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

HCC occurs in a higher incidence in some subsets of human populations residing in specific geographic areas around the world. These include black populations residing south of the Sahara, particularly in South and East Africa; in populations of Southeast Asia and the Western Pacific; in India, China, and in some other circumscribed areas. These epidemiologic observations strongly suggest that environmental factors are involved in the etiology of HCC. Evidence from human and animal data point toward a multicausal etiology, including dietary or environmental contamination with mycotoxin carcinogens, acting in concert with hepatitis B viral infection and, in some areas, with malnutrition. Dietary factors that appear to influence susceptibility to HCC include fat, protein and amino acids, vitamin A, selenium, and zinc. In addition, alcohol consumption, environmental chemicals that are natural or man made, and genetic predisposition must also be considered. It seems likely that identification of etiologic agents (hepatitis B infection, aflatoxin, malnutrition) and correction or prevention of these are the most promising means for controlling HCC in man.
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PMID:Chemical carcinogenesis: mycotoxins and other chemicals to which humans are exposed. 608 58

During the past 20 years, trends have been observed in primary hepatocellular carcinoma in Thailand. There is a definite increase in the association between HCC and cirrhosis of liver from 16.6% in 1958 to 50.78% in 1968 and 73.93% in 1978 series. The increase in percentage is associated with increase in mean age group from 44.61 +/- 9.77 in 1958, to 48.84 +/- 12.35 (p < 0.01) in 1978. This reflects the important role which hepatitis B plays in the etiology of HCC-associated with cirrhosis in Thailand. Also, the aggregation of people in the city of Bangkok may cause an increase in the hepatitis B carrier.
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PMID:Carcinoma of the liver in Thailand, trends in two decades. 625 11

A review of 205 primary hepatic cancers from different geographic areas reveals that HCC which forms the vast majority (86%) of these, commonly presents as the trabecular variety (76%). The compact and pseudoglandular forms are rare (18% and 6%). Relatively fewer cases of undifferentiated cancer, hepatoblastoma and cholangiocarcinoma are encountered. HCC is often associated with the presence of hepatitis B virus surface antigen (HBsAg) in the liver. This is particularly true of the trabecular variety (81%). A proportion of the compact variety as well as undifferentiated cancers do not appear to be related to HBV infection. Cholangio carcinomas are considered to be related to infection by liver flukes. Hepatoblastomas occur in infancy and childhood and show no known aetiologic association. Aflatoxin may be aetiologically related to same cases of HCC. Continued use of oral contraceptives can occasionally induce HCC.
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PMID:Relationship between histology and aetiological factors in primary liver cancer. 625 13

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

A continuous human cell line was established from a hepatocellular carcinoma of an HBsAg-positive Japanese male. The cell line, designated HCC-M, grows as an adhering monolayer with a doubling time of 24 h in medium RPMI-1640 supplemented with 10% FCS and grows with 30% clonal efficiency in soft agar. The cells have been shown by light and electron microscopy to be of epithelial type. When they were transplanted subcutaneously into the back of athymic nude mice (BALB/c, nu/nu), tumors developed at the sites of inoculation, which were shown to be hepatocellular carcinoma, similar in morphology to the original tumor from which they were derived. HCC-M had a chromosome mode of 63 with five identifiable marker chromosomes. HCC-M produced albumin at the 10th passage but this property was lost by the 30th passage. This cell line has not secreted alpha-fetoprotein. Hepatitis B viral particles or HBsAg have not been demonstrated in the cells from the primary culture nor in several subsequent subcultures tested.
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PMID:Establishment of a cell line (HCC-M) from a human hepatocellular carcinoma. 630 92

The prevalence of serum hepatitis B virus markers was studied in three groups of age- and sex-matched patients: a. 31 patients with liver cirrhosis and hepatocellular carcinoma (c-HCC); b. 31 patients with chronic liver disease (CLD) and c. 62 hospitalized control subjects. The overall exposure rate to the hepatitis B virus was 90% in c-HCC, 80% in CLD and 58% in control subjects. The prevalence of hepatitis B surface antigen (HBsAg) was 29%, 13% and 1.6% in the three groups, respectively. The prevalence of hepatitis B surface antibody was significantly lower in c-HCC (9.6%) than CLD (42%) and control subjects (40%). The serological evidence of continuous viral replication (HBsAg positivity or isolated high titre hepatitis B core antibody positivity) was more common in c-HCC (39%) than CLD (12%) and control subjects (1.6%). The prevalence and patterns of aggregation of serum hepatitis B virus markers were similar in the 31 patients with c-HCC and in 11 patients with HCC without concomitant liver cirrhosis (n-HCC). In conclusion, the overall exposure rate to the hepatitis B virus is similar in c-HCC and CLD. However, serological evidence of continuous viral replication is more common in the former group. A defective clearance of the hepatitis B virus in hepatocellular carcinoma is a possible explanation of the phenomenon. The strength of the association between hepatitis B virus infection and hepatocellular carcinoma appears to be similar in c-HCC and n-HCC.
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PMID:Case-control study of hepatitis B virus infection in chronic liver disease and hepatocellular carcinoma. 632 29

Hepatitis C and B viruses are associated with hepatocellular carcinoma in Europe, Asia and Southern Africa. A study of hepatitis C and hepatitis B virus infection was carried out on 70 patients with HCC, from the National Cancer Institute, Cairo University. Sera from patients were tested for anti-HCV and HBsAg markers. Twenty patients (30%) were anti HCV positive alone, 15 (21.4%) were HBsAg positive alone, 28 (40%) were positive for both anti-HCV and HBsAg and the remaining 6 patients (8.6%) were negative for the two markers. The total positivity for anti-HCV and for HBsAg in these patients was 70% and 61.4% respectively. The comparable figures in a recent study on 90 blood donors from Egypt, were 24.4% for anti-HCV and 4.4% for HBSAg. These data suggest a possible link between HCV and HBV infection and the development of hepatocellular carcinoma in Egypt, as has been found elsewhere in the world.
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PMID:Hepatitis C and B viruses, and their association with hepatocellular carcinoma in Egypt. 750 48

We designed a multicenter cross-sectional study to evaluate the role of alcohol abuse, the hepatitis viruses and other pathogenic factors in cirrhosis and hepatocellular carcinoma. A total of 1,829 consecutive cirrhosis patients, with or without HCC, was enrolled over 6 mo in 21 centers throughout Italy. The etiological categories and diagnostic criteria were preestablished. The median age of the patients was 59 yr (range, 13 to 85 yr); 63.6% of the patients were graded as Child class A, 23.4% as Child class B and 13% as Child class C. Hepatitis C virus antibodies were found in 72.1% of cases (47.7% alone, 21.2% with alcohol abuse, 3.2% with hepatitis B virus); HBsAg was present in 13.8% (4.2% alone, 3.2% with hepatitis D virus, 3.2% with hepatitis C virus, 3% with alcohol abuse), alcohol abuse with no concomitant viral infection was recorded in 8.7%, primary biliary cirrhosis was found in 1.8%, other causes were found in 1.4% and cryptogenic cirrhosis was only present in 5.3%. Hepatocellular carcinoma was detected in 11.9% of patients (217 cases). The presence of hepatocellular carcinoma was more frequent in males than females (14.7% vs. 7.3%; p < 0.001) and increased with worsening Child class (8.3% in Child class A, 16.9% in Child class B, 19.9% in Child class C, p < 0.001). The highest prevalences of hepatocellular carcinoma were observed in hepatitis B virus infection, with or without alcohol abuse (20% and 16%, respectively) and in hepatitis C virus cirrhosis, with or without alcohol abuse (16% and 10.3%, p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenic factors in cirrhosis with and without hepatocellular carcinoma: a multicenter Italian study. 752 73

Subclinical hepatocellular carcinoma (SCHCC) is defined as HCC without obvious HCC symptoms and signs. During 1958-1991, 391 patients with SCHCC were analyzed. In the entire series, 1) 67.3% was detected by natural population screening using alpha-fetoprotein (AFP) serosurvey, while the others were discovered by high-risk population screening or regular health checkup using AFP and/or ultrasonography (US); 2) AFP > 20 micrograms/L was found in 77.6% of patients; 3) serum hepatitis B surface antigen (HBsAg) was positive in 68.9%; 4) associated liver cirrhosis occurred in 89.1%; 5) the median tumor size was 5 cm, and small HCC (< or = 5 cm) amounted to 61.1%; 6) resection was done in 81.4%, and limited resection was performed in the majority (71.3%); 7) re-resection for subclinical recurrence was done in 44 patients; and 8) cytoreduction and sequential resection was carried out in 13 patients with unresectable SCHCC. Comparison between SCHCC and clinical HCC (n = 1,251) revealed higher resectability (81.4% vs. 46.8%), lower operative mortality (1.9% vs. 6.0%), and higher 5-year survival (entire series: 50.7% vs. 20.6%; resection: 60.5% vs. 36.8%). It is concluded that the study of SCHCC has resulted in marked improvement of ultimate outcome of HCC; screening in high-risk populations using AFP and/or US, limited resection, and re-resection for subclinical recurrence are some of the key features.
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PMID:Subclinical hepatocellular carcinoma: an analysis of 391 patients. 768 16

A double case control study evaluated the role of hepatitis C virus (HCV) and hepatitis B virus (HBV), alcohol drinking, and tobacco smoking as potential risk factors for cepatocellular carcinoma (HCC). Fifty-one patients with HCC, 34 of whom had underlying cirrhosis, were analyzed against 51 hospital controls and 34 patients with cirrhosis, respectively. Sera from patients of all three groups were tested for HBV markers and anti-HCV antibodies. The polymerase chain reaction technique was used to detect HCV RNA in the anti-HCV-positive samples. Alcohol drinking and smoking habits were recorded for all patients. HCC risk was significantly related to the presence of hepatitis B surface antigen (HBsAg) [relative risk (RR) = 18], HCV infection (RR = 8), and alcohol abuse (RR = 4). When the presence of cirrhosis was taken into account, only HBsAg positivity was significantly associated with HCC development (RR = 6.7), indicating that HCV infection and alcohol abuse are related to HCC indirectly through the cirrhotic process. No significant interaction between HCV and HBV infection in the causation of HCC was found. Through the computation of population-attributable risk, it was found that 46% of the HCC cases in Greece could be attributed to HBsAg positivity but only 4% to HCV infection. In conclusion, HBV infection is the major risk factor in the development of HCC in Greece, either by inducing cirrhosis or by direct oncogenic effect. HCV infection is also related to HCC development, albeit indirectly through the cirrhotic process.
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PMID:The leading role of hepatitis B and C viruses as risk factors for the development of hepatocellular carcinoma. A case control study. 779 31


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