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)

Cross immunoelectrophoresis of serum A1AT (Pi M) shows "frequent" patterns with M2 less than M6 less than M4. Other "particular" patterns were found with M6 greater than M4 and M6 less than M2. The most often found patterns among the Negroid population in our study appeared dissimilar to that found among Caucasians. The "super-gene" concept and the variability of genetic flow may explain this difference. The "particular" patterns are often found in cord blood samples and in patients with hepatocarcinoma. They show similaritis between embryonic and cancerous processes. These different patterns also agree with the "super-gene" concept.
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PMID:[Variation of the profile phenotype M of alpha-1-chymotrypsine : trial of interpretation (author's transl)]. 21 Jun 93

The hepatoma-specific band of serum gamma-glutamyl transferase II (GGT II) and other three markers were evaluated in 77 patients with primary hepatocellular carcinoma (PHC). The positive rate of GGT II (87%) was much higher than that of the increased alpha-fetoprotein (AFP greater than or equal to 400 ng/ml, 54.5%), the increased alpha-1-antitrypsin (AAT greater than or equal to 400 mg/dl, 64.9%) and alkaline phosphatase isoenzyme I (ALP I, 13.0%). In patients with AFP less than 400 ng/ml, the positive rate of GGT II was 95.2%, higher than that of ALP I (22.8%) and AAT (60.0%). The positive rate of GGT II was positively correlated to the volume of PHC (r = 0.324, P less than 0.05), but even in patients with small PHC (less than or equal to 65 cm3), the positive rate of GGT II (78.6%) was higher than that of AFP (50.0%) and AAT (28.6%). The ALP I positivity was only seen in patients with larger PHC. Follow-up study showed that GGT II, like AFP, might occur before liver tumor could be detected by B-mode ultrasonography and computerized tomography. Therefore, GGT II is a valuable marker of PHC, especially in patients whose AFP was negative or slightly increased; GGT II may be useful for relatively early diagnosis of PHC.
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PMID:Reappraisal of diagnostic significance of a hepatoma-specific band of serum gamma-glutamyl transferase. 197 81

Ascitic fluid alpha 1-antitrypsin (AF-AAT) was compared with ascitic fluid total protein (AF-TP) and the serum-ascites albumin gradient (SAAG) in the differential diagnosis of ascites. The study included 82 consecutive patients of which 42 had cirrhosis, 8 hepatoma (with cirrhosis), and 27 malignant ascites (peritoneal 18, liver 9). The concentration of AF-AAT (milligrams per deciliter) was significantly elevated (P less than 0.001) in hepatoma (174 +/- 123), malignant liver disease (232 +/- 119) and peritoneal neoplasms (376 +/- 106) in comparison with cirrhotics (66 +/- 33). In separating ascites caused by cirrhosis or malignancy, AF-AAT (discriminating limit of 120 mg/dl) had a 96% sensitivity, 95% specificity, and 96% diagnostic efficacy, which was superior to the 87% observed for AF-TP and 86% for the SAAG. Similar results were obtained for the A/S AAT ratio but this test was not available in all patients. AF-AAT was particularly useful in patients with malignancy causing portal hypertension as assessed by SAAG (hepatoma, malignant liver disease). We conclude that AF-AAT may be a valuable parameter in the differential diagnosis of ascites.
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PMID:Ascitic fluid alpha 1-antitrypsin. 216 27

The presence and distribution of AFP, AAT and HBsAg in peritumoral non-neoplastic hepatocytes (NNH) of 27 cases and, at the same time, in the neoplastic tissue of 37 liver cell carcinoma (HCC) were studied; AFP and HBsAg were more frequently found in NNH than in HCC cells; no differences were found for AAT. The presence of HBsAg also in normal liver without cirrhosis is probably best explained by its possible role in neoplastic transformation and by the inhibition of replication of the viruses AFP, considered to be expression of dedifferentiated cells, may possible be taken up by NNH for catabolic purposes.
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PMID:Immunohistochemical study of the appearance of some markers in liver adjoining hepatocellular carcinoma. 242 60

Primary liver carcinoma (PLC) may express a certain number of markers. Here we communicate results of an analysis of five such markers (alpha-1-antitrypsin--AAT--, carcino-embryonic antigen --CEA--, alpha-fetoprotein --AFP--, and superficial --HBsAg-- and core --HBcAg-- antigens of hepatitis B virus) by means of PAP techniques in 130 cases of PLC, comparing the neoplastic tissue and the non-tumorous liver. Three variants of PLC are distinguished: hepatocarcinoma (HC) (108 cases); cholangiocarcinoma (CC) (19 cases); and three cases of hepatocholangiocarcinoma (HCC). AAT was positive in 29 HC, 2 HCC, and negative in all 19 CC. CEA appeared positive in 16 HC, 16 CC and only one HCC. AFP was positive in two HC, and negative in all CC and HCC. HBsAg displayed positivity in 15 HC and one HCC, being negative in all 19 CC. HBcAg was positive in 4 HC, and negative in all CC and HCC. HBsAg was also positive in two neoplastic emboli associated with HC. On the non-tumorous liver tissue the immunohistochemical results showed positivity for AAT and CEA, but not for AFP. Therefore the present results confirm that in the geographical area from which these tumors proceed, PLC is closely correlated with HBsAg positivity and with cirrhosis.
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PMID:Immunohistochemical characterization of 130 cases of primary hepatic carcinomas. 244 80

Human alpha-L-fucosidase, a lysosomal enzyme, hydrolyzes alpha-L-fucose from glycolipids and glycoproteins. Its activity is deficient in human fucosidosis an autosomal recessive disease. In order to understand the molecular basis of this lysosomal storage disorder we have cloned several cDNAs coding for human alpha-L-fucosidase from a human hepatoma and a human liver cDNA library constructed in lambda gt11. Compiling the cDNA sequences of these clones we have identified 1,829 base pairs (bp) encoding human alpha-L-fucosidase. This includes an open reading frame of 1,172 bp, a consensus polyadenylation signal AAT AAA and a poly(A)+ tail. The sequence is incomplete at the 5'-end, and clones encoding the amino terminus of the native protein, the propeptide and leader signal have not yet been isolated. The open reading frame encodes for 390 amino acids with a calculated Mr of 45,557. This represents 78-95% of the mature processed alpha-L-fucosidase. The availability of these cDNA clones has enabled us to map the structural gene for alpha-L-fucosidase to chromosome 1p34.1-1p36.1 by Southern blot analysis of DNA from human-rodent somatic cell hybrids and by in situ hybridization. Furthermore, a Pvu II restriction fragment length polymorphism (RFLP) has been identified at the human alpha-L-fucosidase gene locus. Analysis of mRNA by Northern blotting gives a major species of 2.25 kb. In 4 patients with fucosidosis no mRNA signal was detected and Western blots gave no immunoreactive enzyme. Southern blotting after Eco RI digestion in two fucosidosis families revealed a banding abnormality (extra 6-kb band).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular biology of the alpha-L-fucosidase gene and fucosidosis. 289 6

The tightness of DNA-protein binding in the nuclei of mouse spleen T- and B-lymphocytes was assessed, using nucleoprotein celite chromatography, and changes in the number of T- and B-suppressors in the course of o-AAT-induced chemical hepatocarcinogenesis were studied. Attenuation of DNA-protein bonds in T-lymphocytes at the early stages (up to 3 months) was observed, and by the time of hepatoma formation (8 months) about 50% of T-lymphocyte DNA was loosely bound to proteins, which is a typical feature of quiescent cells. In B-lymphocytes attenuation of DNA-protein interaction was only observed by the 8th month of carcinogenesis. By the time of hepatoma formation the number of T-suppressors in mouse spleen increased 2.8-fold, while the number of B-suppressors in lymph nodes remained unchanged.
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PMID:[Change in the strength of DNA-protein binding in T- and B-lymphocytes of the spleen of C3HA mice during chemical hepatocarcinogenesis]. 387 31

Alpha 1-antitrypsin has been examined in formalin-fixed, paraffin-embedded liver specimens from Greek patients with cirrhosis (35 cases) and hepatoma (55 cases) by peroxidase-antiperoxidase (PAP) method. Ring-like AAT globules were found in the non-neoplastic cells in 12% of the cases of hepatoma and in 11% of the cases of cirrhosis. Atypical globules were seen in neoplastic cells in 5.4% of the cases of hepatoma and in 17% of the cases of liver cirrhosis. A diffuse fine granular pattern of AAT distribution was present in 31% of the cases of hepatoma in the neoplastic cells and in 27% of those in the non-neoplastic cells. The relatively high incidence of ring-like AAT-globules, and of atypical globules in cases of hepatoma and cirrhosis is not in agreement with the extremely low gene frequency of Z allele in a Greek population of patients with cirrhosis and hepatoma. Thus, there is some doubt whether AAT-globules in the liver represent a histopathologic marker of genetically determined AAT deficiency. A relationship between AAT deposits and the degree of differentiation of hepatoma was noted in this series. AAT-positive cells were found in 55% of moderately differentiated, in 29% of highly differentiated and in 20% of poorly differentiated hepatomas.
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PMID:Demonstration of alpha 1-antitrypsin in paraffin sections of hepatoma and cirrhosis. 629 75

Treatment with synthetic MDP inhibited growth of transplantable, chemically induced tumors in syngeneic mice. The tumor-inhibitory effect was dependent on the schedule of MDP administration. Growth of SC transplants of a nonmetastasizing, MC-induced fibrosarcoma, MC11, was inhibited by local treatment with 200 micrograms and 1,000 micrograms MDP given SC 5-7 weeks before challenge. Treatment with lower (10 micrograms and 100 micrograms) doses of MDP and shorter (1-4 weeks) time intervals was not effective. Single doses of MDP (10-1,000 micrograms) 1-3 weeks after challenge had no effect. Growth of IV-inoculated, metastasizing AAT-induced hepatoma A was inhibited by IV injections of 20 micrograms MDP given 1 and 2 days prior to the challenge. Significant increases in the survival of hepatoma-bearing mice were observed only after injections of MDP incorporated in multilamellar liposomes.
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PMID:Inhibition of tumor growth in mice treated with synthetic muramyl dipeptide. 656 71

Activities of the cytoplasmic and mitochondrial isozymes of aspartate aminotransferase (aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1, AAT) in transplantable mouse hepatomas BW7756 and H-4 are reduced when compared to normal adult liver. Both proteins have been purified to homogeneity from a single preparation of mouse liver and monospecific antibodies raised to each isozyme. By quantitative immunotitration analysis, the activity of each isozyme in liver and hepatoma has been shown to correlate with levels of immunoprecipitable protein. Furthermore, for each isozyme, the liver versus hepatoma species is indistinguishable by heat inactivation kinetics, Km's for substrates, and molecular weights. Thus, the reduction of mitochondrial and cytoplasmic AAT activities in hepatoma tissue is due not to alterations in the catalytic activity of the enzyme molecules, but to a decrease in the number of enzyme molecules present. Turnover of the isozymes was studied in liver and hepatoma tissue using in vivo radiolabeling and specific immunoprecipitation techniques. The cytoplasmic isozyme has a similar rate of degradation in liver and hepatoma, while the rate of synthesis of this isozyme in hepatoma is approximately tenfold less than in liver. The mitochondrial isozyme is also degraded at a similar rate in both tissues, but the rate of synthesis is sixfold greater in normal liver tissue than in hepatoma. It is concluded that decreased amounts of both isozymes in hepatoma as compared to liver are the result of a reduction in the rate of synthesis of each isozyme without any change in the rate of degradation.
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PMID:Turnover of cytoplasmic and mitochondrial aspartate aminotransferase isozymes in mouse liver and transplantable hepatomas. 685 79


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