cell cycle in G(1) phase and lead to apoptosis in HCC-9204 cells. This study is to investigate whether p27(KIP1) plays an important role in this process.METHODS:In order to elucidate the exact function of p27(KIP1) in this process, a zinc inducible p27(KIP1) stable transfectant and transient p27(KIP1)-GFP fusion transfectant were constructed. The effects of inducible p27(KIP1) on cell growth, cell cycle arrest and apoptosis were examined in the mock, control pMD vector, and pMD-KIP1 transfected HCC-9204 cells.RESULTS:This p27(KIP1)-GFP transfectant may transiently express the fusion gene. The cell growth was reduced by 35% at 48 h of p27(KIP1) induction with zinc treatment as determined by trypan blue exclusion assay. These differences remained the same after 72h of p27(KIP1) expression. p27(KIP1) caused cell cycle arrest after 24 h of induction, with 40% increase in G(1) population. Prolonged p27(KIP1) expression in this cell line induced apoptotic cell death reflected by TUNEL assay. Fourty-eight h and 72 h of p27(KIP1) expression showed a characteristic DNA ladder on agarose gel electrophoresis.CONCLUSION:Bak may induce cell cycle arrest in G(1) phase through upregulating expression of p27(KIP1) and subsequently lead to apoptosis in HCC-9204 cells. The p27(KIP1) -GFP fusion protein can be transiently expre-ssed in HCC-9204 cells. The inducible p27(KIP1)-expressing cell line provides a model to assess p27(KIP1) function.

Journal Article↗
PubMedDate not supplied

Clinical significance of alpha-fetoprotein mRNA during perioperative period in HCC.

BACKGROUND/AIMS: The presence of alpha-fetoprotein (AFP)mRNA in the peripheral blood of patients with HCC suggested that carcinoma cells still existed. We investigated the influence of an alternation of human AFPmRNA perioperatively detected in peripheral blood in matters of recurrence, prognosis and operative performance. METHODOLOGY: Thirty-three patients with HCC were enrolled for this study. AFPmRNA in peripheral blood before the operation, and on 1, 3, 7, 14, 21 and 28 post-operative days was examined by means of the reverse-transcriptase polymerase chain reaction (RT-PCR). RESULTS: In 18 of 33 patients (54.5%) with HCC, AFPmRNA was detected in peripheral blood pre-operatively. Ten of 22 (45.4%) who were detected with AFPmRNA in peripheral blood during the perioperative period were diagnosed with intrahepatic recurrence or distant metastasis within 12 months post-operatively. In contrast, 10 (90.8%) of 11 patients who were not detected with AFPmRNA in peripheral blood anytime during hospitalization were diagnosed as free of intrahepatic recurrence or distant metastases within 9 months after the operation. CONCLUSIONS: These results suggested that an alternation of AFPmRNA from HCC patients' peripheral blood during the perioperative period by means of this technique may be a practical tool in the detection of early recurrence or distant metastases after surgery.

Adult↗
PubMed2001

[Expression of telomerase reverse transcriptase and its relationship with tumor suppressor gene p53 in HCC].

OBJECTIVE: To explore the expression of human telomerase reverse transcriptase (HTERT) and its relationship with tumor suppressor gene p53. METHODS: RNA-RNA in situ hybridization (ISH) technique was applied to localize the expression of HTERT mRNA and immunohistochemistry (IHC) was used to observe the p53 protein expression in 34 specimens of HCC and their corresponding non-cancerous tissues. Both the significance of HTERT mRNA expression in the different histopathologic characters and its relationship with p53 protein were investigated. RESULTS: HTERT was detected in tumor tissue in 30 of 34 cases (88.2%), and all the 6 cases of small cancer (diameter<3cm) were positive. The positive rate of HTERT mRNA was higher in the tumor tissues with low-differentiation, extra- or intra-hepatic metastasis, uncompleted fibrotic capsule and/or the non-cancerous tissue with chronic active lesions or positive HBsAg. Intensive signal was seen both in the HCC cells along the front of invasive area and in a few non-cancerous liver cells with dysplasia. Of all 34 HCC, p53 protein was presented in 25 cases. There was a correlation between the expression of HTERT mRNA and of p53 protein. The coincidence rate of the expression (HTERT+/p53+ and HTERT-/p53-) was 79.4%. More intensity of HTERT signal could be seen in the cases of positive p53. HTERT mRNA was not found in normal liver tissues. CONCLUSIONS: High expression of HTERT mRNA is proved in most cases of HCCs. HTERT expression may relate to the pathogenesis and the invasion of HCC. p53 may play a role in regulating the expression of HTERT.

Adult↗
PubMed1992

[Therapeutic difference by TAE between HCC with HCV-Ab and HBV-Ag].

Transarterial infusion therapy using adriamycin-Lipiodol emulsion (TAE) was used for 30 patients of HCC with HCV-Ab and 20 patients with HBV-Ag. We compared the tumor effect and prognosis in terms of several clinico-pathological factors. The response rate (PR+MR) after TAE was 43% in HCC patients with HCV-Ab and 30% in those with HBV-Ag. One-year survival rate was 89% in HCC patients with HCV-Ab and 58% in HCC patients with HBV-Ag. Thus, there was a significant difference between the two groups. No definite reasons between two groups influencing tumor effect and prognosis is obviously revealed except for portal vein invasion.

Carcinoma, Hepatocellular↗
PubMed2005

[Estimation of an NY-ESO-1 expressing HCC cell line by NY-ESO-1b specific CD8+T cells in vitro induced by HLA-A2 restricted NY-ESO-1b peptide].

OBJECTIVE: To analyze the effect of an NY-ESO-1 expressing HCC cell line by NY-ESO-1b specific CD8(+)T cells in vitro induced by HLA-A2 Restricted NY-ESO-1b peptide and to further analyze the possibility of NYjESOj1 as a vaccine in HCC treatment. METHODS: Peripheral blood mononuclear cells (PBMCs) were obtained from an HLA-A2(+) HCC patient and NY-ESO-1 specific CD8(+)T cells were in vitro induced by HLA-A2 Restricted NY-ESO-1b peptide. Next we estimated the effect that NY-ESO-1 specific CD8(+)T cells recognized and killed NY-ESO-1 expressing HepG2 cells by enzyme-linked immunospot(ELISPOT). RESULTS: These in vitro induced NY-ESO-1b specific CD8(+)T cells could recognize HepG2 cells stably transfected with NY-ESO-1 in both IFN-gamma and Granzyme B ELISPOT assays. And the data also showed that NY-ESO-1 specific CD8(+)T cells could efficiently kill NY-ESO-1 expressing HepG2 cells. CONCLUSION: NY-ESO-1 protein can be processed by HCC cells, and that HLA-A2 restricted NY-ESO-1b peptide (157-165) can also be presented on the surfaces of cells and recognized by NY-ESO-1b specific CD8(+)T cells in vitro induced.

Antigens, Neoplasm↗
PubMed1991

Pathobiology of chronic hepatitis virus infection and hepatocellular carcinoma (HCC).

Hepatitis viruses may cause liver cancer (HCC) through an indirect mechanism inducing inflammation and cirrhosis. Only hepatitis B virus (HBV) was shown to have a direct oncogenetic potential. Hepatitis D virus (HDV) infection, superimposed on the oncogenetic background provided by chronic HBV infection, appears to provide an additional risk for HCC. Patients with florid infections from both HBV and HDV and active liver inflammation develop HCC at a significantly younger age than those infected by HBV alone or infected by hepatitis C virus (about 10 years earlier). In patients positive for serum HBV-DNA/HDV-RNA and/or IgM anti-HBc/IgM anti-HD it is mandatory to program a more frequent (thrice a year) schedule of screenings (ultrasound scan, alpha-1-phetoprotein, etc.) for prophylaxis of HCC.

Animals↗
PubMed1989

Strategy for early diagnosis of hepatocellular carcinoma (HCC).

Two hundred and eighty-two patients with HCC including 89 with tumors 2 cm or smaller in size and 193 of 2-5 cm were studied on clinical and pathological findings and correlated with the value of various diagnostic imaging modalities. There were apparent differences in histological findings of HCC between 2 cm or smaller in size and larger ones; the former had much less invasion of malignant cells to the extracapsule and portal vein neighbouring the HCC than the latter. In 83 patients with HCCs 2 cm or less in diameter AFP level was normal (less than 20 ng/ml) in 39.8%, 20-200 ng/ml in 44.6% and more than 200 ng/ml in only 15.6%. Detectability of HCC measuring 2 cm or less by various imaging modalities was as follows: 97.8% by US, 54% by X-ray computed tomography (CT), 61.6% by magnetic resonance imaging (MR) and 75.4% by angiography. There was considerable limitation of imaging modalities in making a definitive diagnosis of the smaller HCCs, particularly in the differentiation from regenerative nodules of liver cirrhosis. Tissue biopsy under ultrasound control provided a correct diagnosis in 36 out of 41 patients (87.8%) with HCCs 2 cm or less in size, a better ratio than for aspiration biopsy.

Adult↗
PubMed1995

[Detection of HBV DNA and HBsAg in HCC and pericarcinomatous tissues using double labelling technique].

40 cases of hepatocellular carcinoma (HCC) and their surrounding tissues were studied on paraffin-embedded sections by in situ hybridization and immunohistochemical double labelling techniques. The positive rates of HBV DNA and HBsAg were 65% and 82.5% respectively, suggesting that HBV infection is a significant cause of HCC. HBV DNA and HBsAg signals in the pericarcinomatous tissues were stronger than that in cancer cells. Reduced replication caused by integration of HBV DNA in HCC may explain this phenomenon. We found that the small "piece-meal like" inclusions which existed only in HCC may be a special cancer related pattern of HBsAg. There were stronger signals of HBsAg in the small cell LCD than in other pericarcinomatous lesions, supporting the theory that the small cell LCD is more likely to be a precarcinomatous lesion.

Carcinoma, Hepatocellular↗