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)

Response to hepatitis B virus (HBV) infection [HBV surface antigen (HBsAg) and antibody to HBsAg (anti-HBs)], serum iron, total iron-binding capacity, hematological status (erythrocytes, Hb, and hematocrit), and evidence of liver damage (serum glutamic pyruvic transaminase; aspartate aminotransferase, L-aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1) were determined for 201 patients on chronic renal dialysis. Four factors-serum iron level, transminase level, sex, and HBV response [i.e., infected-HBsAg(+) (HBsAg positive), anti-HBs(+) (anti-HBs positive), or no response]-were analyzed simultaneously to test the hypothesis that serum iron is higher in those with HBsAg in their serum than in those without HBsAg, independent of the transaminase level. Four independent, statistically significant two-factor interactions were identified. (i) Serum iron is higher in those HBsAg(+). (ii) Serum iron is higher in those with increased transaminase. (iii) Transaminase is higher in those HBsAg(+). (iv) Males are more likely to be HbsAg(+) and females are more likely to be anti-HBs(+). Also, those who are HBsAg(+) have significantly higher percent iron saturation (serum iron/total iron-binding capacity). That is, the hypothesis was supported by the findings. Several additional biological hypotheses are suggested, including a possible role of increased iron levels in susceptibility and response to HBV infection and the possible relationship between higher iron levels and the likelihood of HBV infection progressing to primary hepatocellular carcinoma. In addition, further tests of the initial hypothesis in nonhospitalized populations with endemic HBV infection are proposed.
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PMID:Serum iron levels and response to hepatitis B virus. 28 82

Iron uptake rate of the tumor tissues of the rat liver was compared with that of the nontumor tissues of the same rat liver. Ferric[59Fe] citrate was injected to rats bearing hepatoma induced by the administration of diethylnitrosamine. The tumor and nontumor tissues were enucleated from the liver and radioactivity (cpm/10 mg tissue) of the individual tissue was calculated to estimate the iron uptake rate of the tissue. Eleven rats were finally available for the study. Population mean of radioactivity of the tumor group was larger than that of the nontumor group when examined 6 hr after the injection, so far as the specimens of both groups were sufficient in number, more than 19. The variance of radioactivity of the tumor group was always larger than that of the nontumor group, probably in part due to cytological and histological varieties of the tumor tissues. These results suggest that the tumor tissues can take up more iron than the nontumor tissues.
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PMID:Radio-iron uptake of rat hepatoma. 52 Jul 51

Iron overload was found in 3 patients who had undergone partial gastrectomy: a 61-year-old woman developed iron overload because she may have had idiopathic haemochromatosis and had also been given parenteral iron; in a 62-year-old man with thalassaemia minor, iron overload may have developed because of increased oral iron ingestion, low serum folate, increased, albeit ineffective, erythropoiesis and sideroblastic anaemia; a 74-year-old man with thalassaemia minor developed iron overload without exogenous therapy and died from a hepatoma. These cases illustrate that partial gastrectomy fails to protect patients from developing iron overload, particularly if given uncontrolled iron therapy.
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PMID:Iron overload despite partial gastrectomy. 53 65

A significant anemia develops in Buffalo rats bearing the Morris hepatoma 7777. By indiceal measurements the red blood cells (RBCs) appear to be microcytic and hypochromic. Ferrokinetic studies demonstrate a decreased uptake of iron in the bone marrow and an increased incorporation of iron in the spleens of the tumor-bearing animals. RBC survival studies indicate the presence of a hemolytic component which appears to contribute to the anemia. The RBCs from tumor-bearing animals (T-RBC) have a greatly increased fragility in sodium chloride solutions. Inspection of these T-RBCs by electron microscopy demonstrates significant echinocytosis when they are compared to normal cells. Electrophoretic separation of the hemoglobin from T-RBCs shows a pattern different from normal cells and consistent with the pattern described for hemoglobin from spleen and bone marrow. The findings are consistent with bone marrow inadequacy and an increased splenic erythropoiesis which is insufficient to maintain normal hematological values. The hypothesis is presented that the RBCs synthesized under these circumstances appear in the circulation with an "immature" hemoglobin pattern and are hemolyzed more readily. This process then contributes to the hemolytic component and development of the anemia.
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PMID:Host-tumor interactions: basis for the anemia in rats bearing the hepatoma 7777. 53 90

Two hundred twelve Italian patients with genetic hemochromatosis (181 men, mean age 50 +/- 11 yr; and 31 women, mean age 49 +/- 10 yr) were followed for a median period of 44 mo (range = 3 to 218 mo). Alcohol abuse was present in 31 subjects (15%), and chronic HBV and HCV infection were seen in 19 (9%) and 35 (24%) of 145 cases tested, respectively. Twenty-four patients (11%) had concomitant beta-thalassemia trait. Liver biopsy revealed cirrhosis in 146 and a noncirrhotic pattern in the other 66. Perls' stain was degree III in 37 patients and IV in 171 patients. One hundred eighty-five patients underwent weekly venesection, and iron depletion was achieved in 122 cases after total iron removal of 3 to 41 gm. Death occurred in 44 patients after 3 to 198 mo and was due to hepatocellular carcinoma in 20 cases, liver failure in 10, extrahepatic cancer in six, heart failure in three and hemochromatosis unrelated causes in five. Cancer has developed in seven other patients still alive (hepatocellular in five and extrahepatic in two). No deaths were observed among noncirrhotic patients; cumulative survival rates in cirrhotic patients were 85%, 75%, 60% and 47% at 3, 5, 8 and 10 yr, respectively. Univariate analysis in the 146 cirrhotic patients showed that age greater than 60 yr, alcohol abuse, cardiomyopathy, skin pigmentation, portal hypertension, hypoalbuminemia, hypergammaglobulinemia and Child class B or C had significant negative prognostic value. At multivariate analysis, only alcohol abuse, gamma-globulins greater than 2.0 gm/dl and Child class B or C maintained their negative prognostic values (p less than 0.01, hazard ratio 2.7; p less than 0.001, hazard ratio 2.8; and p less than 0.001, hazard ratio 4.3, respectively).
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PMID:Survival and prognostic factors in 212 Italian patients with genetic hemochromatosis. 131 85

Copper (Cu), iron (Fe), zinc (Zn) and manganese (Mn) levels in organs of LEC rats (Long-Evans rats with a cinnamon-like coat color), which develop spontaneous jaundice with hereditary hepatitis, were determined by instrumental neutron activation analysis method. Unusual accumulations of Cu in the liver of LEC rats were found, depending on the age of the animals, the metal concentration being more than approximately 20-40 times those of normal LEA rats (Long-Evans rats with an agouti coat color). Fe and Zn were also accumulated, in addition to Cu, significantly in the LEC rats. The unusual Cu accumulations in the liver of LEC rats were associated with the induction of metallothionein, estimated by radioimmunoassay method, in the liver of LEC rats, rather than that of superoxide dismutase, estimated by electron spin resonance -spin trapping method. These findings suggest that the unusual Cu accumulation in LEC rats is involved in the development of jaundice, hepatic injury and hepatocellular carcinoma.
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PMID:Unusual accumulation of copper related to induction of metallothionein in the liver of LEC rats. 131 72

The two human hepatoma cell lines, HepG2 and Hep3B, have been demonstrated to metabolize ethanol efficiently even in the absence of alcohol dehydrogenase. By using specific metabolic inhibitors, it was found that the microsomal ethanol-oxidizing system (MEOS) plays a significant role in ethanol metabolism in these two cell lines. There is a strong positive correlation between the rates of ethanol metabolism and the total cytochrome P-450 levels in the hepatoma cells. The involvement of the cytochrome P-450 system was further supported by the induction of aniline p-hydroxylase activity after ethanol treatment. However, the 3- to 4-fold elevation in aniline p-hydroxylase activity was not accompanied by an increase in cytochrome P450IIE1 mRNA level. Exposure of HepG2 and Hep3B cells to ethanol resulted in an increase of accumulation of apoA-I (15%-45% over control) in a dose-dependent manner (from 5 to 50 mM) of ethanol over a 24-hr period. All other major apolipoproteins which included apo CII, apo CIII and apoE, with the exception of apoB, were not affected by these treatments. At a concentration of ethanol of 25 mM or greater, accumulation of apoB, VLDL and LDL triglyceride were increased by 20% to 25% over the control level. Elevation of HDL cholesterol (40%-70% over control) was observed when the cells were exposed to an ethanol concentration of > or = 10 mM. Metyrapone, which inhibited the MEOS, was capable of blocking the induction of apoAI caused by ethanol treatment.
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PMID:Effect of ethanol on lipoprotein secretion in two human hepatoma cell lines, HepG2 and Hep3B. 133 18

The uptake of transferrin-bound iron by receptor-mediated endocytosis has been the subject of extensive experimental investigation. However, the path followed by iron (Fe) after release from transferrin (Tf) remains obscure. Once Fe is released from Tf within the endosome, it must be transported across the endosomal membrane into the cell. The present investigation describes the presence of a cytoplasmic Tf-free Fe pool which is detectable only when cells are detached from their culture dishes at low temperature, after initial incorporation of diferric transferrin at 37 degrees C. This cellular iron pool was greatly reduced if incubation temperatures were maintained at 37 degrees C or if cells were treated with pronase. Human melanoma cells (SK-MEL-28) in culture were prelabeled by incubation with human 125I-59Fe-transferrin for 2 h, washed, and reincubated at 4 degrees C or 37 degrees C in balanced salt solution in the presence or absence of pronase. The cells were then mechanically detached from the plates and separated into "internalized" and supernatant fractions by centrifugation. Approximately 90% of cellular 59Fe and 20% of 125I-Tf remained internalized when this reincubation procedure was carried out in balanced salt solution at 37 degrees C. However, at 4 degrees C, cellular internalized iron was reduced to approximately 50% of the initial value. The release of this component of cellular 59Fe (approximately 40% of total cell 59Fe) at 4 degrees C was completely inhibited in the presence of pronase and other general proteinases at 4 degrees C and at 37 degrees C, without affecting internalized transferrin levels. Similar results were obtained in fibroblasts and hepatoma cells, indicating that this phenomenon is not unique to melanoma cells. The characterization of this Tf-free cellular Fe pool which is detectable at low temperature may yield valuable insights into the metabolic fate of iron following its transport across the membrane of the endocytotic vesicle.
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PMID:Intermediate steps in cellular iron uptake from transferrin. Detection of a cytoplasmic pool of iron, free of transferrin. 140 Apr 50

Detection and exclusion of focal liver lesions is especially difficult in patients with diffuse liver disease. Magnetic resonance (MR) imaging may be particularly valuable in these patients. By judicious comparison of appropriate pulse sequences, normal and hypertrophic liver may be distinguished from atrophic, neoplastic, or otherwise abnormal hepatic parenchyma. Chemical shift (lipid-sensitive) techniques allow definitive identification of fatty liver, including focal fatty infiltration or focal sparing. T2-weighted and T2*-weighted images allow identification of iron overload, depicting malignancies as focal masses without iron. Analysis of signal intensity and internal morphology allows confident distinction between regenerative nodules and hepatocellular carcinoma in most instances, and allows diagnosis of early carcinoma within regenerative nodules. MR imaging provides capabilities for noninvasive characterization of liver tissue beyond those available with other noninvasive modalities.
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PMID:Focal manifestations of diffuse liver disease at MR imaging. 911 25

We examined the properties of a new iron-binding protein purified previously from rat liver (T. Furukawa, S. Taketani, H. Kohno, and R. Tokunaga, 1991, Biochem. Biophys. Res. Commun. 181, 409-415). The protein was digested with trypsin and the peptides were analyzed by reverse-phase high-performance liquid chromatography. The partial amino acid sequences of the tryptic peptides coincided with that of rat ribosomal protein P2. Immunoblot analysis and iron-binding assay confirmed that the iron-binding protein and ribosomal protein P2 are identical. Then the iron binding ability of ribosomal protein P2 was examined in rat hepatoma H4IIEC3 cells incubated with radioactive iron. When immunoprecipitation with anti-iron-binding protein serum was performed using cells incubated with 59Fe-citrate, about 4% of the 59Fe radioactivity in cells was associated with the iron-binding protein through 30 to 90 min of incubation. About 1.5% of radioactive iron in cells incubated with 59Fe-transferrin was found in immunoprecipitates with anti-iron-binding protein serum during 1 to 5 h of incubation, and 4 to 7% of the radioactivity was found in immunoprecipitates with a monoclonal antibody against ribosomal P proteins in the same incubation. These results demonstrate that ribosomal proteins P2 binds iron taken up by the cells.
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PMID:Ribosomal protein P2, a novel iron-binding protein. 152 26


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