Epidemiology of hepatocellular carcinoma and its viral risk factors.
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Adult↗
Biomedical subjects
M C Kew
Publications and source records attributed to M C Kew.
The pathogenesis of raised serum alpha-fetoprotein levels in amoebic and pyogenic hepatic abscesses.
Serum alpha-fetoprotein (AFP) concentrations may be slightly raised in patients with amoebic hepatic abscesses. In an attempt to learn more about the pathogenesis of the raised levels, we studied 74 patients with amoebic and six with pyogenic hepatic abscesses. Serum (AFP) levels were slightly elevated (24-72 ng/ml) on admission in four patients and markedly raised (2000 ng/ml) in one, who had hepatocellular carcinoma in addition to a pyogenic hepatic abscess. The pattern of the early rise in AFP levels could not be determined because these four patients were lost to follow-up. However, serial serum AFP estimations were obtained in 29 patients with a normal value on admission and in none of these did the concentration rise during recovery. Our findings do not support the prevailing hypothesis that regenerating hepatocytes are responsible for the raised serum AFP levels in non-neoplastic hepatic disorders, including hepatic abscesses.
Adolescent↗
Research into the cause, diagnosis and treatment of primary liver cancer.
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Aflatoxins↗
Serum alpha-foetoprotein levels in amoebic hepatic abscess.
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Humans↗
Membranous obstruction of the inferior vena cava and invasion of the inferior vena cava by tumour in hepatocellular carcinoma.
A 28 yr old Zulu presented with a painful swelling in the right hypochondrium and severe swelling of the legs of short duration. The serum alpha-fetoprotein concentration was over 2 X 10(5) ng/ml and imaging showed a large hepatic mass-lesion. Radionuclide venography revealed no flow through the inferior vena cava but flow through a large collateral vessel. Contrast venography showed the upper portion of the inferior vena cava to be occluded: large collateral vessels arose from the lower vena cava and the iliac veins. The histological features were those of longstanding hepatic venous outflow obstruction with irregular centrizonal and portal fibrosis: severe acute centrizonal congestion was not seen. This combination of findings indicates the presence of both membranous obstruction of the inferior vena cava, a rare developmental abnormality which predisposes to hepatocellular carcinoma formation, and invasion by the tumour of the inferior vena cava via the hepatic veins, an uncommon complication of hepatocellular carcinoma.
Adult↗
Unusual clinical presentations of hepatocellular carcinoma.
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Abdomen, Acute↗
Hepatic scintoscans.
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Carcinoma, Hepatocellular↗
Analysis of ras gene mutations in hepatocellular carcinoma in southern African blacks.
Paired samples of hepatocellular carcinoma and non-tumorous liver tissue from 12 southern African blacks were examined for mutations in codons 12, 13, and 61 of the three ras proto-oncogenes (H-, K-, and N-ras). Deoxyribonucleic acid was isolated from carcinoma and non-tumorous tissues and amplified with the polymerase chain reaction. Using the single-stranded conformational polymorphisms method, products of the polymerase chain reaction amplification of codons 12, 13, and 61 of H-, K-, and N-ras were analysed for mutations. Mobility shifts were not detected except in one tumour in the region of codon 61 of K-ras. By sequencing the relevant polymerase chain reaction products, this sequence of deoxyribonucleic acid was proved to be normal, indicating that the single-stranded conformational polymorphisms result was an artifact of the polymerase chain reaction. Thus, no mutations were detected in the regions of interest in any of the tumours studied. These results indicate that activation of ras proto-oncogenes by mutations in codons 12, 13, and 61 does not play an important role in hepatocellular carcinogenesis in southern African Blacks despite the fact that dietary exposure to aflatoxin B1 is a risk factor in this population.
Artifacts↗
The prevalence of antibodies to the hepatitis A virus in Owambo children.
The prevalence of hepatitis A virus infection, in a population as well as the age at which it is usually acquired reflect the prevailing socio-economic conditions and standards of public hygiene. Infection occurs equally in both the sexes. Black Africans are known to have a high prevalence of hepatitis A virus infection and do acquire the infection early in life. This study documents the age-specific prevalence in Owambo children and confirms an equal sex distribution.
Adolescent↗
Loss of heterozygosity in chromosome 4q12-q13 in hepatocellular carcinoma in southern African blacks.
Paired samples of hepatocellular carcinoma and non-tumorous hepatic tissue from 12 southern African blacks were examined for loss of heterozygosity at two loci (D4S409 and D4S392) in chromosome 4q12-q13 (mapping to the same region as the locus for the gene for alpha-fetoprotein). Deoxyribonucleic acid was extracted from carcinoma and non-tumorous tissues and amplified using the polymerase chain reaction. The primers used were based on flanking regions of minisatellite DNA specific for the loci. Products of PCR amplification were separated by denaturing polyacrylamide gel electrophoresis and analysed for allelic losses. At the D4S409 locus one of seven informative samples showed loss of heterozygosity, whereas none of eight informative samples showed loss of heterozygosity at the D4S392 locus. If these findings are considered together with those previously reported in hepatocellular carcinomas from black Africans, the prevalence of loss heterozygosity in chromosome 4q12-q13 in hepatocellular carcinoma in southern African blacks (33 per cent) is the same as that in tumours from Japanese patients. Loss of heterozygosity at chromosome 4q12-q13 is infrequent during hepatocellular carcinogenesis in southern African blacks.
Alleles↗
Serum alpha-fetoprotein concentrations in urban and rural Southern African blacks with hepatocellular carcinoma.
The reason why only some hepatocellular carcinomas synthesize alpha-fetoprotein is not known. Both the frequency with which this foetal globulin is produced and the major aetiological associations of hepatocellular carcinoma vary between populations with high and low incidences of the tumour, raising the possibility that re-expression of the gene for alpha-fetoprotein is determined, or influenced by, the molecular genetic events that occur during hepatocellular carcinogenesis. This hypothesis could be tested by comparing serum alpha-fetoprotein concentrations in populations in which the major risk factors for hepatocellular carcinoma differ. Two such populations are urban and rural southern African blacks. We measured serum alpha-fetoprotein concentrations by radioimmunoassay in 234 southern African blacks with hepatocellular carcinoma: 78 of the patients were urban and they were age-matched with 156 patients born in rural areas, one-half of whom had remained in a rural environment (rural), whereas the others had migrated to the cities in adulthood (rural-urban). Urban patients were more likely than rural-born patients to have a normal serum alpha-fetoprotein value [23.1% (18/78) compared with 10.2% (16/156); p = 0.02]. There was no significant difference between the concentrations in rural and rural-urban patients. The absolute values of the raised serum alpha-fetoprotein values did not differ between urban (69,558 +/- 176,737 ng/ml; and rural-born patients (53,998 +/- 125,681 ng/ml), or between rural (69,207 +/- 159,975 ng/ml) and urban-rural patients (40,434 +/- 83,028 ng/ml). These findings are compatible with the hypothesis that re-expression of the alpha-fetoprotein gene in hepatocellular carcinoma is related to the aetiology or pathogenesis of the tumour.
Adult↗
Hepatocarcinogenic potential of genotype 5 of hepatitis C virus.
Evidence is emerging that hepatitis C virus genotypes have different carcinogenic potentials. The hepatocarcinogenicity of genotype 5, the predominant subtype in hepatitis C virus isolates in South Africa, is not known. We have compared the prevalence of genotype 5 of hepatitis C virus in 44 southern African blacks with hepatitis C virus-related hepatocellular carcinoma with that in a comparable group of patients with hepatitis C virus-induced chronic liver disease (cirrhosis or chronic hepatitis) in the absence of cancer. Hepatitis C virus serotypes 1 to 6 were identified by measuring type-specific antibodies to NS4-derived peptide antigens. Serotype 5 was present in 48% (21/44) of the patients with hepatocellular carcinoma and 37% (15/41) of those with liver disease in the absence of hepatocellular carcinoma, an insignificant difference. Although the numbers of the other genotypes were small, the differences in the prevalence rates of these serotypes between the two groups of patients were also not significant. We conclude that genotype 5 of the hepatitis C virus is neither more nor less carcinogenic than other genotypes found in isolates in South Africa.
Carcinoma, Hepatocellular↗