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)

The behavior of the activity of arginyl-tRNA synthetase (L-arginine : tRNAArg Ligase(AMP-forming), EC 6.1.1.19) was determined in extracts of rat liver: normal adult, normal proliferating (from developing and from partially hepatectomized rats), and neoplastic (hepatomas of different growth rates) and in extracts of rat kidney cortex and transplantable kidney tumors. The Km values for arginine, ATP, and tRNA of the enzyme of the rapidly growing hepatoma 3924A were the same as those of the enzyme from the liver of control rats. The pH optima of the control and neoplastic livers were in the same range of 7.25-8.0. Taking the hepatic specific activity for arginyl-tRNA synthetase as 100%, deep layer of gut, thymus and testis had higher activity; renal cortex and spleen had the same activity; and skeletal muscle, brain, heart, lung, superficial layer of gut and adipose tissue had lower activity. In a wide spectrum of hepatomas of different growth rates, a significant increase of 1.4-2.4-fold in arginyl-tRNA synthetase activity was observed when compared with that of liver of control normal rats. This elevation in enzyme activity in hepatomas appears to be specific to neoplasia, since it is unaltered in regenerating and low in differentiating liver. The increase in arginyl-tRNA synthetase in the liver tumors appears to be transformation-linked, since the activity was increased in all hepatomas, even in the slowest growing ones. Furthermore, the increase in enzyme activity was not limited to hepatic neoplasms, since a rise was also observed in transplantable rat kidney tumors. Thus, the reprogramming of gene expression in neoplastic tissue entails an increase in arginine-tRNA synthetase activity.
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PMID:Neoplastic transformation-linked alterations in arginyl-tRNA synthetase activity. 42 64

The metabolism of dihydrotachysterol (DHT), a hydrogenated analogue of vitamin D, has been studied in vivo using man and rat and in vitro using the perfused rat kidney, and hepatoma (3B) and osteosarcoma (UMR-106) cell lines. In vivo a large number of metabolites appeared in the plasma of rats given DHT2 and DHT3. Of particular interest was a compound more polar than 25-hydroxy-DHT, which has been designated compound H. Further study of this compound showed that it was composed of two components, one (Ha) being in much lower concentration than the other (Hb). The production of T2/H (peak H from DHT2) was demonstrated in human plasma after administration of oral DHT2. Comparison of the metabolites formed in vivo with those isolated from the rat kidney perfused with 25-hydroxy-DHT3 in vitro showed that 25-hydroxy-DHT3 was metabolized along two metabolic pathways previously described for vitamin D, culminating in the production of 25-hydroxy-DHT3-23,26-lactone and 23,25-dihydroxy-24-oxo-DHT3. The osteosarcoma cell line metabolized 25-OH-DHT3 in vitro along the same two metabolic pathways already demonstrated in the perfused rat kidney. More polar metabolites than compound H seen in rat plasma in vivo were shown to be metabolites of compound H and similar metabolites were also produced in the osteosarcoma cell line from chemically synthesized 1 alpha,25-dihydroxy-DHT3. The hepatoma cell line 25-hydroxylated DHT and no feed-back inhibition was observed. Use of the hepatoma cell to 25-hydroxylate a number of chemically synthesized 1-hydroxy-DHTs indicated that compound Ha was indistinguishable from 1 alpha,25-dihydroxy-DHT whereas compound Hb is possibly 1 beta,25-dihydroxy-DHT. Studies with the VDR in both chick gut and calf thymus indicated that 1 alpha,25-dihydroxy-DHT is very effective in displacing radiolabelled 1 alpha,25-dihydroxyvitamin-D3 and is thus most likely to be the calcaemic metabolite of DHT.
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PMID:The metabolism of dihydrotachysterols: renal side chain and non-renal nuclear hydroxylations in vivo and in vitro. 156 63

HNF1 (Hepatic Nuclear Factor 1) and vHNF1 are transcriptional regulators containing a highly divergent homeodomain. The first was initially found in liver nuclear extracts and is crucial for the transcription of albumin and many other hepatocyte specific genes, while the second was found in dedifferentiated hepatoma cells. Both recognize the same DNA binding site and can form homo and heterodimers in vitro and in vivo. In situ hybridization analyses have been performed to delineate the spatial and temporal pattern of expression of vHNF1 relative to HNF1 during mouse embryogenesis. The results show that accumulation of vHNF1 mRNAs expression is detected in several tissues of the embryo of both endodermal and mesodermal origin. Expression occurs in the yolk sac, the primitive gut, the liver primordium, and at different stages of kidney development in polarized epithelial structures and usually precedes that of HNF1. vHNF1 expression seems particularly prevalent with morphogenetic events in the kidney and may be a marker for certain polarized epithelium.
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PMID:vHNF1 is expressed in epithelial cells of distinct embryonic origin during development and precedes HNF1 expression. 168 90

For assessment of the value of delayed hepatobiliary imaging with technetium 99m (99mTc)-(Sn)-N-pyridoxyl-5-methyltryptophan (99mTc-PMT) for specific diagnosis of hepatocellular carcinoma, 88 patients with various malignant and benign liver diseases (49 with hepatocellular carcinoma, 4 with cholangiocellular carcinoma, 10 with metastatic liver carcinoma, 2 with liver cysts, 2 with liver hemangioma, 1 with liver abscess, 2 with intrahepatic lithiasis, 12 with liver cirrhosis, and 6 with chronic hepatitis) were studied. In 20 (41%) of the 49 patients with hepatocellular carcinoma, greater uptake of 99mTc-PMT by the tumor than by the surrounding liver tissue was seen in delayed hepatobiliary images, whereas in eight patients (16%), equilibrated uptake was seen. No increased uptake of the radioisotope by hepatic lesions was seen in 21 patients with localized liver diseases other than hepatoma. Moreover, in 18 patients with diffuse liver diseases, no focal accumulation of the radioisotope was seen in delayed 99mTc-PMT images. In addition, of 28 patients with hepatocellular carcinoma in whom the serum alpha-fetoprotein level showed little or no increase, 12 showed increased uptake of 99mTc-PMT by the tumor. In assessing delayed 99mTc-PMT images, however, it was necessary to consider following complications: accumulation of tracer in obstructed and dilated biliary trees; retention of radioactivity in nonneoplastic liver tissues; difficulties in evaluating 99mTc-PMT uptake by small hepatic tumors; overlapping of radioactivity in the gut and gallbladder in delayed 99mTc-PMT images of tumors. This study indicates that delayed 99mTc-PMT images can be useful in the diagnosis of hepatocellular carcinoma.
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PMID:Specific diagnosis of hepatocellular carcinoma by delayed hepatobiliary imaging. 241 74

The mouse H19 gene was identified by virtue of its coordinate regulation with the mouse alpha-fetoprotein gene. Both genes are expressed in the fetal liver, gut, and visceral endoderm of the yolk sac and are repressed shortly after birth in the liver and gut. They are both under the control of two trans-acting loci: raf, which affects the adult basal levels of the two mRNAs, and Rif, which affects their inducibility during liver regeneration. One crucial difference between the two genes is the activation of the H19 gene in mesoderm derivatives, skeletal and cardiac muscle. As a strategy for explaining both the similarities and differences in their modes of expression, the regulatory domains responsible for the expression of the H19 gene in liver were identified by transiently introducing the gene into a human hepatoma cell line. Two regions necessary for high-level expression of the gene could be identified, a promoter-proximal domain immediately preceding the start of transcription and an enhancer domain which lies between 5 and 6.5 kilobases 3' of the polyadenylation site. The 3' domain consists of two separable enhancer elements, each of which exhibits the properties of tissue-specific enhancers. Nucleotide sequence comparisons between the two H19 and three alpha-fetoprotein enhancers revealed limited similarities which are candidates for binding of common regulatory factors. Sequences which lie 3' of the gene are also required for the expression of the H19 gene following differentiation of teratocarcinoma cells into visceral endoderm.
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PMID:Two regulatory domains flank the mouse H19 gene. 246 63

Autologous mixed lymphocyte reaction (AMLR) and phenotypical composition of circulating lymphocytes obtained from nine subjects with untreated hepatocellular carcinoma (HCC); three HCC patients locally treated by means of intraarterial chemoembolization; six subjects with gut-derived carcinoma (GDC); nine chronic active liver disease patients (CALD), and 14 normal controls have been evaluated, using monoclonal antibodies (MAB) against CD5, CD8, CD4 glycoproteins and anti-LAK-1 molecule, a novel 120-KD surface antigen that is present on the membrane of large granular lymphocytes, by means of classical indirect immunofluorescence technique. Autologous mixed lymphocyte reaction was significantly reduced in all patients, along with CD4-positive cells that are the responder cells in this reaction. A relative increase in the percentage of LAK cells was also observed in neoplastic patients with a normalization after local treatment of the HCC. In the light of promising results obtained by Rosenberg et al. by adoptive transfer of LAK cells activated with Interleukin-2 (IL2) in various cancers, our results support a similar therapeutic trial in HCC patients.
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PMID:Circulating LAK-1 cells and autologous mixed lymphocyte reaction in patients with hepatocellular carcinoma. 253 11

The case is reported of a 66-year old man who developed Streptococcus bovis endocarditis on a fairly loose aortic stenosis and who also presented with alcoholic cirrhosis complicated by an ultimately lethal hepatoma. On this occasion, comments are made on the following points: -Str. bovis is increasingly responsible for bacterial endocarditis. This micro-organism is now rapidly and reliably identified. -Str. bovis endocarditis has some clinical features of its own. -Patients in whom the usual portals of entry of bacterial infection (i.e. benign or malignant tumours of the colon or rectum) cannot be identified should be investigated systematically for hepatic cirrhosis. -Drug sterilization of the gut is useful to prevent bacteremia of intestinal origin in cirrhotic patients.
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PMID:[Infectious endocarditis caused by Streptococcus bovis and alcoholic cirrhosis complicated by hepatoma]. 282 37

Thirteen patients with cancer of the gut, six with hepatocellular carcinoma and three with cancer of the bile duct have been treated with tegafur. All the patients were in an advanced stage of the disease with metastases to lymph-nodes or elsewhere. Each patient was given tegafur (oral daily dose of 600-1200 mg for 15-30 days with a dose-free interval of 25 days). Tegafur with other antiblastic drugs (such as cyclophosphamide, methotrexate, vincristine, doxorubicin, mitomycin) was given to ten patients. The results observed after the first treatment were as follows: partial remission in 14 patients (64%), no change in 4 (18%) and progression of the disease in 4 (18%). Only 10 patients among the 22 who were first treated, underwent one to three subsequent cycles of therapy obtaining with resultant partial remission in four cases, no change in two and progression of the disease in four patients. Side-effects (nausea and vomiting) during the treatment were recorded only in 14% of the patients. No significant impairment of blood functional tests has been documented. A comparison of the results obtained with tegafur and intravenous 5-fluorouracil has been made: the therapeutic effects of these two drugs are similar, but side-effects seem to be less during tegafur treatment.
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PMID:Tegafur chemotherapy for the treatment of gut and liver cancer. 309 13

A case of hemochromatosis and hepatocellular carcinoma secondary to hereditary spherocytosis is very rare and this is only the second case reported in an English language bulletin. When the patient, a 56 years old man, was admitted for receiving cholecystectomy for cholelithiasis, a diagnosis of hemochromatosis secondary to hereditary spherocytosis was made by liver biopsy and hematological examination data. The patient did not receive a blood transfusion nor was administered iron during the entire duration of the illness. Hepatoma was suspected at the time of splenectomy which was performed in 1981 because of severe anemia. Eight months later he died of massive abdominal cavity bleeding and subsequent autopsy findings were consistent with the disease mentioned above. Clinical and postmortem examinations suggested that conspicuously enhanced erythropoiesis in the bone marrow and unknown factors may be responsible for an increase in iron absorption from the gut and in the amount of stored body iron, leading to the development of hemochromatosis.
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PMID:An autopsy case of hemochromatosis and hepatoma combined with hereditary spherocytosis. 608 95

The effect of Fe3+ citrate on carrier-free 67Ga and 59Fe kinetics was studied in a Buffalo rat-Morris 7777 hepatoma model. Two mg Fe3+ citrate/Kg were administered intravenously in a variety of time sequences, prior to and following the tracers, and the rats were killed at 4 or 24 hours. 67Ga concentrations could be increased in tumor and decreased in most normal tissues. Administering Fe3+ both one half hour before and 2 hours after the tracers produced 67Ga values equivalent to 72-hour carrier-free values after 4 hours, while simultaneously decreasing gut secretion and increasing urinary excretion. The 59Fe and 67Ga kinetics suggested that events at both vascular and cellular levels were responsible for these changes. This study demonstrated the potential utility of Fe3+ citrate for improving both conventional 67Ga and positron (68Ga) imaging of tumors.
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PMID:The effect of certain variables on the tumor and tissue distribution of tracers V: false carrier effect, II, Fe. 707 35


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