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)

Rat hepatoma cells were fused with cells of an established mouse lymphoma line, with normal diploid mouse macrophages, lymphocytes and fibroblasts and with normal diploid rat macrophages and lymphocytes. The liver-specific enzyme tyrosine aminotransferase was produced by almost all the hybrid cells, but usually at a lower level than in the parental hepatoma cells. Most of the hybrids also showed increased levels of this enzyme after exposure to dexamethasone. In the rat x mouse hybrids, the electrophoretic mobility of the enzyme indicated that only the rat hepatoma enzyme was produced. The findings are difficult to explain in terms of simple models involving a single diffusible repressor or activator of tyrosine aminotransferase synthesis.
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PMID:Synthesis of a liver enzyme in hybrid cells. 1 Mar 12

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

Type-B mammary tumor virus particles were detected by electron microscopy in the submaxillary glands of 6 of 27 freshly trapped, pregnant wild mice (Mus musculus). Type-B particles were also detected in 3 9f 24 seminal vesicles and 2 pulmonary adenomas from wild mice. Intracytoplasmic type-A virus particles were found in 7 spontaneous nonmammary tumors (lymphoma, hepatoma, lung adenoma) of aging wild mice. Type-C virus particles were also detected in many of these tissues.
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PMID:Mammary tumor virus particles in the submaxillary gland, seminal vesicle, and nonmammary tumors of wild mice. 16 6

Herpesvirus saimiri (HVS) is an oncogenic virus for a variety of nonhuman primates. HVS does not produce overt disease upon inoculation in the natural host (squirrel monkey) but consistently induces neoplasms including lymphomas and lymphocytic leukemias in 4 other species of monkeys. Various drugs inhibit replication of HVS in vitro including cytosine arabinoside and adenine arabinoside. In addition, the lymphoma and leukemia induced in owl monkeys responds to vincristine and prednisolone, cyclophosphamide, cytosine arabinoside, and human interferon. Of the various chemical carcinogens studied, the antitumor agent procarbazine induces neoplasms in a variety of species including monkeys. Thus far this compound has induced acute myelogenous leukemia (AML), lymphoma, and hemangiosarcomas in macaques. We have induced primary liver tumors in macaques with several nitrosamines and aflatoxin B1 and these tumors produce alpha-fetoprotein (AFP) which can be assayed for both diagnosis and therapy. Thus far, therapy of hepatocellular carcinoma has been most successful with surgical resection; and the tumor mass and serum AFP have been less responsive to single agent chemotherapy. These nonhuman primate models are useful for an understanding of the cause, diagnosis, prevention, and treatment of the human disease.
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PMID:Nonhuman primate models for lymphoma, leukemia, and other neoplasms. 16 36

This paper reports the radiographic findings in 84 cases of biopsy-proven pancreatic and biliary malignancies studied by endoscopic retrograde cholangiopancreatography. In the 73 successful studies a diagnosis of tumor could be made in 67 patients (92%). The study was successful in 40 of 43 patients with pancreatic carcinoma and the diagnosis could be made in 37 on the basis of stenosis or obstruction of the ducts. There were 33 successful studies in the 41 patients with miscellaneous tumors including primary bile duct, ampullary, gallbladder, metastatic carcinoma, lymphoma, and hepatoma. A diagnosis of tumor was made in 30 studies. As has been observed in carcinoma of other hollow structures, the hallmark of malignancy in the pancreatic and biliary tract is obstruction and stenosis. This study indicates that malignant disease of the pancreas and tract is accurately assessed by this endoscopic method.
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PMID:Diagnostic accuracy of endoscopic retrograde cholangiopancreatography in hepatic, biliary, and pancreatic malignancy. 17 13

Thirty-eight subjects from Hong Kong with chronic infestation by Clonorchis sinensis were studied. Ten of the patients died of hepatocellular carcinoma, seven of cholangiocarcinoma, and one each of carcinoma of the common bile duct and lymphoma. The major difference between the patients having cholangiocarcinoma and hepatocellular carcinoma was cirrhosis. Only one patient with cholangiocarcinoma had cirrhosis; whereas all but one patient with hepatocellular carcinoma had cirrhosis. The etiopathogenesis of these two tumors is substantially different.
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PMID:Clonorchiasis and hepatic neoplasms. 18 75

Considerable thymidine kinase and pyrroline-5-carboxylate reductase activities were found in the plasma of rats bearing a transplanted lymphoma; neither activity was detected in plasma of hosts carrying hepatic, renal, mammary, or submaxillary gland tumors. All host livers exhibited signs of biochemical immaturity as indicated by the appropriate increases or decreases in the concentrations of the nine enzymes measured. The extent and time schedule of the changes in host liver varied with the enzyme and with the tumor that caused them. The hepatic concentrations of ornithine aminotransferase, arginase, pyrroline-5-carboxylate reductase, and glucokinase (all diminished), and of peptidyl proline hydroxylase and hexokinase (increased) were sensitive indicators of tumor growth in general. The concentration of ornithine aminotransferase decreased before the tumors became palpable. At more advanced stages, the high hepatic thymidine kinase activity distinguished the presence of hepatoma and lymphoma from those of all other equally fast-growing tumors. However, only in lymphoma-bearing rats did a fivefold elevation of hepatic thymidine kinase occur as early as 4 days after implantation. Additional observations on the lymphoma itself, on blood cells, and on the involuting thymus of normal rats indicate that the striking systemic effects of this tumor cannot be explained by a release of enzymes from the thymus or by the increased number of lymphoma cells present in blood or liver.
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PMID:The effect of lymphoma and other neoplasms on hepatic and plasma enzymes of the host rat. 18 34

We examined whether hormones would modify the carcinogenic action of aflatoxin B1 (AFB1). Four groups of inbred Fischer rats received AFB1, 125 mug per animal, weekly per os. In three of the groups, certain hormones were administered simultaneously: One group received 1 U growth hormone (GH) sc weekly, another was given 4 U adrenocorticotropin (ACTH) weekly, and a third received 0.5 U insulin weekly sc. AFB1, ACTH, and insulin were given for 20 weeks; GH was given for only 10 weeks. The control group did not receive hormone adjuvant. In each group, 4 animals were killed at 7, 14, 21, 28, and 35 weeks; the remaining rats were killed at 77 weeks. Their livers were carefully examined and samples prepared for light and electron microscopy. Animals receiving AFB1 and ACTH failed to exhibit hepatocellular carcinoma. On the other hand, malignant lymphoma appeared at 56 weeks in 3 of the 6 surviving males on this regime. AFB1, alone or when given with insulin or GH, caused hepatocellular carcinoma in all animals; in these, lymphoma was not observed. Lymphoma comprised two cell types, each with similar neclear characteristics but differing in their nucleocytoplasmic ratios and in the amount and distribution of cytoplasmic organelles. Alterations leading to hepatocellular carcinoma were examined at various stages of development. "Basophilic hyperplasia" reflected an increase in free ribosomes. "Hyperplastic nodules" were composed of hepatocyte aggregates with characteristics similar to those encountered in the earlier stage. Both the "neoplastic nodules" and hepatocellular carcinomas were formed by cells containing large, "smooth fingerprints" and free ribosomal aggregates. These features supported the concept that AFB1 impairs ribosomal binding to endoplasmic reticulum membranes. The failure of ACTH-treated animals to develop hepatocellular carcinoma was ascribed to the effect of adrenal cortical stimulation upon membrane-polysome binding.
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PMID:Inhibition of hepatocarcinogenesis by adrenocorticotropin in aflatoxin B1-treated rats. 18 49

To study malignant invasion, we associated tissue and cell culture fragments, with adhesive and non-adhesive living substrates in vitro (11). Non malignant mesonephros, quail heart and BHK-cells, as well as malignant HeLa-, Hepatoma-, Harding-Passey melanoma-, Py-, TLX5 lymphoma- and Schmidt-Ruppin sarcoma cells, were transplanted into cultured organ fragments of chick embryos and chick blastoderms. Malignant invasion was evaluated on the basis of the following histological criteria: 1. changes in organization of the graft. 2. infiltration of cells from the graft into the substrate, 3. degenerative alterations of the substrate. It was shown that adhesion of the graft to the substrate is a prerequisite for malignant invasion. Invasion into non-adhesive substrates, such as the apical side of epithelia, was never observed. Contrary, all malignant cells did invade into adhesive substrates. Interposition of a vitelline membrane always inhibited the expression of invasiveness. The morphological pattern of invasion depended mainly on the architecture of the substrate and differential resistance of its various components explained well all histological pictures. From the latter observation and from the localization of degenerative changes in the substrate we inferred that malignant cells exert their deleterious effect most probably upon immediate contact with their host.
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PMID:Invasion of malignant cells into cultured embryonic substrates. 19 48

The standard analytical and preparative electrophoresis in polyacrylamide gel did not reveal qualitative differences in the fraction composition of c-RNA of the ascitic tumour cells (Zaidel hepatoma, Ehrlich carcinoma, NK/ly lymphoma) and normal liver cells. In vitro the tumour and normal cells efficiently incorporated the labeled uridine into the all main classes of c-RNA (4S, 18S, 28S, fractions above 28S), the process being more intensive in the tumour cells. The presence of tumours in the animal organism had a significant effect on RNA biosynthesis in the liver, the effect being dependent on the tumor nature. Lucantone (miracyl D) had practically no effect in vitro on the quantitative content of the summation c-RNA and its fractions in all cells studied. However, it markedly inhibited the metabolism of the main fractions of c-RNA in the cells of Zaidel hepatoma and Ehrlich carcinoma. The effect of lucatone in the cells of NK/ly lymphoma was contrary.
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PMID:[Molecular mechanism of the action of lucanthone on tumor and normal cells]. 19 13


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