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 diagnostic value of whole body scanning using 99mTc-N-pyridoxylmethyltryptophan (PMT) was evaluated in 16 patients with bone metastases from hepatocellular carcinoma, in comparison with 99mTc-MDP. Of the 72 known lesions of bone metastases, 63 (87.5%) were detected by 99mTc-PMT scintigraphy, which demonstrated increased uptake of radionuclide. However, 99mTc-MDP bone scintigraphy detected only 45 lesions (62.5%), which were shown as increased, decreased, or mixed patterns of uptake. Thus 99mTc-PMT scintigraphy was more sensitive than 99mTc-MDP bone scintigraphy. In addition, the latter showed poor specificity because of its high false positive rate due to degenerative change. All lesions undetected by 99mTc-PMT scintigraphy were located in areas that overlapped the liver or bowel activity. In conclusion, it is recommended that whole body 99mTc-PMT scintigraphy be combined with 99mTc-MDP bone scintigraphy for the detection of bone metastases from hepatocellular carcinoma.
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PMID:[Clinical usefulness of 99mTc-PMT whole body scans in the diagnosis of bone metastases from hepatocellular carcinoma]. 131 62

Prognosis of patients affected with hepatocellular carcinoma (HCC) has been improved by the modern imaging techniques allowing an early diagnosis and by the value of the therapeutic protocols employed. Staging has also become more and more important. Bone metastases from HCC are reportedly rare. The authors observed a 5.5% incidence in 90 cases of hepatocarcinoma. The metastases were demonstrated by radiography, CT, and nuclear scintigraphy, in patients with skeletal pain. The plain film appearance of skeletal metastases from HCC was osteolytic in all cases; no surrounding sclerosis was seen. CT scans demonstrated the destructive nature of these lesions, which were associated with bulky soft-tissue masses. Metastases exhibited increased radiotracer (99mTc-MDP) uptake at bone scintigraphy. The authors believe that bone scintigraphy should be included in the staging protocols of the HCCs which need a potentially curative therapy.
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PMID:[Bone metastasis of hepatocarcinoma. Review of the literature, radiologic pictures and personal caseload]. 165 79

The metabolism of the glutathionyl leukotriene LTC4 in the mercapturic acid pathway was studied in suspensions of AS-30D hepatoma cells and hepatocytes, as well as in vivo in the bile duct-cannulated rat and in primates. 1. Isolated hepatocytes actively took up cysteinyl leukotrienes and metabolized LTC4 not only to LTD4 and LTE4 but also to N-acetyl-LTE4 and to metabolites more polar than LTC4. 2. AS-30D hepatoma cells are deficient in the transport system for the uptake of cysteinyl leukotrienes. Peptide cleavage of LTC4 to LTD4 and LTE4 was catalyzed by ectoenzymes of these cells. Inactivation of gamma-glutamyltransferase by acivicin and inhibition of LTD4 dipeptidase by penicillamine largely prevented further catabolism of LTC4 and LTD4, respectively. 3. [3H]LTC4 injected i.v. into rats was rapidly eliminated from the circulating blood, taken up by the liver, and excreted into bile where 77% of the administered radioactivity was recovered within 1 hr. The biliary LTC4 metabolites included LTD4, N-acetyl-LTE4, and metabolites more polar than LTC4. 4. Inhibition of [3H]LTC4 metabolism in vivo by i.v. penicillamine shifted the pattern of biliary cysteinyl leukotrienes; an extended half-life of [3H]LTD4 was associated with a retarded formation of N-acetyl-LTE4 and of polar metabolites. 5. Endogenous cysteinyl leukotrienes elicited by trauma were measured after HPLC separation by radioimmunologic analysis in plasma and bile of rats. The biliary concentration of these leukotrienes was up to 100 times as great as in plasma. N-Acetyl-LTE4 was the predominant endogenous metabolite in rat bile. 6. In the monkey Macaca fascicularis, cysteinyl leukotrienes were predominantly eliminated from blood via the liver into bile; renal excretion amounted to about 50% of the hepatobiliary elimination. Absorption of cysteinyl leukotrienes from the intestine resulted in enterohepatic circulation of these mediators. 7. Metabolites of [3H]LTC4 injected i.v. in the monkey were analyzed in bile and urine. In addition to polar metabolites and a small percentage of [3H]LTD4, [3H]LTE4 was a predominant metabolite particularly in bile. LTE4 was also the major endogenous cysteinyl leukotriene detected by radioimmunologic analysis in monkey bile. 8. LTE4 was the predominant endogenous cysteinyl leukotriene measured in human bile in patients suffering from acute pancreatitis. The detected amounts of LTE4 may be sufficient to induce known phenomena associated with acute pancreatitis including the shock-like reaction.
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PMID:Leukotriene C4 metabolism by hepatoma cells and liver. 289 Feb 80

A transplantable hepatocarcinoma of strain 2 guinea pigs was used as an experimental model for immunotherapy of cancer. 6,6'-Dideoxy-6,6'-bis-mycoloylamino-alpha,alpha- trehalose (TDNM) was found to be more effective in producing regression of transplantable line-10 tumours than 6,6'-di-O-mycoloyl-alpha,alpha-trehalose (TDM) when combined with 6-O-stearoyl muramyldipeptide (L18-MDP). TDNM showed potent antitumour activity in combination with synthetic lipid A of Escherichia coli (compound 506), but not with the lipid A analogues (GLA-59 and 60). As with the combination of MDP derivative and lipid A analogue, MDP derivatives conjugated with GLA-60 (GMD compounds) showed no tumour regression activity of line-10 cells in guinea-pigs.
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PMID:Regression of line-10 hepatocellular carcinoma by a less toxic cord factor analogue combined with L18-MDP or synthetic lipid A analogues. 319

Inhibition of the catabolism of the most biologically potent cysteinyl leukotriene, LTD4, was studied in rat hepatoma cells in vitro and in the rat in vivo. LTD4 dipeptidase, an ectoenzyme on the surface of AS-30D hepatoma cells, exhibited an apparent Km value of 6.6 microM for LTD4. D-Penicillamine and L-penicillamine inhibited this enzyme activity with apparent Ki values of 0.46 mM and 0.21 mM respectively. Bestatin, an inhibitor of the aminopeptidase activity of hepatoma cells, did not affect LTD4 hydrolysis at concentrations as high as 5 mM, indicating that the aminopeptidase did not contribute to LTD4 catabolism. In the rat in vivo, D-penicillamine also inhibited LTD4 catabolism. After intravenous injection of [3H]LTC4 an accumulation of [3H]LTD4 and a retarded formation of [3H]LTE4 were observed in the circulating blood after D-penicillamine pretreatment. Within 1 h after intravenous [3H]LTC4 injection, about 80% of the administered radioactivity was recovered in bile. After D-penicillamine pretreatment [3H]LTD4 was the major biliary leukotriene metabolite, whereas in untreated controls leukotriene metabolites more polar than LTC4 predominated in bile. After stimulation of endogenous leukotriene production in vivo by platelet-activating factor, N-acetyl-LTE4 was the major cysteinyl leukotriene detected in bile. D-Penicillamine treatment prior to platelet-activating factor resulted in the accumulation of LTD4, which under these circumstances was the major endogenous leukotriene metabolite detected in bile.
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PMID:Inhibition of leukotriene D4 catabolism by D-penicillamine. 362 11

The pharmaceutical properties of quinonyl-MDP-66 were discussed with special reference to the stability of oil-in-water emulsion, distribution capacity into regional lymph nodes and tumor regressive activity. The oil-in-water emulsion of quinonyl-MDP-66, which was prepared by treatment of quinonyl-MDP-66 with squalane (25 x) and emulsified with aqueous solution of 5% HCO-60 and 5.6% d-mannitol, was kept in lyophylized state and used after reconstitution by the addition of water before use. The reconstituted suspension of quinonyl-MDP-66 in oil-in-water emulsion was stable for more than 24 hrs. The oil-in-water emulsion of quinonyl-MDP-66 as prepared above was effective for the distribution of quinonyl-MDP-66 into regional lymph node in rats and for the regression of line 10 hepatoma in strain 2 guinea pigs by intralesional injection.
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PMID:Antitumor activity on line 10 hepatoma in strain 2 guinea pigs and pharmaceutical properties of quinonyl-MDP preparations. 370 41

A glutathione conjugate of aflatoxin B1 (AFB1) which has previously been identified as 8,9-dihydro-8-(S-glutathionyl)-9-hydroxy aflatoxin B1 (AFB1-GSH) (E.J. Moss, D.J. Judah, M. Przybylski and G.E. Neal, Biochem. J., 210 (1983) 227-233) has been degraded in vitro to all of the intermediates of the mercapturic acid pathway (MAP) and the chromatographic and spectral characteristics of each of these compounds investigated. The cysteinylglycyl conjugate (AFB1-Cys.Gly) was prepared by incubating the AFB1-GSH conjugate with a rat hepatoma cell line rich in gamma-glutamyl-transpeptidase (GGT). Incubations of the AFB1-Cys.Gly conjugate with dipeptidase produced a metabolite, which was purified and characterized by 1H-NMR spectroscopy as 8,9-dihydro-8-(S-cysteinyl)-9-hydroxy aflatoxin B1 (AFB1-Cys). The N-acetyl derivative of the AFB1-Cys conjugate resulted from the incubation of the AFB1-GSH conjugate in vitro with isolated rat kidney cells. Mass spectral data were consistent with the compound being 8,9-dihydro-8-(S-cysteinyl-(N-acetyl))-9-hydroxy aflatoxin B1 (AFB1-Nac.Cys). A chromatographically identical compound was obtained by the chemical acetylation of AFB1-Cys.
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PMID:The mercapturic acid pathway metabolites of a glutathione conjugate of aflatoxin B1. 393 41

Patients with diffusely increased uptake in both kidneys (often referred to as "host kidneys") on Tc-99m-MDP bone imaging were evaluated. Among 2056 patients reviewed, this finding was seen in 13 patients (0.63%): four with liver cirrhosis, two with lung cancer, one each with primary hepatoma, Hodgkin's disease, malignant lymphoma, thyroid cancer, leukemia, sideroblastic anemia and diabetes mellitus. Renal vascular disease and iron overload are considered to be the major causes of this finding.
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PMID:Diffusely increased Tc-99m-MDP uptake in both kidneys. 645 33

Treatment with synthetic MDP inhibited growth of transplantable, chemically induced tumors in syngeneic mice. The tumor-inhibitory effect was dependent on the schedule of MDP administration. Growth of SC transplants of a nonmetastasizing, MC-induced fibrosarcoma, MC11, was inhibited by local treatment with 200 micrograms and 1,000 micrograms MDP given SC 5-7 weeks before challenge. Treatment with lower (10 micrograms and 100 micrograms) doses of MDP and shorter (1-4 weeks) time intervals was not effective. Single doses of MDP (10-1,000 micrograms) 1-3 weeks after challenge had no effect. Growth of IV-inoculated, metastasizing AAT-induced hepatoma A was inhibited by IV injections of 20 micrograms MDP given 1 and 2 days prior to the challenge. Significant increases in the survival of hepatoma-bearing mice were observed only after injections of MDP incorporated in multilamellar liposomes.
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PMID:Inhibition of tumor growth in mice treated with synthetic muramyl dipeptide. 656 71

Although bone scintigraphy with 99mTc-MDP is a sensitive diagnostic method to detect bone metastasis, it is not specific for malignancy. A radioactive substance which accumulates specifically into metastatic lesions should be of value. 123I-IMP and bone scintigraphy with 99mTc-MDP were consecutively performed in patients with vertebral bone metastases from hepatocellular carcinoma and lumbar spondylosis deformans in a 7-day interval or shorter. The intensity of uptake was compared. Eighteen of the 20 metastatic lesions (90%) were classified as increased uptake areas in 123I-IMP scintigraphy. MDP-scintigraphy disclosed 16 metastatic lesions (80%), 9 as "hot" lesions (56%) and 7 as "cold" lesions (44%). 123I-IMP scintigraphy was negative in all 12 lesions of lumbar spondylosis deformans. Compared to MDP-scintigraphy, 123I-IMP scintigraphy was more sensitive in detecting vertebral bone metastases of hepatocellular carcinoma with smaller rates of false-positive and false-negative findings.
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PMID:Clinical experience of 123I-IMP scintigraphy in detecting vertebral bone metastases of hepatocellular carcinoma. A comparison with bone scintigraphy with 99mTc-MDP. 817 43


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