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PubMed2003

Impact of N-acetyltransferase polymorphism (NAT2) in hepatocellular carcinoma (HCC)--an investigation in a department of surgical medicine.

In the multifactorial aetiology of hepatocellular carcinoma (HCC), an association and interaction between genetic polymorphisms of xenobiotic metabolizing enzymes, lifestyle factors, and cancer risk has been postulated. N-acetyltransferase (NAT2) is involved in the metabolic activation and detoxification of aromatic amines. Aromatic amines are potential hepatocarcinogens in humans. In the present study, we investigated if genetic NAT2 polymorphism is related to HCC. Genotyping of NAT2 was performed in 70 HCC patients and 87 controls using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. The results of this investigation show that 46 out 70 HCC patients (65.7%) and 50 out of 87 controls (57.5%) were of the slow acetylator genotypes. The frequency of distribution of slow and rapid acetylators (genotypes) was not significantly different between cases and controls (p > 0.05). Slow acetylator genotypes were not associated with a significantly increased HCC risk (odds ratio, 1.4; 95% confidence interval, 0.74-2.72). A significant association between NAT2 genetic polymorphism and HCC was observed among smokers. Slow acetylator genotypes significantly increased the HCC risk in cigarette smokers (odds ratio, 3.5; 95% confidence interval, 1.38-9.05). Our results suggest that genetic NAT2 polymorphism may play a role in lifestyle factors-related hepatocarcinogenesis. NAT2 activity may be particulary critical in smoking related hepatocarcinogenesis.

Acetylation↗
PubMed1996

HCC-1, a novel chemokine from human plasma.

A novel CC chemokine, HCC-1, was isolated from the hemofiltrate of patients with chronic renal failure. HCC-1 has a relative molecular mass of 8,673 and consists of 74 amino acids including four cysteines linked to disulfide bonds. HCC-1 cDNA was cloned from human bone marrow and shown to code for the mature protein plus a putative 19-residue leader sequence. Mature HCC-1 has sequence identity of 46% with macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta, and 29-37% with the other human CC chemokines. Unlike MIP-1 alpha and the other CC chemokines, HCC-1 is expressed constitutively in several normal tissues (spleen, liver, skeletal and heart muscle, gut, and bone marrow), and is present at high concentrations (1-80 nM) in plasma. HCC-1 has weak activities on human monocytes and acts via receptors that also recognize MIP-1 alpha. It induced intracellular Ca2+ changes and enzyme release, but no chemotaxis, at concentrations of 100-1,000 nM, and was inactive on T lymphocytes, neutrophils, and eosinophil leukocytes. In addition, HCC-1 enhanced the proliferation of CD34+ myeloid progenitor cells. It was as effective as MIP-1 alpha, but about 100-fold less potent.

Amino Acid Sequence↗
PubMed2006

Molecular techniques for identifying HCC origin and biology after orthotopic liver transplantation.

Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world. Liver transplantation represents the potentially curative treatment for small HCC. Recurrence after surgical resection and liver transplantation remains one of the major obstacles in further prolonging survival of patients with HCC. In the new liver, HCC might be of recipient or donor origin. One approach for investigating this question is by performing human identification and/or engraftment analysis. Distinction between recurrent and de novo HCC after orthotopic liver transplantation could allow for the development of important clinical and therapeutic strategies. Polymerase chain reaction amplification of highly polymorphic short tandem repeat DNA sequences, gene expression profiling, and fluorescence in situ hybridization were applied in a patient who developed a second HCC after orthotopic liver transplantation from an opposite gender donor. These techniques provided consistent evidence that the second HCC was a recurrence of the primary tumor.

Amelogenin↗
PubMedDate not supplied

Differentially expressed genes between early and advanced hepatocellular carcinoma (HCC) as a potential tool for selecting liver transplant recipients.

Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world. Liver transplantation (LT) represents a curative treatment for "small" HCC. Preoperative staging is critical in selecting optimal candidates for LT to optimize the use of this scarce resource. From December 1997 to February 2004, 148 patients diagnosed with cirrhosis and HCC were evaluated at our center. After staging, the patients were listed for LT according to United Network for Organ Sharing (UNOS) criteria. When pretransplant liver MRIs were compared with the findings of the explanted livers, 8 of 35 patients (22.8%) were understaged. Three of the 8 patients (37.5%) had recurrence post-LT. A retrospective gene expression profiling study was done using microarray technology for tumor samples in the pretransplant hepatitis C virus (HCV)-HCC understaged patients and in a contemporaneous group of HCV-HCC patients that were accurately staged. Two sample t tests comparing the early versus advanced HCV-HCCs with respect to gene expression showed an important set of genes differentially expressed among the samples. Hierarchical clustering analysis of the gene expression profiling classified 93.8% of the total tumor samples and 85.7% of the understaged samples in concordance with the explanted pathological staging. We found a distinctive pattern of gene expression between early and advanced HCV-HCCs. These results suggest that gene expression profiling could improve the pre-LT HCC staging to more closely mimic the explant pathology. Whether gene expression profiling of HCC will be refined to the point of predicting potential metastatic biologic behavior to predict post-LT recurrence will require longitudinal prospective study of this gene array technology.

Aged↗
PubMed2026

Multi-Target HCC Blood Test Demonstrates Consistent Performance Across Subgroups of Patients with Chronic Liver Disease.

BACKGROUND: Early detection of hepatocellular carcinoma (HCC) is critical for improving patient outcomes; however, ultrasound-based surveillance has limited sensitivity and variable performance across patient populations. We evaluated the performance of a multitarget HCC blood test (mt-HBT), incorporating methylated DNA markers, alpha-fetoprotein (AFP), and patient sex, across clinically relevant subgroups. METHODS: We performed a subgroup analysis of a multicenter, prospective case-control study that included 159 patients with early-stage HCC (Barcelona Clinic Liver Cancer Stage 0/A) and 649 control patients with cirrhosis or chronic hepatitis B without HCC. The mt-HBT combined methylated HOXA1, TSPYL5, and B3GALT6 markers with AFP and sex. Sensitivity and specificity were evaluated overall and according to age, sex, obesity, liver disease etiology, Child Pugh class, and tumor size. Performance was compared with AFP and GALAD. RESULTS: Overall sensitivity and specificity of mt-HBT for early-stage HCC detection were 76.7% (95% CI, 69.6-82.6) and 87.5% (95% CI, 84.8-89.8), respectively. Sensitivity was significantly higher than that of AFP (35.2%, p < 0.001) and comparable to that of GALAD (78.6%, p = 0.56), whereas specificity was lower than that of AFP (98.5%, p < 0.001) but higher than that of GALAD (76.9%, p < 0.001). Sensitivity was maintained across key subgroups, including patients with obesity (68.9%), Child Pugh B cirrhosis (75.0%), hepatitis C (80.0%), hepatitis B (72.2%), alcohol-associated liver disease (80.5%), and metabolic dysfunction-associated steatotic disease (69.0%) (all p > 0.05 between subgroups). Specificity exceeded 80% in all examined populations and was significantly higher in women than in men (92.5% vs. 83.9%, p < 0.001). Sensitivity increased with tumor size, ranging from 60.0% for tumors < 2 cm to 100% for tumors > 5 cm. CONCLUSIONS: The mt-HBT demonstrated robust, consistent performance for early-stage HCC detection across diverse patient populations, including subgroups in which ultrasound surveillance commonly underperforms. These findings support the prospective validation of mt-HBT as a blood-based surveillance strategy for HCC.

liver cancer↗
PubMed2004

Disseminated tumor cells homing into rats' liver: a new possible mechanism of HCC recurrence.

AIM: To detect the origin of hepatocellular carcinoma (HCC) recurring and attempt to propose a new recurrent mechanism. METHODS: Orthotopic liver allotransplantation was performed on male rats with HCC- induced by diethylnitrosamine using female donors. Metastatic tumors in transplanted livers were obtained. A DNA probe that exhibits specificity for the rat Y chromosome was generated by using a set of primers specific to murine sry gene. In situ hybridization (ISH) for Y chromosome was used to detected the origin of HCC recurring. Male HCC tissue was designed to be positive control. ISH on female tissue and using non-labeled with DIG probe was thought to be negative control. RESULTS: Positive marks were seen through ISH for Y chromosome in recurrent tumor tissue and positive control. No signal was detected in both negative controls. CONCLUSION: Recurrent HCC after liver transplantation originated from disseminated tumor cells in recipients. Extrahepatic cells homing into liver may be a new HCC recurrence mechanism. Likewise, it implicates that this mechanism is responsible for HCC recurring after hepatectomy.

Animals↗
PubMed2004

[Expression of human telomerase reverse transcriptase gene in HCC does not depend on proliferating cell nuclear antigen and P53].

AIM: To investigate the expression of human telomerase reverse transcriptase(hTERT) gene and its relationship with proliferating cell nuclear antigen and P53. METHODS: Immunohistochemical staining was used to detect the expressions of hTERT, PCNA and P53 in 42 hepatocellular carcinoma(HCC) tissues. The relationship between hTERT expression, pathological characters of HCC and PCNA and P53 expression was analyzed. RESULTS: The expression rates of hTERT, PCNA and P53 in HCC tissues were 71.4%(30/42),76.2%(32/42) and 73.8%(31/42), respectively. hTERT was not expressed in normal liver tissues. The expression rates of hTERT gene in HCC tissues of different pathological grades (I, II and III)were 40.0%(4/10), 70.0%(14/20) and 100%(12/12), respectively. The expression of hTERT was correlated with HCC recurrence. CONCLUSION: The expression of hTERT gene may relate to the genesis and progression of HCC. There is no significant correlation between the expression of hTERT and PCNA and P53. The detection of hTERT gene expression may be regarded as a marker for recurrence of HCC.

Aged↗
PubMed2005

[Changes in the immune function of dendritic cells (DC) derived from HBV-related hepatocellular carcinoma (HCC) patient's peripheral blood monocytes (PBMC) pulsed with tumor antigen].

OBJECTIVE: To identify the phenotype and immune function of dendritic cells derived from HBV-related HCC patients's peripheral blood monocytes pulsed with soluble tumor antigen, and their relation to immune escape. METHODS: Peripheral blood monocytes were isolated from 18 HBV-related hepatocellular carcinoma (HCC) patients, 11 HBV-related liver cirrhosis patients (LC) and 10 health blood donors; DCs were induced in the completed medium containing GM-CSF and IL-4. The morphology of DCs was studied using a confocal microscope and scanning electronic microscope, and the phenotype of DCs were detected by flow cytometric analysis. The mixed leucocyte reaction test was employed to determine the stimulatory capacity of DCs before and after being pulsed with soluble tumor antigen (prepared from HCCLM6 cell line). IL-12 ELISA kit was used to investigate IL-12 secretion of DCs in the supernate of MLR. RESULTS: The amount of PBMC and DCs was significantly lower in LC and HCC compare to those in the healthy subjects; the expression levels of HLA-DR, CD1a, CD80 and CD86 on DC surfaces were lower in LC and HCC patients than those of the healthy group; the stimulating capacity of DC in MLR and levels of IL-12 in supernate of MLR were also lower in LC and HCC, but were enhanced after tumor antigen pulsed in all three groups, particularly in the LC group; the secretion of IL-12 in MLR supernate was still lower than that of the healthy group. CONCLUSION: The phenotype and function defects of DC derived from PBMC of LC and HCC patients might play a key role in immune escape in HBV infection and HCC. The function of DC of LC patients can be enhanced after the tumor was antigen-pulsed.

Antigens, Neoplasm↗
PubMed2006

[Mechanical properties of rat HCC adhesion to collagen I and its relationship with cell cycle].

The mechanical properties of tumor cells adhering to extracellular matrix (ECM) are closely related with their invasion and metastesis. In this study we investigated the adhesive mechanical properties between hepatocellular carcinoma cells(HCC) and the collagen I coated surfaces from the viewpoint of cell cycle by coupling cellular biology and cellular mechanics, using micropipette aspiration and cell synchronization technique. The results showed that the synchronous G1 and S phase HCC cells were achieved by use of thymine-2-desoryriboside, colchicines sequential blockage method and double thymine-2-desoryriboside blockage method, and that the synchronous rates of G1 and S phase HCC amounted to 74.09% and 90.39% respectively. Within the ranges of dosing and timing in this study, the adhesion of HCC cells to collagen I displayed dose dependent and time dependent patterns. S phase cells had small force of adhesion to collagen I as compared with G1 phase and controlled cells(P<0.001), which suggested that G1 phase HCC may play an important role in the step of invading interstitial connective tissue in the metastasis pathway of HCC through blood circulation. These are of significance to unveiling the mechanism of HCC metastasis.

Animals↗
PubMedDate not supplied

Expression of laminin in HCC treated with transcatheter arterial embolization. Usefulness of laminin staining as a post-surgical detection procedure at the tumor invasion boundary.

The distribution of laminin was studied in sixty surgically resected hepatocellular carcinomas (HCC) treated with transcatheter arterial embolization (TAE) using immunoperoxidase procedure. When increased, laminin patterns consisted of thick basement membranes, organized in a trabecular pattern, and were lined by sinusoid structures. A marked increase of laminin was seen in 63.4% of well differentiated HCC, and in only 9.1% of poorly differentiated HCC. No laminin positive cases were found among 8 cases of adenomatous hyperplasia (AH) containing HCC foci. Thus, laminin patterns in HCC may be related to the degree of tumor differentiation. At the tumor-non tumor boundary, differential expression of laminin has made it possible to discriminate overt cancerous regions from normal tissues. Thus, laminin status proved to be an effective marker for tumor invasion in well-differentiated, laminin positive tumors. Assessment of HCC by laminin staining, together with a thorough and precise pathological examination of viable tumor cells after TAE treatment, may be recommended as a detection procedure for tumor invasion and for the transition from AH to the premalignant condition which culminates in HCC.

Adolescent↗
PubMed2026

PSMA1, PSMA5, and PSMB2 serve as prognostic biomarkers and are correlated with tumor-infiltrating leukocytes in HCC.

Hepatocellular carcinoma (HCC) ranks as the third leading cause of cancer-related death. Proteasome (PSM) is the main intracellular proteolytic system in higher eukaryotic cells. It has been reported to be involved in the tumor's onset, metabolism, and survival, and it has been recognized as a therapeutic target for many human cancers. The 20S proteasome subunits, specifically proteasome 20S subunit alpha 1 (PSMA1), proteasome 20S subunit alpha 5 (PSMA5), and proteasome 20S subunit beta 2 (PSMB2), are overexpressed in various malignancies, including HCC. Nevertheless, the exact role of these genes in HCC prognosis remains only partially understood. Moreover, a reliable predictive biomarker for HCC is essential for supporting the implementation of personalized therapies. Therefore, this study employed a comprehensive bioinformatics approach, integrating data from cBioPortal, Human Protein Atlas (HPA), Oncomine, STRING Viruses, Kaplan-Meier plotter, and other established high-throughput databases and tools. The current study thoroughly examined the expression levels, methylation, and genomic alterations of PSM and their correlation with tumor-infiltrating leukocytes. PSMA1, PSMA5, and PSMB2 are overexpressed in various cancers, including HCC, and their expression levels are associated with tumor grade and stage. The abundance of these genes is linked to diminished DNA methylation levels and genome alterations. Moreover, there was a significant association between the expression levels of these genes and poor prognosis and immune cell infiltration. In conclusion, this study proposes PSMA1, PSMA5, and PSMB2 as biomarkers for HCC.

Humans↗
PubMed1997

Hepatitis B and C virus infection, alcohol drinking, and hepatocellular carcinoma: a case-control study in Italy. Brescia HCC Study.

We performed a case-control study to assess the association of hepatocellular carcinoma (HCC) with hepatitis B virus (HBV) and hepatitis C virus (HCV) infection and alcohol drinking. We recruited as cases 172 subjects with an initial diagnosis of HCC, who were admitted to the two major hospitals in the province of Brescia, northern Italy, and 332 subjects, sex-, age-, and hospital-matched, who were admitted to the Departments of Ophthalmology, Dermatology, Urology, Cardiology, and Internal Medicine, as controls. Of the HCC cases, 23.8% were positive for HBsAg and 37.8% for HCV RNA; among the controls, 5.4% were positive for HBsAg and 4.8% for HCV RNA. History of heavy alcohol intake (>80 g of ethanol per day for at least 5 years) was found among 58.1% of the cases and among 36.4% of the controls. The relative risks (RRs) for HBsAg, HCV RNA positivity, and heavy alcohol intake were, respectively: 11.4 (95% confidence interval: 5.7-22.8), 23.2 (95% confidence interval: 11.8-45.7), and 4.6 (95% confidence interval: 2.7-7.8). Positive interactions (synergisms) between both HBsAg positivity and HCV RNA positivity and heavy alcohol intake were found, suggesting more than additive effects of viral infections and alcohol drinking on the risk of HCC. Infection with HCV genotype 1b showed a higher risk than type 2 (RR = 2.9; 95% confidence interval: 0.9-10), suggesting a major role for the former type in causing HCC. On the basis of population attributable risks (AR), heavy alcohol intake seems to be the single most relevant cause of HCC in this area (AR: 45%), followed by HCV (AR: 36%), and HBV (AR: 22%) infection.

Adult↗
PubMed1999

A case-control study on a novel DNA virus (TT virus) infection and hepatocellular carcinoma. The Brescia HCC Study.

We performed a case-control study to evaluate the association of a new human DNA virus named TT virus (TTV) with hepatocellular carcinoma (HCC). We recruited 174 subjects hospitalized for HCC (84% males; mean age: 64 years) and 118 patients hospitalized for non-liver diseases in Brescia, northern Italy, as controls (94% males; mean age: 66 years). TTV DNA was found in serum by polymerase chain reaction (PCR) in 26 cases (15%) and 11 controls (9.3%) (P >. 1). TTV group 2 infection was identified in 16 cases (61.5%) and 4 controls (36.4%) (P >.1) using a type-specific PCR method. Sequence analysis of 222 nt of TTV DNA demonstrated that the remaining 10 cases and 7 controls were all infected by group 1. The odds ratio (OR) for TTV-DNA positivity, adjusted for demographic variables, hepatitis B surface antigen (HBsAg), hepatitis C virus (HCV) RNA, and heavy alcohol intake was 1.8 (95% CI: 0.7-4.8; P >.1). The OR did not change when the analysis was restricted to 14 HCC cases and 56 controls who were negative for each known risk factor for HCC (OR = 1.7; 95% CI: 0.8-4.0). TTV-DNA positivity was not associated with transfusion history. The prevalence of TTV DNA was higher among HCC cases positive for HBsAg (10 of 38 [26.3%]) than among those positive for HCV RNA (8 of 62 [12.9%]) or negative for hepatitis B virus (HBV), HCV, and hepatitis G virus (HGV) infections (5 of 62 [8. 1%]) (P =.02). This study does not support the hypothesis of an association between TTV infection and HCC.

Adult↗
PubMed2004

Hcc-1 is a novel component of the nuclear matrix with growth inhibitory function.

Hcc-1 is a novel nuclear protein containing the SAF-box DNA-binding domain. It binds to both double-stranded and single-stranded DNA with higher affinity for the single-stranded form. In addition, it also binds specifically to scaffold/matrix attachment region DNA. These nucleic acid-binding characteristics suggest a potential function for Hcc-1 as a component of the heterogeneous ribonucleoprotein complex. Using a yeast two-hybrid screen, two DEAD-box RNA helicases, BAT1 and DDX39, were identified as proteins that interact with Hcc-1. Interactions with these RNA helicases suggested a role for Hcc-1 in nucleic acid biogenesis. Expression of Hcc-1 in the HEK293 cell line resulted in a slower growth rate compared to controls (p = 0.0173) and an accumulation of cells at the G2/M phase (p = 0.0276 compared to control HEK293 cells). Taken together, these results suggest a role for Hcc-1 in growth regulation and nucleic acids metabolism.

ATP-Binding Cassette Transporters↗
PubMed2002

[Shoulder metastasis as the initial manifestation of hepatocellular carcinoma (HCC)].

BACKGROUND: Primary diagnosis of hepatocellular carcinoma (HCC) by a shoulder metastasis is a rare event. HISTORY AND CLINICAL FINDINGS: A 68-year-old man was admitted with swelling of his left shoulder. No further clinical symptoms. Alcohol consumption: 1 l beer/day. On ultrasound, the clinically impressing tumor of the left shoulder showed calcifications. INVESTIGATIONS: Histologic examination of the tumor of the shoulder showed a well-differentiated, trabecular carcinoma consistent with the metastasis of an HCC. Subsequent ultrasound of the abdomen gave evidence of liver cirrhosis. In addition, an infiltrating mass was found, which encompassed 75% of the right liver lobe and was subsequently shown by histology to be a well-differentiated HCC with identical features of the tumor of the shoulder. Further metastases with pathologic rib fractures were found on CT scan of the thorax. DIAGNOSIS: Based on clinical findings, laboratory investigations and imaging studies, the patient suffered from an HCC owing to ethyl-toxic liver cirrhosis stage Child C, and initially presented with a shoulder metastasis. THERAPY: Due to the advanced tumor stage, no curative or palliative therapy was administered. CONCLUSION: This is an interesting case of an atypical primary diagnosis of HCC. The most important information was given by the pathologists who raised the suspicion of a metastasizing HCC by examining the tumor of the shoulder.

Aged↗
PubMed2005

Dendritic cells pulsed with gp96-peptide complexes derived from human hepatocellular carcinoma (HCC) induce specific cytotoxic T lymphocytes.

Dendritic cells (DCs) are one of the most potent antigen-presenting cells (APCs) capable of activating immune responses. Different forms of tumor antigens have been used to load DCs to initiate tumor-specific immune responses. Heat shock proteins (HSPs) are considered natural adjuvants which have the ability to chaperone peptides associated with them presented efficiently by interaction with professional APCs through specific receptors. In the present study, we used HSP, gp96-peptide complexes, derived from human hepatocellular carcinoma (HCC) cells as antigens for pulsing DCs. We found that gp96-peptide complexes derived from HCC cells induced the maturation of DCs by enhancing expression of human leukocyte antigen class II, CD80, CD86, CD40, and CD83. The matured DCs stimulated a high level of autologous T cell proliferation and induced HCC specific cytotoxic T lymphocytes, which specifically killed HCC cells by a major histocompatability complex (MHC) class I restricted mechanism. These findings demonstrate that DCs pulsed with gp96-peptide complexes derived from HCC cells are effective in activating specific T cell responses against HCC cells.

Antigen Presentation↗
PubMed2005

Increased incidence of hepatocellular carcinoma (HCC) in HIV-1 infected patients.

BACKGROUND: The likely increased incidence of hepatocarcinoma (HCC) in HIV-1 infected patients has not yet been demonstrated. METHODS: We studied all cases of HCC occurring in HIV-1 infected patients in our hospital during the past 15 years. Incidence and survival time were compared with those of the general population in the same area and the same time of the study. RESULTS: We found 6 cases of HCC in a cohort of 2383 HIV-1 infected patients between 1986 and 2001. This is a higher than expected incidence rate of HCC compared with the general population, with a standardized incidence ratio of 13.95. Chronic hepatitis virus infection and alcohol abuse were present in four and two cases, respectively. In one patient, no liver disease was known before the HCC and the surrounding liver was normal in the necropsy study. CONCLUSION: The improved survival of patients on highly active antiretroviral treatment (HAART) and the increasing incidence of end-stage liver disease in these patients caused by chronic hepatitis virus infection and alcohol abuse may be responsible for an increase in the incidence of HCC in HIV-1 infected patients.

Journal Article↗
PubMed2002

Neoadjuvant and adjuvant therapies for resectable hepatocellular carcinoma (HCC) and palliation strategies.

Hepatocellular carcinoma (HCC) is the most common primary malignancy in the liver worldwide. The incidence of the tumor varies geographically. Thus, in the eastern area (China, Taiwan, and Japan) there are more than 20 cases per year per 100'000 population compared to less than 5 cases per 100'000 in most western countries [1]. The etiology of HCC is multifactorial. The two most important factors are the presence of cirrhosis and chronic hepatitis [2]. Early detection of HCC still remains a challenge. At the time of diagnosis, only 20-30% of all patients have tumors that are surgically resectable. Survival after curative resection is 30%-50% at five years. The poor outcome of the disease led to the development of different adjuvant and neoadjuvant therapies. There are numerous studies dealing with the treatment of HCC. Unfortunately, only few randomized controlled trials exist. In addition, there is no consensus on staging of HCC and no standardization of the outcome in the literature, which makes it difficult to compare the different procedures. This paper summarizes the current strategies in the treatment of HCC.

Carcinoma, Hepatocellular↗