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)

A new common antigen, preneoplastic (PN), was found in every early and late hyperplastic nodule and in every primary hepatoma induced by N-2-fluorenylacetamide, ethionine, 3-methyl-4-dimethylaminoazobenzene, dimethylnitrosamine, or diethylnitrosamine in three strains of rats (CFN, F344, and BUF). It so far has not been found in normal adult rat liver, liver surrounding nodules or cancer, fetal liver, amniotic fluid, adult rat serum, sera from rats with hyperplastic nodules or primary hepatomas, or various normal rat tissues. Immunofluorescent staining indicated the PN antigen was present in the cytoplasm of hepatocytes in hyperplastic nodules and in primary hepatomas.
J Natl Cancer Inst 1975 Jan
PMID:A new common marker for premalignant and malignant hepatocytes induced in the rat by chemical carcinogens. 16 16

In 1970, a staging based on surgical resectability of hepatic tumors was devised. Adjuvant chemotherapy with vincristine, 5-fluorouracil, and cyclophosphamide has been given to seven recent cases. Objectives of this study were to set up unified clinical staging and followup; to evaluate the effect of combination chemotherapy on survival in advanced disease; and to evaluate early adjunctive combination chemotherapy in surgically resectable lesions to, hopefully, prevent metastasis. Results to date in seven patients are: no change in the poor prognosis of the three female patients presenting with Stage III-IV hepatocellular carcinoma; the three males with Stage I-II hepatoblastoma have done well and survive the free of disease at 47 months, 44 months, and 28 months; one patient with hepatoblastoma had lung metastasis at diagnosis and died at 7 months with tumor. No toxicity was noted with the use of adjunctive combination chemotherapy following major hepatic resection.
Cancer 1975 Apr
PMID:A multiple chemotherapeutic approach to the management of hepatoblastoma. A preliminary report. 16 73

Homogenate and plasma membrane fractions of Morris hepatoma 5123tc (h) and rat liver were studied with regard to their relative basal activties of adenylate cyclase and to the comparative responsiveness of this enzyme to glucagon, sodium fluoride, epinephrine, prostaglandin E1, and insulin. The basal adenylate cyclase activities of the hepatoma fractions were found to be similar to those of liver at an adenosine 5'triphosphate concentration of 3.2 mM; if the substrate affinity (Km adenosine 5'-triphosphate) of the tumor enzyme is comparable to that of liver, these findings suggest that the reduced basal cyclic adenosine 3':5'-monophosphate levels found to occur in hepatoma 5123tc (h) probably are not due to a decreased basal rate of formation of this cyclic nucleotide. Glucagon (5.6 muM) significantly stimulated adenylate cyclase in both fractions of hepatoma and livers; however, the responsiveness of the tumor enzyme to this hormone was substantially lower than the responsiveness of liver for both homogenate and plasma membrane preparations; i.e., activities were enhanced 18-fold (relative to the basal activity)for liver homogenate compared with only a 6-fold increase for tumor. With the plasma membrane preparations, glucagon increased the activities 5- and 3.5-fold in liver and hepatoma, respectively. Sodium fluoride (10mM), in contrast to glucagon, increased the adenylate cyclase activity to approximately the same extent (about 10-fold) in the liver and hepatoma preparations. Epinephrine (100 muM) enhanced the liver and hepatoma homogenate activites 3- to 4-fold and the hepatoma plasma membrane activities 2-fold; however, the liver plasma membrane activites were not increased. Prostaglandin E1 (56.6 MUM) significantly increased adenylate cyclase activites of liver and hepatoma homogenates (i.e., 1.5- and 3-fold, respectively) but not of the plasma membrane preparations. Insulin (0.7 muM) did not significantly alter adenylate cyclase activities in any of the preparations.
Cancer Res 1975 Mar
PMID:Comparative adenylate cyclase activities in homogenate and plasma membrane fractions of Morris hepatoma 5123tc (h). 16 85

The total cyclic adenosine 3':5'-monophosphate (cAMP) phosphodiesterase activities as well as the activities of the low- and high-K-m enzyme forms were investigated in homogenates, 100,000 X g supernatants, and plasma membrane fractions of rat liver and Morris hepatoma 5123tc(h); the responsiveness of hepatoma and liver plasma membrane (low-K-m) phosphodiesterases to imidazole (40 mM) and theophylline (5mM) were also compared at cAMP concentrations of 1 and 7.5 muM. The total cAMP phosphodiesterase activities of tumor homogenates and 100,000 X g supernatant fractions were found to be less than one-half those of liver; kinetic studies of homogenates indicated that this finding was largely due to a substantial reduction (53%) in activity of the hepatoma high-K-m enzyme. In contrast, low-Km cAMP phosphodiesterase activities for tumor homogenate and plasma membrane fractions were significantly (50%) higher than liver; this was particularly evident when cAMP concentrations were between 0.5 and 2 muM. Since these concentrations are in the range of basal physiological levels of cAMP in hepatocytes, the present results suggest that the reduced levels of cAMP, previously observed in hepatoma 5123tc (h), are primarily due TO An increased rate of cAMP metabolism by low-Km cAMP phosphodiesterase in plasma membranes of the tumor. Imidazole increased the activity of the low-K-m cAMP phosphodiesterase of liver plasma membranes by 22 (1 muM cAMP) and 38% (7.5 muM camp); tumor activity was enhanced 35 and 50%, respectively, at 1 and 7.5 muM cAMP. Theophylline inhibited the plasma membrane phosphodiesterase activity of liver 79 and 53% at cAMP concentrations of 1 and 7.5 muM, respectively; hepatoma activity was inhibited 82 (1 muM cAMP) and 62% (7.5 muM cAMP).
Cancer Res 1975 Mar
PMID:Increased activity of low-Km cyclic adenosine 3':5'-monophosphate phosphodiesterase in plasma membranes of Morris hepatoma 5123tc (h). 16 86

Mitochondrial DNA's (mtDNA) isolated from rat liver and the Novikoff hepatoma grown as both solid tumors and cells in monolayer culture were examined by a variety of physicochemical techniques. Buoyant densities in analytical CsCl equilibrium gradients and thermal denaturation profiles revealed no significant differences in base composition among the mtDNA's isolated from liver, tumor, and hepatoma cells. Sedimentation in neurtral and alkaline CsCl showed no differences in mtDNA size. However, tumor and hepatoma cell mtDNA's were slightly smaller and more heterogeneous in size than liver mtDNA when molecular contour lengths were measured in the electron microscope. Based on chemical determinations, neoplastic mitochondria contained four to five times more DNA per mitochondrion than liver. Also, electron microscopy showed the proportion of mtDNA in complex forms (catenated dimers and oligomers) to be much higher in tumor (18%) and hepatoma cells (15%) than liver (4%).
Cancer Res 1975 Apr
PMID:Physicochemical characterization of Novikoff hepatoma mitochondrial DNA. 16 98

The M4 isozyme of lactate dehydrogenase was purified to homogeneity from normal rat liver and from two Morris hepatomas (7777 and 7793). Amino-terminal analyses with fluorodinitrobenzene failed to detect the presence of free amino-terminal residues in each enzyme studied. Each enzyme contained between 3.7 and 4.1 moles of protein-bound acetyl groups per mole of enzyme. The amino-terminal peptide, characterized as N-acetylalanylalanine, was isolated from Pronase digests of each isozyme preparation, and quantitative recovery experiments indicated that all acetyl residues were bound at the amino termini. Carboxylterminal analyses demonstrated phenylalanine to be the carboxyl-terminal residue in each enzyme studied. These data indicate no differences in either amino- or carboxyl-terminal regions of the hepatoma M4 isozymes compared to normal liver M4 isozyme.
Cancer Res 1975 May
PMID:Amino- and carboxyl-terminal analyses of hepatoma lactate dehydrogenase isozymes. 16 83

Growth of a guinea pig hepatoma was suppressed when tumor cells were mixed with viable Listeria monocytogenes (LM) before intradermal (id) injection into syngeneic recipients. Heat-killed LM were less effective than viable organisms in suppressing tumor growth. A vaccine containing oil droplets and LM cell walls lacked antitumor activity. Intratumor injection of viable LM on the 7th day after id injection of tumor cells prolonged survival of guinea pigs that did not succumb to LM infection. After intratumor injection of 0.6 times 10-8-1.0 times 10-8 LM, 5 of 22 guinea pigs died from acute infection (23 percent). In the 17 survivors, 3 tumors regressed completely (18 percent). Animals surviving injections of LM and tumor cells were immune to a second challenge with tumor cells. Immunization ofguinea pigs with an intravenous injection of LM decreased the mortality from intratumor injection of LM, but the intratumor injection of LM failed to cure a significant fraction of LM-immune animals bearing 7-day hepatoma transplants. BCG was more effective than LM in producing tumor regression. Synergism between LM and BCG was not observed, and simultaneous intratumor injection of BCG and LM was no more effective than intratumor injection of BCG alone in the treatment of 12-day tumor transplants.
J Natl Cancer Inst 1975 Mar
PMID:Antitumor activity of bacterial infection. II. effect of Listeria monocytogenes on growth of a guinea pig hepatoma. 16 68

Growth of intrapleurally injected cells of immunogenic methylcholanthrene-induced rat sarcomas was suppressed by intrapleural injection of viable or 1 times 10-6 R radiation-sterilized BCG vaccine. As little as 10 mug moist weight of organisms was effective, and treatment could be given several days before or after tumour challenge. Pleural effusion growth of a moderately immunogenic ascitic hepatoma was also controlled by intrapleurally administered BCG. In contrast, BCG injected intravenously, subcutaneously or intraperitoneally was without influence on pleural tumour growths. Similarly, intraperitoneal growth of these tumours was suppressed only by intraperitoneal injection of BCG. With two other transplanted tumours, a chemically induced mammary carcinoma and a spontaneous sarcoma, both of which lack significant immunogenicity, BCG treatment of pleural and peritoneal growths was less successful and more variable. Nevertheless, these studies indicate the potential of this type of treatment of thoracic and peritoneal tumour deposits for possible clinical application in the treatment of malignant mesothelioma.
Int J Cancer 1975 Feb 15
PMID:BCG therapy of pleural and peritoneal growth of transplanted rat tumours. 16 55

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.
J Natl Cancer Inst 1975 May
PMID:Mammary tumor virus particles in the submaxillary gland, seminal vesicle, and nonmammary tumors of wild mice. 16 6

Administration of 40 ppm diethylnitrosamine (DENA) in the drinking water for 10 weeks to male Fischer rats led to hepatocellular carcinoma in 100 percent with metastasis to the lung in 40 percent, of the animals living for the full experimental period of 20 weeks. Concurrent feeding of phenobarbital and DENA for 10 weeks produced cancer of the liver in 77 percent of the animals, but only 9 percent had metastases in the lung. A brief regimen of DENA for 4 weeks, followed by 16 weeks of observation, induced cancer of the liver in only 13 percent of the rats. Administration of phenobarbital, begun 1 week after cessation of DENA intake and terminated at week 20, led to liver cancer in 64 percent of the rodents. Hydroxyurea had no effect on this enhancement. Treatment with a purified gamma fraction of antilymphocytic serum after the DENA did not influence the outcome. Thus phenobarbital given together with DENA reduced the severity of the carcinogenic process, but when it was given after the hepatocarcinogen, it increased the effect.
J Natl Cancer Inst 1975 May
PMID:Modification of diethylnitrosamine liver carcinogenesis with phenobarbital but not with immunosuppression. 16 10


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