Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study describes morphometric analysis of nodular changes examined by using fine-needle aspiration biopsy guided ultrasonographically. A group of 49 patients with suspected neoplastic changes of the liver was studied including 4 hepatocellular carcinomas, 21 neoplasms metastasizing to the liver, 23 non-neoplastic changes. The whole material was divided into three major groups: A with neoplastic cells, B with non-neoplastic cells and C with suspected cells. In each case 100 cells were measured, and in each cell the surface area, maximal diameter and coefficient of shape of the cytoplasm, nucleus and nucleolus were measured. It was found that neoplastic cells have larger nuclei and nucleoli; the ratio of nucleus to cytoplasm was shifted in favour of the nucleus. The largest nucleoli are typical for hepatocellular carcinoma. Most rounded are cells of adenocarcinomas metastasizing to the liver. Morphometric measurements automatically isolate large liver cell dysplasia. The present study provides morphometric parameters of the hepatocytes in the cytological material, which may be the basis for further studies.
Patol Pol 1993
PMID:Cytomorphometry of fine-needle aspiration biopsy material from the liver tumours. 830 31

Current diagnostic capabilities of Doppler sonography in solid focal lesions were presented. Diagnostic difficulties were discussed in the case of focal liver lesion, wherein the diagnosis was not reached by sonography backed up by pulsed and color Doppler. The patient was submitted to surgical treatment. A histological specimen disclosed focal nodular hyperplasia. The analysis of the case in question proved that sonography even combined with Doppler method cannot differentiate between hepatocellular carcinoma and focal nodular hyperplasia.
Pol Arch Med Wewn 1993 Mar
PMID:[Focal nodular hyperplasia of the liver in doppler sonography--case report]. 839 70

We present a case report of primary hepatocellular carcinoma with tumor thrombus extending into the right atrium complicated by pulmonary embolism. A 49-year-old man was admitted to our hospital for searching a cause of thrombus in the right atrium. The patient complained of shortness of breath and oedema of the lower extremities. He had a history of hepatitis B. Abdominal sonography and computed tomography revealed a tumor of the liver. A needle biopsy confirmed the diagnosis of hepatocellular carcinoma. Magnetic resonance showed a tumor thrombus also in the inferior vena cava. The diagnosis of pulmonary embolism was confirmed by pulmonary perfusion scintigraphy. This case stresses that clinicians should include hepatocellular carcinoma among the possible causes of intracardiac thrombus and pulmonary embolism.
Pol Arch Med Wewn 1996 Mar
PMID:[A case of primary hepatocellular carcinoma with tumor thrombus in the right atrium and massive pulmonary embolism]. 875 55

Hereditary tyrosinemia type I (HT I, McKusick 276,700) is a metabolic disease with a pattern of autosomal recessive inheritance. The disease is caused by a deficiency of the enzyme involved in the last step in the degradation of the amino acid tyrosine, fumarylacetoacetate hydrolase (FAH). The result of this block is the accumulation of catabolites some of which have been proposed to be highly toxic due to their alkylating potential. In humans, hereditary tyrosinemia is often associated with the development of hepatocellular carcinoma in young patients. The reasons for the high incidence of hepatocellular carcinoma are unknown but it has been suggested that it may be caused by accumulated metabolites such as fumarylacetoacetate (FAA) and maleylacetoacetate (MAA). The various mutational defects in the FAH gene are reviewed. The use of two mouse models of this disease to study the molecular basis of the pathologies associated with HT I are discussed. Finally, some preliminary data on the mutagenic potential of FAA and MAA in a gene reversal assay are presented.
Acta Biochim Pol 1996
PMID:Tyrosine and its catabolites: from disease to cancer. 879 Jul 25

Plasma prekallikrein (PPK) is a single-chain glycoprotein synthesized in the liver. The aim of our study was to evaluate a plasma prekallikrein as the marker reflecting liver protein synthesis in patients with chronic liver diseases. PPK levels have been measured by own modification of amidolytic micro-assay in 43 patients with chronic liver diseases and 37 healthy volunteers as control group. As compared to control group, PPK level was significantly decreased in patients with chronic active hepatitis and with decompensated liver cirrhosis and significantly increased in patients with liver cirrhosis complicated by hepatocellular carcinoma. There was no difference in plasma prekallikrein between patients with compensated liver cirrhosis and controls. The results suggest that PPK might be a useful index for the assessment of residual functional liver mass in patients with chronic liver diseases.
Pol Arch Med Wewn 1995 Nov
PMID:[Plasma prekallikrein in chronic liver diseases]. 883 36

In erythrocytes of rats bearing Morris hepatoma 5123 the activities of superoxide dismutase, glutathione peroxidase and glutathione reductase as well as the level of reduced glutathione increased on the 10th day after transplantation of the tumor. In the second phase of the tumor growth (20 days after transplantation), the activities of glutathione peroxidase, glutathione reductase and the level of reduced glutathione in erythrocytes of the experimental animals were lower than in controls, whereas the activity of superoxide dismutase was at that time higher than in controls. On the other hand, the activity of catalase did not significantly differ from that found in healthy rats.
Acta Biochim Pol 1996
PMID:The activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in erythrocytes of rats with experimental neoplastic disease. 886 87

Monomeric G-actin, total actin and filamentous F-actin were examined during the growth of experimental tumour hepatoma Morris 5123. Actin was measured by the inhibition of the standard DNase I from bovine pancreas. A remarkable increase in total actin, and F-actin content, as well as in the state of actin polymerization (measured by the F:G actin ratio) was shown in the cytosol of the tumour cells in the second week of the tumour growth, followed by a rapid decrease in the third week. Parallel observations were made in the cytosol of the liver and in the serum of the tumour bearing rats. The results were compared with the data obtained for control healthy rats. It was shown that hepatoma Morris tumour growth is accompanied by the changes in the actin content and polymerization, occurring also in the liver of the host animal. Only G-actin was found in the serum. It increased significantly in the second week of tumour growth as compared with the G-actin level in the serum of the control healthy rats.
Mater Med Pol
PMID:Actin content and polymerization in tumour, liver and serum of the hepatoma Morris 5123 tumour bearing rats. 893 49

Repair of alkylated bases in DNA is performed by O6-methylguanine-DNA methyltransferase (MGMT) and a set of enzymes of the base excision repair pathway involving N-methylpurine-DNA glycosylase (MPG), apurinic endonuclease (APE), DNA polymerase beta (Pol beta) and DNA ligase. The level of expression of these enzymes may exert a profound effect on resistance of cells towards alkylating drugs. We have comparatively analyzed the expression of MGMT and the different base excision repair genes in rat hepatoma cells (line H4IIE) after exposure to alkylating agents, X-rays and the glucocorticoid hormone dexamethasone. Furthermore, the effect of these agents on the activity of the cloned human MGMT promoter was assayed. Exposure of cells to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or ionizing radiation increased MGMT mRNA levels up to 4.5-fold. Under the same conditions of treatment, exerting only a weak toxic effect, MPG and DNA ligase I mRNA levels were not enhanced, whereas the amounts of APE and Pol beta mRNA transiently increased by approximately 2-fold after X-ray and MNNG treatment, respectively. Dexamethasone induced both MGMT, APE and Pol beta mRNA and the induction paralleled the increase in mRNA of the glucocorticoid-dependent gene tyrosine aminotransferase. The observed increase in MGMT mRNA was due to promoter activation, which was shown in transient transfection assays with MGMT promoter-CAT reporter constructs in H4IIE cells. In these assays, the human MGMT promoter was found to be induced by methylating agents (MNNG and methyl methanesulfonate), ionizing radiation and dexamethasone. Weak induction of the promoter was observed after UV irradiation. Treatment with the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate was ineffective in promoter activation. The transfected MGMT promoter was not inducible by mutagens in HeLa S3 cells, which do not respond with induction of the endogenous MGMT gene. This is the first report showing hormone induction of a DNA repair gene (MGMT). The induction of MGMT and other genes encoding enzymes involved in DNA alkylation damage repair may be relevant in cancer therapy by causing resistance of tumor cells to alkylating drugs.
 ...
PMID:Induction of the alkyltransferase (MGMT) gene by DNA damaging agents and the glucocorticoid dexamethasone and comparison with the response of base excision repair genes. 896 45

The 19,094 autopsy examinations carried out between 1976-1990 revealed 698 (3.65%) case of cirrhosis, of which 64.6% were men. During the last 5 years the percentage of coexistance of hepatoma (hepatocellular carcinoma) with cirrhosis was higher 5-year periods (5.8%; 5.4%). Moreover, the same changing interrelation was observed for other malignancies and cirrhosis-higher (15%) in the last period than in the proceeding years (11.1%; 11.3%). The severity of atherosclerotic changes and coexistance of peptic ulcers, gall bladder disease and productive pulmonary tuberculosis in cirrhotic patients were also assessed. Finally the direct causes of these patients' death were discussed.
Pol Merkur Lekarski 1996 Sep
PMID:[Coexistence of some diseases and analysis of death causes based on autopsy examinations carried out in liver cirrhosis patients based on autopsy observations in 1976-1990]. 913 85

The highest amount of N-acetylneuraminic acid (AcNeu) was found in pyruvate kinase isoenzyme L from normal rat liver (24 moles/mole of enzyme tetramer), with the highest electrophoretic mobility. On the other hand, isoenzyme M2 from Morris hepatoma 7777, with the lowest electrophoretic mobility, had the lowest AcNeu content (5 moles/mole of enzyme tetramer). This tumour isoenzyme M2 of pyruvate kinase was, however, characterised by the highest phosphate content (12 moles/mole protein), in comparison to isoenzyme L (3 moles/mole protein) or normal liver isoenzyme M2 (6 moles/mole protein). This could indicate a regulatory change caused by reversible enzyme phosphorylation and dephosphorylation or sialization and desialization. Despite these differences, the sum of the two negatively charged residues was lower in tumour pyruvate kinase isoenzyme M2, with the slowest migration rate, than in normal rat liver isoenzyme M2. Moreover, isoenzyme M2 from tumour material, in comparison with isoenzyme M2 from normal rat liver, had a twice as high content of thiol groups (20 moles/mole protein), especially of free and superficially located ones, than the isoenzyme M2 from normal liver (10 moles/mole protein). This may explain abnormal susceptibility of tumour isoenzyme M2 to stereospecific inhibition by exogenous L-cysteine, and indicate genetically dependent changes in amino-acid content of tumour enzyme which take place during cell tumourigenic transformation.
Acta Biochim Pol 1997
PMID:N-acetylneuraminic acid, phosphate and thiol groups of pyruvate kinase isoenzymes from Morris hepatoma 7777 and normal rat liver. 936 Jul 8


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>