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)

Radial immunodiffusion assay was used to measure fetal hemoglobin (HbF) concentrations in 312 patients with various malignancies. In 305 of these, alpha-fetoprotein (AFP) was measured by radioimmunoassay. The concentration of HbF exceeded 3 SDs above the normal mean in 68 of 312 patients, most notably in patients with leukemia, multiple myeloma, lymphoma, bladder carcinoma and testicular tumors. HbF was correlated with total hemoglobin concentration and with serum AFP concentration in hepatoma and bladder carcinoma.
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PMID:Fetal proteins in various tumors. 8 98

The binding of the "activated" receptor-glucocorticoid complexes of cultured rat hepatoma cells to nuclei, chromatin, and DNA has been studied under cell-free conditions. A critical factor in determining the shape of the binding curve is shown to be an inhibitory material which is present in crude cytosol and which can be removed without destroying the receptor-steroid complex. These and other results argue that the apparent saturation observed in earlier experiments may have been due to the inhibitors. Thus, the actual number of acceptor sites in hepatoma tissue culture cell nuclei is much larger than previously estimated and their affinity for the complex is lower. Nuclear binding experiments indicate that the inhibitory material interacts with the receptor-steroid complex. The inhibitors appear to be macromolecular; but their effects cannot be mimicked by albumin or hemoglobin. The acceptor capacity at low ionic strength for binding receptor-glucocorticoid complexes increases when proceeding from nuclei to DNA. An analysis of the kinetics of association and dissociation and of the relative binding behavior of nuclei and DNA argues that the affinity of complex for nuclei is much greater than for DNA. DNA-associated histones reduce the amount of complex that binds to DNA. These and perhaps other chromosomal proteins may be responsible for the ordering of acceptor capacity. Evidence is presented that the difference in affinities of nuclear and DNA acceptors could also be due to chromosomal proteins. In nuclei, these proteins may thus both reduce the amount of complex binding by rendering regions of DNA less accessible and increase the binding affinity of some, or all, of those DNA binding sites which remain exposed.
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PMID:Interaction of glucocorticoid receptor-steroid complexes with acceptor sites. 17 16

In this case report, the patient had been delivered by Caesarean section and weighed only 4 pounds at birth. The mother was O negative, the father A positive, and the infant A positive. Initial red cell count was 2.85 million/cu mm; white cell count, 19,200/cu mm; and hemoglobin 70% of normal. At 3 months of age hemoglobin was 10% of normal. Bone marrow examination revealed marked erythroid hyperplasia. A diagnosis of Blackfan-Diamond syndrome was made. He received blood transfusions every 2 or 3 weeks for the first 4 years of his life. During his lifetime he received 433 units of packed cells for the treatment of congenital hypoplastic anemia. Vitamin-B12, folic acid, and iron were given without benefit. At 8 years of age a spelectomy was done. 20 months after surgery he recovered from pneumonococcal meningitis without sequelae. Progressive signs of hemochromatosis developed and finally progressive signs of heart failure with edema. At 24 years of age severe epigastric pain developed. An open liver biopsy disclosed multiple liver nodules which proved to be hepatoma. Severe ascites followed the surgery. Pulmonary metastases of the liver tumor developed and heart failure. He died at age 25. This patient had received no androgen. He was consistently hepatitis antigen negative. He was prepubertal at the age of 25 and had almost no endogenous androgens. Alpha-fetoglobin was present. This test may be useful as a screening test for hepatoma.
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PMID:Hepatocellular carcinoma, transfusion-induced hemochromatosis and congenital hypoplastic anemia (Blackfan-Diamond syndrome). 18 Aug 2

Two different factors chemotactic for cancer cells were extracted in pseudoglobulin fraction of rat ascites hepatoma transplanted tissue. After chromatography on Sephadex G-50 and CM-sephadex, these factors were separated by gel filtration on Sephadex G-100. The factor a was further fractionated by immunoadsorbent chromatography with goat antirat gamma-globulin antibody and then with rabbit antirat hemoglobin antibody; it was a protein with a molecular weight of about 78,000, resembling a chemotactic factor previously reported, and its activity was thermolabile. The previously undescribed factor b was also a protein with a molecular weight of about 14,000 and its activity was thermostable. Intradermal injection of these factors at low concentrations induced an extravascular migration of circulating tumor cells and formation of metastatic secondary tumors; and little difference in the in vivo effect between these factors was observed. It was thus assumed that the combined action of these two factors may be involved in malignant invasion.
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PMID:Characterization of two different factors chemotactic for cancer cells from tumor tissue. 18 49

Somatic cell hybrids between hepatoma and Friend erythroleukemia parental cells were studied for the expression of liver-specific and erythroid properties. Several independent clones were isolated using HAT selection and were shown to be true hybrids by isozyme and chromosome analysis. All displayed a complete extinction of hemoglobin and globin mRNA production, but a retention of albumin and transferrin secretion. The data suggest that erythroid differntiation is being actively inhibited by the hepatoma genome. Possible mechanisms that might explain these results are discussed in the light of current hypotheses regarding the mechanism of cell differentiation.
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PMID:Somatic cell hybrids between Friend erythroleukemia cells and mouse hepatoma cells. 20 66

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

The uptake of radio-labeled hemoglobin-haptoglobin complex (Hb-Hp) by human hepatoma PLC/PRF/5 and HepG2 cells was investigated in an attempt to characterize the uptake process and intracellular transport. Human hepatoma cells took up Hb-Hp in a receptor-mediated manner. Scatchard analysis of binding revealed that PLC/PRF/5 and HepG2 cells exhibited about 21,000 and 63,000 haptoglobin receptors/cell, with a dissociation constant (Kd) of 8.0 and 17 nM, respectively. Human hepatocytes in primary culture also expressed about 84,000 receptors/cells, with a Kd of 7.4 nM. The hemoglobin-haptoglobin complex was internalized and subsequently the internalized Hb-Hp was slowly degraded in the cells. Preincubation of the cells with Hb-Hp resulted in a decrease in binding of the radioactive Hb-Hp to the cell surface, and was accompanied with an accumulation of intracellular receptors. The uptake of Hb-Hp by the cells was not inhibited by 100 microM chloroquine or by 10 mM methylamine, but was inhibited by 50 microM monodansylcadaverine. Hemoglobin-heme taken up by the cells induced microsomal heme oxygenase. Thus, human hepatoma PLC/PRF/5 and HepG2 cells can take up Hb-Hp by haptoglobin receptor-mediated endocytosis and Hb-Hp probably causes translocation of the haptoglobin receptors from the cell surface to the cell interior where they can be degraded. The internalized heme-moiety of hemoglobin can regulate the expression of heme oxygenase.
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PMID:Expression of haptoglobin receptors in human hepatoma cells. 135 88

Iron is essential for life, but iron overload is toxic and potentially fatal. The liver is a major site of iron storage and is particularly susceptible to injury from iron overload, especially when (as in primary hemochromatosis) the iron accumulates in hepatocytes. Iron can be taken up by the liver in several forms and by several pathways including: (1) receptor-mediated endocytosis of diferric or monoferric transferrin or ferritin, (2) reduction and carrier-facilitated internalization of iron from transferrin without internalization of the protein moiety of transferrin, (3) electrogenic uptake of low molecular weight, non-protein bound forms of iron, and (4) uptake of heme from heme-albumin, heme-hemopexin, or hemoglobin-haptoglobin complexes. Normally, pathway 2 is probably the major one for uptake of iron by hepatocytes. Iron is stored in the liver in the cores of ferritin shells and as hemosiderin, an insoluble product derived from iron-rich ferritin. Iron in hepatocytes stimulates translation of ferritin mRNA and represses transcription of DNA for transferrin and transferrin receptors. The major pathologic effects of chronic hepatic iron overload are: (1) fibrosis and cirrhosis, (2) porphyria cutanea tarda, and (3) hepatocellular carcinoma. Although precise pathogenetic mechanisms remain unknown, iron probably produces these and other toxic effects by increasing oxidative stress and lysosomal lability. Vigorous efforts at diagnosis and treatment of iron overload are essential since the pathologic effects of iron are totally preventable by early vigorous iron removal and prevention of iron re-accumulation.
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PMID:Iron and the liver. 184 76

Knowledge of the endogenous blood level of erythropoietin (Epo) has gained recent interest in view of the advances in Epo replacement therapy in anemic patients. By radioimmunoassay, we have carried out comparative measurements of the serum Epo level in patients suffering from chronic enterocolitis or leukemia. In chronic enterocolitis, the Epo level showed an exponential increase with the degree of anemia (up to 250 U Epo/1 serum at 70 g hemoglobin/1 blood). Similarly anemic patients with leukemia and severe bone marrow insufficiency of erythropoiesis had much higher Epo levels (usually above 500 U/1). Our findings indicate that the level of Epo is not only dependent on the blood hemoglobin concentration but also on the type of anemia. In fact, additional in vitro studies showed that immunomodulatory peptides can significantly influence the production of Epo in the hepatoma cell culture HepG2.
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PMID:Immunoreactive erythropoietin in the anemia of non-renal chronic diseases. 216 83

A severe anemia develops in recipient C57L/J mice after syngeneic transplantation of the BW7756 murine hepatoma. The tumor undergoes an exponential growth spurt in the 14-21 days post-implantation, accompanied by a parallel increase in serum alpha-fetoprotein levels and a significant decrease of hemoglobin concentration and hematocrit extending to the 28th day. Concomitant with the decreased hematocrit, the blood volume displayed a 10% increase. The blood cell population was generally one of reticulocytosis and leukocytosis. Mild icteric plasma was observed and both "cold" and "warm" antibodies were detected in the sera of tumor-bearing mice. An elevation of IgM was observed by day 7, followed by a depletion of IgG1 and IgG2 throughout the tumor growth period. When RBCs of tumor-bearing mice were compared to those of normal mice, the same degree of osmotic fragility was found. However, the lifespan of the transfused RBC was shorter in tumor-bearing mice than in normal mice (half-life: 2 days vs. 4 days). The data suggest a type of auto-immune hemolytic anemia which is analogous to various hematopoietic disturbances described for murine hosts bearing solid tumors distal to hematopoietic sites.
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PMID:Characterization of murine hepatoma BW7756. III. Hematological profile of a tumor-associated anemia. 240 35


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