Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gene product expression in normal and chronic hepatitis C virus infection was determined in an attempt to improve our understanding of the molecular events leading to the development of cirrhosis and liver carcinoma. Activation of CD95 (Fas) causes apoptosis of cells and liver failure in mice and has been associated with human liver disorders. c-myc is involved in cell proliferation and EGFR in regeneration of cells. The material of the current study included 50 cases of chronic hepatitis C (CHC) (and negative hepatitis B virus infection), 29 cases of liver cirrhosis and HCV (LC), and 19 cases of hepatocellular carcinoma and HCV (HCC) admitted to the Theodor Bilharz Research Institute (TBRI) during the years 2003-2004. Ten wedge liver biopsies - taken during laparoscopic cholecystectomy - were included in the study as normal controls. Laboratory investigations, including liver function tests, serological markers for viral hepatitis and serum alpha fetoprotein level (alpha-FP), were determined for all cases. Histopathological study and immunohistochemistry using monoclonal antibodies for CD95, c-myc and EGFR were also done. In CHC cases, the histological activity index (HAI) revealed more expression of Fas antigen in liver tissues with active inflammation than in those without active inflammation (p < 0.01). EGFR and c-myc act synergistically in liver tumorigenesis. Upregulation of Fas in chronic hepatitis C infection and of c-myc & EGFR in malignant transformation was concluded from this study. c-myc expression may obstruct the induction of apoptosis of HCC cells and lead to uncontrolled cell growth.
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PMID:Immunohistochemical expression of CD95 (Fas), c-myc and epidermal growth factor receptor in hepatitis C virus infection, cirrhotic liver disease and hepatocellular carcinoma. 1685 63

There is a continuing need for innovative, alternative therapies for hepatocellular carcinoma (HCC). Immunotherapy of cancer is attractive because of the exquisite specificity of the immune response. Activation of an HCC-specific response can be accomplished by strategies targeting tumour-associated antigens (for example: alpha fetoprotein (AFP)) or viral antigens in those patients infected with hepatitis B or C. Uncharacterised and mutated antigens can also be targeted with whole tumour cell or tumour lysate-based immunisation strategies. Viral vectors coding for genes which make the patient's tumour immunogenic can allow the immune system to naturally evolve specificity against immunogenic target antigens. Strategies which have been tested in human clinical trials include adoptive transfer of lymphocytes, cytokine injections, autologous tumour-pulsed dendritic cells (DC) as well as AFP-derived peptides in adjuvant and pulsed onto autologous DC. These trials, testing novel immune-based interventions in HCC subjects, have resulted in immunological responses and some have impacted recurrence and survival of HCC subjects.
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PMID:Recent advances in immunotherapy for hepatocellular cancer. 1737 Jan 44

Saudi Arabia appears to have an usually high incidence of hepatocellular carcinoma, which has been causally associated with a high prevalence of hepatitis B virus (HBV). Other risk factors, including hepatitis C virus (HCV) infection are currently not known. A study was undertaken to establish the risk factors and clinicopathological features of hepatocellular carcinoma in Saudi Arabia. The profiles of 140 patients with a biopsy-proven hepatocellular carcinoma were analyzed. Demographic data revealed a strong male preponderance (male:female = 5.7:1) and 114 patients (81.4%) were found to have or have had HBV infection. The data concerning HCV infection were incomplete, but suggest a causal association (nine of 33 patients). An absence of alcohol as a risk factor was noteworthy. Clinical jaundice and right upper quadrant abdominal pain were the most frequent presenting features. Abnormal liver function tests were present in 125 patients 989.3%) at diagnosis and serum alpha fetoprotein was elevated in 112 patients (80%). The majority of patients had locally advanced, inoperable disease and the prognosis was uniformly dismal. The median survical was 61 days.
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PMID:Hepatocellular carcinoma: A review of 140 cases. 1737 9

The purpose of this study was to identify factors influencing prognosis after resection for hepatocellular carcinoma in the noncirrhotic liver and to measure the impact of moderate fibrosis on presentation and prognosis. A series of 116 primary procedures were performed for hepatocellular carcinoma in the noncirrhotic liver. These cases accounted for 42% of hepatic resections performed for hepatocellular carcinoma during the study period (1987-2005). Seventy-seven cases (58%) occurred in patients with nonfibrotic livers (Metavir score F0). The mean age was 61 years. The sex ratio was 3.5, with a female predominance before 50 years. Hepatitis B virus (HBV) or hepatitis C virus infection was found in 30% of patients. Symptoms were present in 64% of cases. Elevated serum alpha fetoprotein levels were observed in 44% of cases. Procedures involved minor hepatectomy in 40 cases, major hepatectomy in 72 cases, and transplantation in 4 cases. Postoperative mortality was 6% and morbidity was 31%. Complete resection was achieved in 90% of cases. The tumor was isolated in 72% of cases. The mean tumor diameter was 10.6 cm. Vascular invasion was observed in 48% of cases. Hepatocellular carcinoma in the nonfibrotic liver was associated with younger age and female sex, but there was no difference with other hepatocellular carcinoma with regard to histological or prognostic features. With a median follow-up of 79 months, overall survival was 40% for a median of 41 months. Multivariate analysis identified incomplete resection, vascular invasion, and HBV infection as independent factors of poor prognosis. In case of recurrence, repeat resection was feasible in 30% of cases with 69% survival at 5 years. Although hepatocellular carcinoma in the noncirrhotic liver is generally diagnosed at an advanced stage, its resectability remains high. As a result, hepatocellular carcinoma in the noncirrhotic liver accounts for a large proportion of cases in surgical series and has a better prognosis than hepatocellular carcinoma in the cirrhotic liver. Vascular invasion, incomplete resection, and HBV infection are independent factors of poor prognosis.
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PMID:Prognostic factors after resection for hepatocellular carcinoma in nonfibrotic or moderately fibrotic liver. A 116-case European series. 1746 20

Hepatocellular carcinoma (HCC) is a common cancer in the world due to high prevalence of hepatitis B or C virus infection. Research in recent years has uncovered important molecular pathways involved in development and progression of HCC. Several genetic aberrations and molecular mechanisms responsible for initiation of hepatocarcinogenesis have been identified. Novel biomarkers for HCC are being developed for better detection and prognostication. Alpha-fetoprotein, the conventional marker of HCC, has limited sensitivity and specificity. Serum levels of isoforms of AFP based on differential lectin binding of the glycan moiety appear to be more sensitive and specific than total AFP level in early detection of HCC. The clinical usefulness of other HCC biomarkers such as des-gamma-carboxy prothrombin and glypican-3 are under investigation. HCC is an aggressive tumor with early vascular invasion and metastasis. Studies over the past two decades have elucidated the clinical predictors of outcome, leading to several staging systems for HCC based on clinical parameters. However, the predictive accuracy of clinical staging systems is limited. Recent studies suggested that biological factors may provide additional prognostic information. In particular, gene expression profiling appears to be a promising approach. Study of tumor angiogenesis in HCC reveals that the expression of angiogenic factors such as vascular endothelial growth factor and angiopoietins may also predict prognosis. The elucidation of tumor biology of HCC is of particular importance in the current era of rapid development of anti-cancer molecular targeting agents, which provide hope for an effective systemic therapy for HCC.
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PMID:Biology of hepatocellular carcinoma. 1823 13

Hepatocellular carcinoma (HCC) is an important cause of cancer death in the world. It has great regional differences in the pathology and epidemiology. The variation is greatly influenced by the aetiologies of the disease. Hepatitis B and C infection are the most important risk factors. HCC incidence rates are higher but in decreasing trend in developing countries. However, the figures in the developed countries are contrary. Successful hepatitis B virus (HBV) vaccination programs, better food hygiene, increased global hepatitis C virus (HCV) prevalence and population migration are the possible explanations. A number of clinical and pathogenic differences exist between HBV- and HCV-related HCC. HBV infection leads to the development of HCC through direct and indirect pathways as it has the ability to integrate into the host genome affecting cellular signaling and growth control. HCV causes HCC mainly through indirect pathways: chronic inflammation, cell deaths and proliferation. As a result, HCC is almost exclusively found in cirrhotic HCV patients while HCC is sometimes found in HBV patients without significant liver cirrhosis. Due to the different severities of liver cirrhosis and HCC extent, therapeutic strategies from resection, liver transplantation to symptoms palliation are available. Poorly differentiated histology, lack of fibrous capsule, large tumour size, early vascular invasion and elevated serum levels of alpha fetoprotein (AFP) are the features for more aggressive disease. Combined with markers of liver reserve and performance status, accurate scoring systems and models have been developed to predict patients' survival and match best treatment option.
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PMID:Natural history of hepatitis-related hepatocellular carcinoma. 1835 May 95

Non-alcoholic steatohepatitis (NASH) has been associated with hepatocellular carcinoma (HCC) often arising in histologically advanced disease when steatohepatitis is not active (cryptogenic cirrhosis). Our objective was to characterize patients with HCC and active, histologically defined steatohepatitis. Among 394 patients with HCC detected by ultrasound imaging over 8 years and staged by the Barcelona Clinic Liver Cancer (BCLC) criteria, we identified 7 cases (1.7%) with HCC occurring in the setting of active biopsy-proven NASH. All were negative for other liver diseases such as hepatitis C, hepatitis B, autoimmune hepatitis, Wilson disease, and hemochromatosis. The patients (4 males and 3 females, age 63 +/- 13 years) were either overweight (4) or obese (3); 57% were diabetic and 28.5% had dyslipidemia. Cirrhosis was present in 6 of 7 patients, but 1 patient had well-differentiated HCC in the setting of NASH without cirrhosis (fibrosis stage 1) based on repeated liver biopsies, the absence of portal hypertension by clinical and radiographic evaluations and by direct surgical inspection. Among the cirrhotic patients, 71.4% were clinically staged as Child A and 14.2% as Child B. Tumor size ranged from 1.0 to 5.2 cm and 5 of 7 patients were classified as early stage; 46% of all nodules were hyper-echoic and 57% were <3 cm. HCC was well differentiated in 1/6 and moderately differentiated in 5/6. Alpha-fetoprotein was <100 ng/mL in all patients. HCC in patients with active steatohepatitis is often multifocal, may precede clinically advanced disease and occurs without diagnostic levels of alpha-fetoprotein. Importantly, HCC may occur in NASH in the absence of cirrhosis. More aggressive screening of NASH patients may be warranted.
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PMID:Does hepatocellular carcinoma in non-alcoholic steatohepatitis exist in cirrhotic and non-cirrhotic patients? 1978 50

Alpha-fetoprotein (AFP) is a marker of the presence of hepatocellular carcinoma (HCC), but is also elevated in advanced chronic hepatitis B. The detection and usage of AFP tests need to be improved. A cohort of 101 patients with advanced chronic hepatitis B and elevated AFP values was treated with entecavir (ETV) or peginterferon-alpha2a. ETV was more effective in reducing AFP levels; mean time to AFP normalization was 11.9 weeks after ETV treatment initiation vs 22.3 weeks in peginterferon treated patients (P = 0.000). An additional cohort of 93 hepatitis B virus (HBV) cirrhotic patients with elevated AFP were treated with ETV prospectively and maintained under intensive surveillance. HCC developed in 16 (17.2%) patients in whom the strongest independent predictor was a continued AFP rise in spite of ongoing treatment. In this context, nodules of sizes 10-14 mm and 15-20 mm were detected in 40% of patients each. In conclusion, HBV cirrhotic patients with rising AFP levels were at very high risk of HCC development. Early detection of minute lesions may be possible by monitoring AFP levels, whilst patients are on treatment in conjunction with enhanced computed tomography examination.
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PMID:Effect of antiviral treatment on alfa-fetoprotein levels in HBV-related cirrhotic patients: early detection of hepatocellular carcinoma. 1981 3

A 47-year-old otherwise healthy woman, presented elevation of alpha fetoprotein (AFP) and des-gamma-carboxy prothrombin (DCP) levels at a general health checkup. Both HCV antibody and hepatitis B surface antigen were negative. A screening abdominal CT revealed no abnormal change. An abdominal MRI and repeated CT, however, revealed a 20-mm tumor adjacent to the inferior vena cava and adjacent to or involving the liver. A surgical resection of the tumor was performed. The tumor was adjacent to, but distinct from, the liver. The Capsule of the tumor was connected to the liver but it was distinct from hepatic, renal, and adrenal tissue. A histological examination yielded a diagnosis of moderately differentiated hepatocellular carcinoma, with positive staining of hepatocyte-specific antigen and AFP.
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PMID:[A case of ectopic hepatocellular carcinoma]. 1996 20

Chronic viral hepatitis C and B are one of the major public health and medical problems. Both viruses cause life threatening liver diseases, i.e. cirrhosis, liver failure and hepatocellular carcinoma (HCC). Effective treatment for both hepatitis B and hepatitis C to reduce the rate of adverse outcomes is now available. There is no recommendation for mass screening for HBV and HCV in the general population but only in the high risk groups. There is wide availability of diagnostic tests for HCV and HBV infection with high sensitivity and specificity. Prior to therapy initiation, serum HCV RNA by quantitative assay and HCV genotype should be determined. Liver biopsy is performed to assess the disease severity, not always including genotype 3. Response to antiviral therapy should be assessed by AST, ALT and qualitative HCV RNA, and in patients with liver cirrhosis early detection of HCC by alpha fetoprotein, ultrasound, CT, or MR should be done every 6 months. Chronic HCV infection with cirrhosis and HCC is the leading indication for liver transplantation. The current hepatitis B vaccination policy is universal neonatal vaccination. HBsAg, HbBeAg and antiHBe positive patients should be qualitatively tested for HBV DNA and liver biopsy is performed according HBV DNA level. Patients are treated with interferon and nucleos(t)ide analogues. Treated patients should be tested for HBsAg, HBeAg and HBV DNA every 3 and 6 months. The optimal duration of therapy for oral drugs is not well established and life long treatment is generally recommended. Chronic HBV infection is the leading cause of HCC and its early detection is essential. Liver transplantation is successfully performed for HBV cirrhosis, liver failure and HCC. Patients with HBV/HDV, HBV/HCV or HIV/HBV/HCV co-infection should be treated accordingly. TTV, GBV-C and HEV hepatitis do not cause chronic liver diseases.
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PMID:[Monitoring patients with chronic hepatitis during and after therapy]. 2019 95


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