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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case/control study has been carried out to determine the prevalence of hepatitis B surface antigen (HBsAg) and antibody (anti-HBs) in patients with primary liver cancer (PLC), and age/sex matched hospital controls with cancers of other sites (OCC) and similarly matched controls without cancer (NCC). HBsAg was found in 61.2% of 165 cases of PLC, as compared to 11.7% of 154 OCC and 11.3% of 328 NCC. The frequency of HBsAg in PLC patients was significantly higher (72.2%) in those with detectable alpha-fetoprotein as compared to those without (40.3%).
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PMID:[Primary liver cancer and hepatitis B infection in Senegal. Comparison of cancer patients with 2 control groups]. 6 Jan 44

The prevalence of serological markers of active of past hepatitis-B virus (H.B.V.) infection was determined in 80 Greek patients with primary hepatocellular carcinoma (P.H.C.), 160 age and sex matched controls and 40 patients with metastatic liver cancer (M.L.C.). The relative risk of the various patterns of H.B.V. serological markers for P.H.C. was calculated. Active H.B.V. infection, as indicated by positive tests for hepatitis-B surface antigen (HBsAg), or antibody to hepatitis-B core antigen (anti-HBc) without antibody to HBsAg) (anti-HBs), was associated with P.H.C. (relative risk 10.4) but not with M.L.C. (relative risk 1.2). Patients without markers and those who had recovered from hepatitis B (anti-HBs-positive) had approximately the same low risk for P.H.C. (relative risk 0.8). Active infection was more common in P.H.C. patients with co-existing cirrhosis than in those without cirrhosis (67% versus 26%). Thus the relationship between active hepatitis B and P.H.C. seen in African and Asian populations is now seen in a European Caucasian population with different racial, environmental, and dietary circumstances.
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PMID:Hepatitis B and primary hepatocellular carcinoma in a European population. 8 32

The human hepatoma cell line, PLC/PRF/5, was shown to produce hepatitis B surface antigen (HBsAg). Immunologically reactive material was present in the supernatant tissue culture medium in significant amounts, and was associated with spherical particles approximately 20 nm in diameter. The rate of antigen production by the cells was estimated at 500 ng/day/10(6) cells by reference to a purified HBsAg standard. All immunological activity was neutralized by specific antibody and the subtype was ad. The studies reported here broaden the scope of investigations on both the in vitro production of HBsAg and the association between this antigen and primary liver cancer.
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PMID:Hepatitis B surface antigen produced by a human hepatoma cell line. 18 8

Although hepatocellular carcinoma is probably caused by one or more environmental carcinogens, a genetically determined susceptibility to the development of the tumor has not been excluded. In looking for such a predisposition, we have compared the histocompatibility antigens (HLA) of 102 southern African blacks with histologically proved HCC with those of 208 healthy blacks. The standard two-stage lymphocyte microcytotoxicity method was used to test for 40 antigens: 17 in the A locus, 20 in the B locus, and 3 in the C locus. None of the HLA antigens had a frequency that was significantly different in the patients and the controls. A close association undoubtedly exists between chronic hepatitis B virus infection and hepatocellular carcinoma. If this virus is proved to be oncogenic with respect to hepatocellular carcinoma, a genetic predisposition to the hepatitis B virus carrier state may have an indirect bearing on the etiology of the tumor. Sera from the hepatocellular carcinoma patients were therefore tested for hepatitis B virus markers (HBV surface antigen and antibody against HBV core antigen), and these were related to the patients' histocompatibility antigens. None of the HLA antigen frequencies was significantly different in the surface antigen-positive and the surface antigen-negative patients. As 88% of the patients were anticore positive, no meaningful correlation could be carried out with this marker. Analysis of histocompatibility antigens thus failed to show evidence of a genetic predisposition either to hepatocellular carcinoma or to chronic hepatitis B surface antigenemia in patients with this tumor.
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PMID:Histocompatibility antigens in patients with hepatocellular carcinoma and their relationship to chronic hepatitis B virus infection in these patients. 22 45

Hepatitis type B is hyperendemic in Greenland with serologic evidence of infection in 54% of adults and a hepatitis B surface antigen (HBsAg) carrier rate of 7--25%. The impact of this infection rate on the occurrence of cirrhosis and primary liver cancer (PLC) was studied. Mortality rates for cirrhosis were obtained from official mortality statistics, 1951--1975. PLC was identified by a study of all biopsy and necropsy material taken in the study area during the same period. Neither cirrhosis nor PLC was found to be a more prevalent cause of death in this population than in Northern Europe where hepatitis B is at least 10-fold less prevalent. It is concluded that hepatitis B infection per se does not contribute significantly to the development of cirrhosis or to PLC, at least in the Eskimo population of Greenland.
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PMID:Occurrence of cirrhosis and primary liver cancer in an Eskimo population hyperendemically infected with hepatitis B virus. 70 73

Sera of 184 patients were examined to determine the incidence of hepatitis B surface antigen (HBsAg). Ninety-two patients had primary liver cancer (PLC) and there were 92 matched controls. Thirty-one of the 92 patients with PLC and 8 of the 92 patients with no clinical evidence of liver disease had radio-immunoassay-positive tests for HBsAg. The difference was significant (P less than 0,01). In 56 of the patients with PLC it was possible to assess the nature of associated liver disease histologically. HBsAg was found in the sera of 66,6% of patients with postcollapse cirrhosis and in 22,2% of patients with chronic Budd-Chiari syndrome. It is likely that the role played by hepatitis B infection in the pathogenesis of PLC varies according to local circumstances in different geographical areas.
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PMID:Hepatitis B surface antigen and primary liver cancer. 71 32

A case/control study has been carried out to determine by radioimmunoassay and passive hemagglutination techniques the prevalence of hepatitis B surface antigen (HBsAg) and antibody (anti-HBs) in patients with primary liver cancer (PLC) and age/sex-matched hospital controls with cancers of other sites (OCC) and similarly matched controls without cancer (NCC). HBsAg was found in 61.2% of 165 cases of PLC as compared to 11.7% of 328 NCC. The frequency of HBsAg in PLC patients was significantly higher (72.2%) in those with detectable alpha fetoprotein as compared to those without (40.3%). There was no difference in the frequency of HBsAg in PLC patients with and without accompanying cirrhosis. No significant difference in potential hepatitis exposure history was found in the three study groups.
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PMID:A case/control study of the association between primary liver cancer and hepatitis B infection in Senegal. 117 99

Patients with decompensated liver cirrhosis (n 1441) and those with post-transfusion hepatitis (n 343), whose medical expenses were subsidized by the Aichi Prefectural Government, were followed up for three years by record linkage with the Aichi Cancer Registry. During the follow-up period, 122 incident cases of liver cancer were identified. Compared with the general population, patients with decompensated liver cirrhosis were at a 64.9 times greater risk (50.5 times in males and 100.4 times in females) and those with post-transfusion hepatitis were at a 9.4 times greater risk (8.9 times in males and 13.7 times in females) of developing liver cancer. Information on prognostic factors for 1,068 patients with decompensated liver cirrhosis was also collected in a questionnaire survey by the physicians in charge. Patients positive to hepatitis B surface antigen (HBs Ag) and those positive to HBe Ag had a significantly increased risk of subsequent liver cancer. The risk of developing liver cancer was positively associated with base-line levels of GPT and AFP and age and, inversely associated with total alcohol intake and female sex. In multivariate analyses, the associations with HBe Ag, AFP, sex and age remained statistically significant, whereas the associations with GPT, total alcohol intake and HBs Ag were of borderline significance.
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PMID:The risk and predictive factors for developing liver cancer among patients with decompensated liver cirrhosis. 127 45

A Nigerian series of 890 patients with primary liver cell carcinoma, seen during the recent three years, has been examined with a view to establishing the natural history of the tumour in untreated cases. There were 60 males and the mean age of all the patients was 50 years. Hepatitis B surface antigen was positive in 70 pc of tested patients and there were higher pathologic levels of aflatoxins in these patients when compared to normal controls. Liver cirrhosis was associated with 81 pc of patients. Alcohol and smoking were unlikely to be aetiologically important in these patients. The macroscopic type of tumour was mainly diffusely nodular and the commonest microscopic pattern was the characteristic trabecular pattern. Metastases were present in 52 pc of the patients and were mainly to the lungs. Due to late presentation and underlying cirrhosis, most patients were critically ill with high incidence of ascites, jaundice and hepatic precoma. The mean survival time of all patients was six months after onset of the initial symptoms to death and only three weeks after admission to death. The major causes of death were advanced cancer in 78 pc, hepatic failure in 48 pc and rupture of tumour, 39 pc. These observations clearly show that the prognosis of liver cancer is dismal in this environment, as elsewhere. Medical education on earlier presentation in hospital and early operative removal of the tumour should be emphasised. It is suggested that an attempt through immunisation should be employed to reduce the incidence of liver cancer in the population.
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PMID:The natural history of primary liver cell carcinoma: a study of 89 untreated adult Nigerians. 132 87

The present paper reviews several studies performed between 1977 and 1986 in Singapore on the 10-year survival outcome of treatment for stage I and II hepatocellular carcinoma (HCC). Of 801 HCC patients evaluated, only 2 survivors (0.3%) remained in complete remission for 13 and 14 years, respectively. One had received four weekly cycles of prednisolone, Adriamycin, vincristine and 5-fluorouracil for an inoperable HCC with a 10-cm diameter, and the other had received localised synchronised hepatic irradiation and Adriamycin. As follow-up, the use of localised hepatic irradiation consisting of 131I-labeled (30 mCi) iodised oil in lipiodol infused via the hepatic artery appeared to benefit patients with small residual tumours but did not affect larger tumours measuring 2 cm in diameter. Prophylactic, intermittent long-term administration of lymphoblastoid interferon-alpha (Wellferon) was carried out in pre-cancerous, high-risk hepatitis B surface antigen (HBsAg)-positive patients with cirrhosis, in immediate male relatives of liver cancer patients, and in persons who had undergone hepatic resection. In the untreated group, 10/162 (6%) cirrhotics, 3/18 (17%) male family members, and 6/10 (60%) post-resection cases developed single or multiple HCCs within 1 year of screening done at 3-month intervals on the basis of alpha-fetoprotein (AFP) levels and real-time hepatic ultrasonography. In contrast, none of the Wellferon-treated group consisting of 518 cirrhotic patients, 82 male relatives of HCC patients and 20 post-resection cases developed HCC. Two HBsAg-positive individuals who had not been treated with interferon (IFN) developed hepatic nodules which that showed dysplasia, AFP elevation and chromosomal changes. These studies demonstrate the poor results of late diagnosis and show that early intervention and prophylaxis with Wellferon can reduce the incidence of HCC in high-risk persons. In addition, transhepatic chemoembolisation and liver resection are suitable methods for treating small HCCs (single or multiple) that are detected by screening. However, some of these early-detected HCCs remain highly malignant. Prophylactic treatment of pre-cancerous conditions appears to be a better option as a long-term programme for HCC.
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PMID:Long-term survival following treatment of hepatocellular carcinoma in Singapore: evaluation of Wellferon in the prophylaxis of high-risk pre-cancerous conditions. 133


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