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 9-year-old boy with non-resectable hepatocellular carcinoma was treated with irradiation and intra-hepatic arterial infusion of antitumor agents. His blood was positive for hepatitis B surface antigen (HBs Ag), but negative for hepatitis B e antigen (HBe Ag). Maternal transmission was suspected, because his mother's blood was positive for HBs Ag and his grand mother died from hepatic cirrhosis. The patient received a total dose of 4000 rad in 30 fractions. A chemotherapy cycle consisted of 5-FU (6 mg/M2/day, given continuously), EX (300 mg/M2, given on 1st, 3rd, 5th, 7th, and 9th week), VCR (1.5 mg/M2, on 2nd, 4th, 6th, 8th, and 10th week), and ADM (30 mg/M2, on 13th and 16th week). Since 6 months after the initiation of the chemotherapy, alpha-fetoprotein has become negative (less than or equal to 100n g/ml), and now, 2 years and 11 months after the diagnosis was settled, the patient remains a disease free state. His blood continues to be positive for HBs Ag.
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PMID:[HBs antigen-positive adult type liver cancer in a child with sustained remission induced by infusion of antineoplastic agents into the hepatic artery]. 630 70

Tumor nucleic acids have frequently been found to be deficient in methylated and other modified nucleotides. In particular, cytoplasmic transfer RNAs (tRNAs) from various neoplasms partially lack the hypermodified nucleoside queuosine, a modification specific for anticodons of histidine-, tyrosine-, asparagine-, and aspartic acid-accepting tRNAs. Using aspartate tRNA as an example, we show here that liver mitochondria contain tRNA fully modified with respect to queuosine, while the corresponding tRNA from mitochondria of Morris hepatoma 5123D completely lacks this constituent. The sequences of these tRNAs, which were determined by a highly sensitive 32P-postlabeling procedure entailing the direct identification of each position of the polynucleotide chains, were found to be (sequence in text) Lack of queuosine in the hepatoma mitochondrial tRNA may be due to the inavailability of queuine in the hepatoma mitochondria for incorporation into tRNA or to inhibition of the modifying enzyme, tRNA (guanine)-transglycosylase, in the tumor. Taking into account results of others indicating a possible involvement of the queuosine modification in differentiation of eukaryotic cells, we hypothesize that the queuosine defect may develop at an early stage of carcinogenesis (i.e., during the promotion phase) and be directly involved in abnormalities of mitochondria which have been observed frequently in transformed cells and tumors.
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PMID:Specific lack of the hypermodified nucleoside, queuosine, in hepatoma mitochondrial aspartate transfer RNA and its possible biological significance. 642 54

We investigated the ability of intracellular ornithine to alter both the biosynthesis of putrescine and the activity of ornithine decarboxylase in Reuber H35 hepatoma cells in culture incubated with 12-O- tetrade - canoylphorbol 13-acetate (TPA). In confluent cultures of H35 cells, the addition of TPA (1.6 microM) caused the activity of ornithine decarboxylase to increase by more than 100-fold within 4 h. When exogenous ornithine (0.1-1.0 mM) was added to the culture medium with TPA, a marked dose-dependent increase in the production of putrescine was observed. The activity of ornithine decarboxylase in the same cultures incubated with ornithine decreased in a similar dose-dependent manner. The addition of arginine (0.1-1.0 mM) (but not lysine or histidine) to the H35 cells in culture concomitant with TPA also led to a relative increase in putrescine biosynthesis and a decrease in ornithine decarboxylase activity compared to cultures not receiving the amino acids. A similar response to exogenous ornithine and TPA was observed in a series of less confluent rapidly growing cultures which were in culture for a shorter period of time. The confluent cultures possessed a basal level of arginase (55 units/mg protein) which increased approx. 2-fold upon treatment with TPA. The intracellular concentration of ornithine in the unstimulated cells was in the order of 0.02-0.03 mM. Upon incubation of the cells with exogenous ornithine or arginine, the intracellular pools of these amino acids increased 4- to 8-fold.
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PMID:A role for ornithine in the regulation of putrescine accumulation and ornithine decarboxylase activity in Reuber H35 hepatoma cells. 653 29

Stimulation of System N transport of glutamine by amino acid starvation of the rat hepatocyte can be repressed by one of its substrates, histidine, but not by two others, glutamine or asparagine. Furthermore, 2-(methylamino)isobutyric acid is also repressive, although it is not perceptibly a substrate or inhibitor of that system. The repression of System A by glutamine proves in contrast not to be dissociated from transport: relatively slow System A uptake of glutamine has now been shown in this cell. System A transport of glutamine is conspicuous in the hepatoma cell HTC and is increased after amino acid starvation of both hepatocytes and the hepatoma cells. Differential repression of the systems could be shown, although lowering the pH prevented the derepression of one system as much as the other on amino acid starvation.
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PMID:Incomplete correspondence between repressive and substrate action by amino acids on transport systems A and N in monolayered rat hepatocytes. 705 75

Adult rat hepatocytes placed in primary culture contain at least two distinct Na+-independent transport systems for neutral amino acids. The characteristics of the two systems do not allow assignment to previously described Na+ independent agencies, so we have tentatively termed the two processes Systems L1 and L2. Uptake by System L1 is substantially inhibited by cysteine, valine, isoleucine, leucine, methionine, histidine, tryptophan, tyrosine, phenylalanine, and 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid. In contrast, System L2-mediated transport is completely inhibited by isoleucine, leucine, phenylalanine, and 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid. Amino acids transported by both systems show biphasic kinetics yielding Km values for the System L1 component in the micromolar range, whereas the corresponding values for System L2 are an order of magnitude higher. In freshly isolated hepatocytes, the activity of System L2 is relatively high and declines over the initial 24 to 48 h of culture. The Na+-dependent Systems N and ASC also show a significant decay in activity during this time period. In contrast to the decrease in uptake by System L2, transport by System L1 increases during culture following an initial lag period of 12 to 24 h. The increase in System L1 activity can be blocked by the addition of either cycloheximide or actinomycin D. System L1 appears to be present also in fetal hepatocytes, although, in the hepatoma cell line, HTC, the Na+-independent component appears to be homogeneous as though one of the two systems present in the normal adult hepatocyte is not expressed in these transformed cells.
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PMID:Evidence for two Na+-independent neutral amino acid transport systems in primary cultures of rat hepatocytes. Time-dependent changes in activity. 711 28

A proband with persistently elevated AFP levels ranging between 21-129 ng/ml with median of 90 ng/ml has been found and observed for 1 year. Family studies have revealed that his father had had persistent AFP elevation for 4 years, ranging from 46 to 198.2 ng/ml, with median level of 93 ng/ml. His brother also has elevated AFP level. However, his mother, paternal uncle and paternal aunt have normal AFP level. Clinical examinations and laboratory tests have shown that AFP elevations are not associated with primary hepatocellular carcinoma, hepatitis, or other malignancies. We believe that such AFP persistency is of hereditary nature. To our knowledge, this is the first family of hereditary AFP persistence reported in China and the fourth one reported in the world literature.
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PMID:[Hereditary persistence of alpha-fetoprotein]. 751 80

The case of a 58-year-old man with clinically-stable and compensated HBsAg-positive liver cirrhosis is reported. In April 1991, the patient underwent partial hepatectomy to treat a solitary 3.5 cm hepatocellular carcinoma (HCC), (Edmonson scale I), in the 5th liver segment. His serum alpha-fetoprotein (AFP) level was 24 ng/ml. After hepatectomy, the AFP level dropped to 8 ng/ml, but between the 4th and 12th month it rose gradually from 72 ng/ml to 4,520 ng/ml. Hepatic recurrence of HCC was excluded, but a 6 cm solitary metastasis (Edmonson scale III-IV) was detected on the right adrenal. Adrenalectomy was performed and two months later the patient is doing well and his AFP level is 51 ng/ml. The methodological approach to diagnosis, treatment and follow-up of HCC, and the relationship between AFP and liver and metastatic HCC, are discussed.
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PMID:Increase in serum alpha-fetoprotein without recurrent disease after hepatectomy for hepatocellular carcinoma. 752 14

The case of a 70-year-old man with clinically-compensated alcoholic liver cirrhosis is illustrated. His serum alpha-fetoprotein level was on the increase but Ultrasonography and Magnetic Resonance detected no focal lesion of the liver. Five months after Ultrasonography, Computed Tomography and Magnetic Resonance were performed because the patient's alpha-fetoprotein level indicated hepatocellular carcinoma, but none of these tests succeeded in locating the neoplasm. Digital subtraction angiography was performed and only then was a small hepatocellular carcinoma revealed under the diaphragm. The patient underwent transcatheter arterial chemo-embolization with the result that the alpha-fetoprotein level dropped immediately and is still normal after 15 months. The case described is a model of what the ideal function of a marker of neoplasia should be, namely early detection, and subsequent precise confirmation of the continuing efficacy of the treatment adopted.
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PMID:A case of hepatocellular carcinoma that resisted identification. 752 3

An autopsy case of a 67 year old man with primary osteosarcoma arising in cirrhotic liver is reported. His son had von Recklinghausen disease and he had had a history of hepatitis C virus infection for 10 years. A large tumor, about 10 cm in diameter, was found in the right liver lobe. This tumor showed marked central necrosis and hemorrhage, and histologically diffuse sarcomatous cell proliferation associated with extensive osteoid formation and calcification of the periphery. Examination of the whole tumor and the cirrhotic liver (155 tissue blocks) showed that the tumor consisted of sarcoma cells mixed with osteoid with no region resembling hepatocellular carcinoma or hepatoblastoma. Minute hepatocellular carcinomas were found in the cirrhotic liver distant from the sarcomatous area. On immunohistochemical examination, the main tumor gave a distinct positive reaction for vimentin, but not for keratin or other epithelial markers. These findings indicate that the tumor was a true primary osteosarcoma, not an osteoid metaplasia of hepatocellular carcinoma.
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PMID:Primary osteosarcoma arising from cirrhotic liver. 755 Oct 4

From October 1987 to November 1993 we evaluated the serum levels of ammonia and amino acids in 85 patients with multiple myeloma. Six of the 85 cases of multiple myeloma demonstrated hyperammonemia and none of the known causes of hyperammonemia, such as liver failure, could be identified in these patients. All six patients also showed serum amino acid disturbances and conscious disorders in various degrees. In this study we compared these abnormalities in multiple myeloma with those in chronic liver failure (n = 14), the basic diseases of which were liver cirrhosis in six cases and liver cirrhosis complicated hepatocellular carcinoma in eight cases. There was a marked difference in the levels of individual serum amino acids between these two groups. The level of glycine was significantly higher in the multiple myeloma group (P < 0.001); on the other hand, that of tyrosine was significantly higher in the liver failure group (P < 0.005). The histidine (P < 0.005) and arginine (P < 0.005) levels were lower in the myeloma group. The ratio of glycine to tyrosine (Gly/Tyr) was 16.7 +/- 4.85 in the myeloma group and 1.7 +/- 0.12 in the liver failure group. The ratio of glycine to tyrosine was an important criterion for differential diagnosis.
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PMID:Serum amino acid disturbance in multiple myeloma with hyperammonemia. 759 24


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