Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By means of an accurate immunoenzymatic assay, the prevalence was studied of antibodies to hepatitis C virus (HCV) in three different populations: 74 patients affected with hepatocellular carcinoma (HCC) on preexisting cirrhosis, 82 patients with liver cirrhosis but with no apparent neoplasm, and 70 control subjects, hospitalized for various conditions, of internal medicine or geriatric interest. 70.2% of HCC patients exhibited anti-HBC antibodies, versus 47.5% of cirrhotic subjects with no tumor and 7.1% of controls. Such results suggest the possible role of HCV in the etiopathogenesis of HCC, and its possible synergy with other agents-e.g., hepatitis B virus, alcohol--in causing chronically injured hepatocytes to become neoplastic.
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PMID:Anti-HCV antibodies and hepatocellular carcinoma. Relationship in a medium-risk population. 133 60

Primary hepatocellular carcinoma (HCC), is reported in three and probably a fourth member of a New Zealand Chinese family, with a high carrier rate of HBsAg. Hepatitis B virus (HBV) markers and HLA tissue types were analysed in the three generations of the expanded family of 35. Twenty-one of the three generations were positive for one or more serum HBV markers, including six of the 18 children. Intrafamilial spread of HBV was seen in four of the eight families. Tissue types did not correlate with HBV status. The two propositi of the four with HCC studied and four of six siblings were positive for HBsAg: both propositi had identical HLA haplotypes, including Bw46/DRw9. Evidence is as yet insufficient that this haplotype may represent a disease susceptibility gene for HCC. Other family members at risk will be those positive for HBsAg and/or anti HBC, but those with Bw46/DRw9 will be monitored with special interest.
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PMID:Familial hepatocellular carcinoma and hepatitis B antigenemia in a New Zealand Chinese family. 631 59

Chronic liver inflammation and hepatic regeneration by infection with hepatitis B (HBV) or C virus (HBC) seem to be important risk factors for hepatocellular carcinoma (HCC). Regarding the hepatocarcinogenesis of HBV DNA integration, it has been variously hypothesized that mechanisms such as the alteration of host chromosomal DNA and transcriptional trans-acting activity of the X gene are activated. On the other hand, integration of HCV virus into chromosomal DNA has not been reported. It is suggested that HCV could replicate more efficiently in noncancerous than in cancerous tissues. Therefore, it might affect some oncogenes or cause an inactivation of tumor suppressor genes in the early stage of HCC. Genetic alterations such as a point mutation and loss of heterozygosity are considered to be late events occurring after tumorigenesis. Regeneration of liver cells through chronic hepatitis increases the incidence of genetic alterations in hepatic cells and/or HCCs in both HBV- and HCV-infected patients.
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PMID:Pathogenesis of hepatocellular carcinoma: a review from the viewpoint of molecular analysis. 872 3

Although the iron-loading disease, hereditary hemochromatosis, has a strong causal association with hepatocellular carcinoma (HCC), the carcinogenic potential of dietary iron overload in Black Africans is not known. We investigated this potential by evaluating iron status, alcohol consumption, markers for hepatitis B (HBV) and C virus (HCV) infections, and exposure to dietary aflatoxin B1 in 24 rural patients with this tumor, 48 race-, sex-, and age-matched hospital-based controls, and 75 related or unrelated close family members of the cancer patients. Iron overload was defined as a raised serum ferritin concentration in combination with a transferrin saturation > or = 60%, and was confirmed histologically when possible. Among 24 patients and 48 hospital controls, the risk of developing HCC in the iron-loaded subjects was 10.6 (95% confidence limits of 1.5 and 76.8) relative to individuals with normal iron status, after adjusting for alcohol consumption, chronic HBV and HBC infections, and exposure to aflatoxin B1. The risk of HCC in subjects with HBV infection was 33.2 (7.2, 153.4) (odds ratio [95% confidence limits]), HCV infection 6.4 (0.3, 133.5), and alcohol consumption 2.0 (0.5, 8.2). Aflatoxin B1 exposure did not appear to increase the risk of HCC. The population attributable risk of iron overload in the development of HCC was estimated to be 29%. Among 20 cancer patients and 75 family members, the risk of developing HCC with iron overload was 4.1 (0.5, 32.2). We conclude that dietary iron overload may contribute to the development of HCC in Black Africans.
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PMID:Dietary iron overload as a risk factor for hepatocellular carcinoma in Black Africans. 962 Mar 27

HBV and HCV are two major etiologic agents of chronic hepatitis, which is closely related to the development of hepatocellular carcinoma (HCC). A possible involvement of HBV co-infection was investigated in ongoing HCV-related liver diseases in HCV-infected patients. A high prevalence of anti-HBC in anti-HCV-positive/HBsAg-negative chronic hepatitis patients was found and a low copy number of HBV DNA was detected in most of the liver biopsy samples of anti-HCV-positive/HBsAg-negative patients. The current data suggest that HBV co-infects frequently with HCV and may play an important role in the development of HCC in HCV-infected patients.
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PMID:[Co-infection of HBV with HCV and a possible role of HBV DNA in hepatocarcinogenesis]. 1003 65

The outcome of liver transplantation for patients with hepatitis B/C virus (HBV/HBC) cirrhosis or with hepatocellular carcinoma(HCC) was deemed pessimistic until the early 1990s due to the high rate of recurrence and mortality. However, with the advent of new antiviral agents and strict adherence transplant indications, the results of liver transplantation in patients with these disease have improved progressively. Coadministration of lamivudine and anti-HBV immunoglobulin, and of interferon and ribavirin inhibits the recurrence of hepatitis B and hepatitis C, respectively. Excluding HCC patients with extrahepatic or lymph node metastasis, vascular invasion, a single lesion more than 5 cm in diameter, or multiple lesions more than 3 cm in diameter, the 5-year patient survival rate has improved from 30% to 85%, with a disease-free survival rate of more than 90%. However, the development of lamivudineresistant mutants after prolonged use of the agent needs to be overcome, possibly by new antiviral agents such as adefovir. In addition, to expand the current limited transplant indications for HCC, the efficacy of perioperative anticancer treatment and the importance of molecular diagnosis of circulating hepatoma cells must be determined in future.
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PMID:[Liver transplantation for patients with hepatitis B/C virus cirrhosis or hepato cellular carcinoma]. 1204 76

Chronic hepatitis B (HBV) and C (HCV) virus infections are the most important factors associated with hepatocellular carcinoma (HCC), but tumor prognosis remains poor due to the lack of diagnostic biomarkers. In order to identify novel diagnostic markers and therapeutic targets, the gene expression profile associated with viral and non-viral HCC was assessed in 9 tumor samples by oligo-microarrays. The differentially expressed genes were examined using a z-score and KEGG pathway for the search of ontological biological processes. We selected a non-redundant set of 15 genes with the lowest P value for clustering samples into three groups using the non-supervised algorithm k-means. Fisher's linear discriminant analysis was then applied in an exhaustive search of trios of genes that could be used to build classifiers for class distinction. Different transcriptional levels of genes were identified in HCC of different etiologies and from different HCC samples. When comparing HBV-HCC vs HCV-HCC, HBV-HCC/HCV-HCC vs non-viral (NV)-HCC, HBC-HCC vs NV-HCC, and HCV-HCC vs NV-HCC of the 58 non-redundant differentially expressed genes, only 6 genes (IKBKbeta, CREBBP, WNT10B, PRDX6, ITGAV, and IFNAR1) were found to be associated with hepatic carcinogenesis. By combining trios, classifiers could be generated, which correctly classified 100% of the samples. This expression profiling may provide a useful tool for research into the pathophysiology of HCC. A detailed understanding of how these distinct genes are involved in molecular pathways is of fundamental importance to the development of effective HCC chemoprevention and treatment.
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PMID:Differential gene expression profiles of hepatocellular carcinomas associated or not with viral infection. 1989 92

Hepatocellular carcinoma (HCC) is known to be associated with both HBV and HCV. While epigenetic changes have been previously reported to be associated with hepatocellular carcinoma (HCC), whether the epigenetic profile of HBC associated HCC differs from that of HCV-associated HCC is unclear. We analyzed DNA methylation of ten genes (APC, CCND2, CDKN2A, GSTP1, HOXA9, RARB, RASSF1, RUNX, SFRP1, and TWIST1) using MethyLight assays on 65 archived liver tissue blocks. Three genes (APC, CCND2, and GSTP1) were frequently methylated in normal liver tissues. Five genes (APC, CDKN2A, HOXA9, RASSF1, and RUNX) were significantly more frequently methylated in malignant liver tissues than normal liver tissues. Among HCC cases, HOXA9, RASSF1 and SFRP1 were methylated more frequently in HBV-positive HCC cases, while CDKN2A were significantly more frequently methylated in HCV-positive HCC cases. Our data support the hypothesis that HCC resulting from different viral etiologies is associated with different epigenetic changes.
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PMID:DNA methylation changes in normal liver tissues and hepatocellular carcinoma with different viral infection. 2007 33

It is evidenced that both HBV and HCV infections may cause chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). HCV is considered as an oncogen virus. The mechanism of carcinogenesis in case of the two distinct viruses shows a number of common and different features. HCC usually develops in stage of liver cirrhosis caused by chronic inflammation of many years or decades. In contrast to HBC, HCV will not be incorporated into the genome of hepatocytes. It induces throughout different mechanisms the development of cancer cells, which will proliferate out of control. Before the discovery of HCV, the connection of non-A non-B (NANB) hepatitis and liver cancer has yet been observed. The subsequent epidemiological studies confirmed this association. A number of publications prove that HCC may develop without cirrhosis in HCV infected patients. The exact mechanism is not known, but data indicate that some proteins of the virus may induce oncogenic process. Differences were found in HCV core gene between HCC patients with and without cirrhosis. It is postulated that the virus evolves its oncogenic effect via endoplasmic and oxidative stress, further on by activation of different oncogenic signal pathways. Recent publications indicate the role of virus induced insulin resistance. Besides the virus determined factors, the host reaction, the deficient tumor cell eliminating capacity may also have a role in the development of liver carcinoma. Monitoring of HCV infected patients for HCC is an important clinical issue. Most relevant is the regular ultrasound cheek up. Serum alpha fetoprotein level is elevated only in a smaller proportion of the patients. The treatment protocol of HCV induced HCC does not differ from the others developed in non-HCV liver diseases.
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PMID:[Hepatitis C virus infection and hepatocarcinogenesis]. 2082 76

Aflatoxin B1 is a carcinogen produced by Aspergillus flavus and a few related fungi that are often present in many food substances. It interacts synergistically with Hepatitis B or C virus (HBV, HBC) infection, thereby increasing the risk of hepatocellular carcinoma (HCC). The G to T transversion at the third position of codon 249 (AGG) of the TP53 gene, substituting arginine to serine, is the most common aflatoxin-induced mutation linked to HCC. This study examined mutations in TP53 by PCR-RFLP analysis and by measurement of an aflatoxin-albumin adduct as a biomarker for human exposure of aflatoxin B1 by indirect-competitive ELISA, in samples collected from healthy controls as well as patients with hepatitis in Hyderabad, Andhra Pradesh, India. A total of 238 blood samples were analyzed the presence of the G to T mutation. Eighteen of these samples were from HBV-positive subjects, 112 of these were from subjects who had HBV-induced liver cirrhosis, and 108 samples were taken from subjects without HBV infection or liver cirrhosis (control group). The G to T mutation was detected in 10 samples, 8 of which were from subjects positive to both HBV and aflatoxin-albumin adduct in blood (p=0.07); whilst two were from individuals who were HBV-negative, but positive for the aflatoxin-albumin adduct (p=0.14). The aflatoxin-albumin adduct was detected in 37 of 238 samples, 29 samples were from HBV-positive subjects and eight were from individuals who were positive for both HBV and the TP53 mutation (p=0.07). The concentration of aflatoxin-albumin adduct ranged from 2.5 to 667pg/mg albumin. Despite low incidence of the G to T mutation, its detection in subjects positive to aflatoxin-adducts is indicative of a strong association between the mutation and aflatoxin exposure in India.
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PMID:The association between exposure to aflatoxin, mutation in TP53, infection with hepatitis B virus, and occurrence of liver disease in a selected population in Hyderabad, India. 2465 65


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