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)

Rats bearing the Morris hepatoma No. 7777 were randomized into three treatment groups. Two of the groups received a nutritionally complete liquid formula diet per os ad libitum. One of these two groups received hydrazine sulfate (HS; an inhibitor of gluconeogenesis) twice daily (15 mg/kg) for 5 days. A third group of tumorous rats received the HS therapy and was given the liquid diet parenterally for 5 days. Tumorous rats fed per os, especially with HS therapy demonstrated inhibition of tumor growth, reduction of body and carcass weight, anorexia and decreased nitrogen retention. The combination of parenteral feeding and HS therapy sustained body and carcass weight with high nitrogen retention but stimulated tumor growth and was associated with liver toxicity. These results support the concept that cancer cachexia involves 'a systemic energy-losing cycle dependent on an interplay of tumor glycolysis and gluconeogenesis'.
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PMID:Total parenteral nutrition and inhibition of gluconeogenesis on tumor-host responses. 11 15

It is reported on the technique of transplantation of a carcinoma on the pancreas of the rat. As to the origin the malignoma used is a tumour induced by Methyl-Yellow and known as solid form of the Zajdela-hepatoma. Out of 50 transplantation experiments 48 were successful (96%). After continuous growth regional formations of metastases were observed. Death took place in the 3rd week after transgression of the borders of the organs under the picture of cachexia.
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PMID:[Pancreas carcinoma in the rat (attempts at implantation)]. 17 9

To ascertain anorexigenic effect of toxohormone-L, a polypeptide extracted and purified from ascites of patients with hepatoma were infused into the rat third cerebroventricle. Food intake decreased on the first day after infusion of an optimum dose of 10.0 micrograms (p less than 0.05). The suppressive effect on feeding was linearly dose dependent (p less than 0.05). Meal size and latency to the first meal decreased in the 12-h dark period, and the first and the second 4-h cumulative blocks after infusion of a 10.0 micrograms dose (p less than 0.01 for each). The suppressive effects on total food intake and meal size were completely recovered within 24 h after infusion. Neither postprandial intermeal interval nor eating speed was affected. Periprandial drinking, a ratio of water intake to food intake, was not affected after infusion of 5.0 and 10.0 micrograms toxohormone-L. Infusion of a 10.0 micrograms dose showed no effect on ambulation. These findings suggest that anorexia and cachexia produced in cancer patients may essentially be due to the suppressive effect of toxohormone-L on food intake.
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PMID:Anorexia induced by toxohormone-L isolated from ascites fluid of patients with hepatoma. 132 17

The influence of eicosanoids on the proliferation of hepatoma (HTC) cells was studied in culture and in tumor-bearing rats. The cells in culture demonstrated a capacity to metabolize arachidonic acid to eicosanoids including thomboxane B2 and the prostaglandins E2 and F2 alpha a. An effect of these eicosanoids on cell proliferation was suggested by the decreased cell division seen with an inhibitor of cyclooxygenase, flurbiprofen. A biphasic effect on the proliferation of HTC cells was observed with increasing concentrations of prostaglandin F2 alpha. These studies were extended to tumor-bearing rats where inhibitory effects on the early stages of tumor growth were seen with flurbiprofen. Bleeding times were decreased in tumor-bearing rats but were restored to control values by treatment with flurbiprofen and an inhibitor of thromboxane synthetase, OKY 046. These drugs and a thromboxane/endoperoxide receptor antagonist, SQ 29, 548, were not observed to have statistically significant effects on isotope-labeled water distribution but they had substantial effects on the maintenance of body weight by tumor-bearing rats. The data suggested that the cachexia of tumor-bearing animals may be mediated at least in part by the action of eicosanoids.
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PMID:Influence of inhibitors of eicosanoid metabolism on proliferation of rat hepatoma cells and on tumor-host interaction. 211 60

Severe cachexia of extremely rapid onset typifies the young Black African patient with hepatocellular carcinoma (HCC). In order to assess whether this is a consequence of tumor-associated increases in protein metabolism or simply due to inadequate dietary intake, the following study was undertaken. The technique of constant i.v. infusion of 14C-labeled leucine was used to measure whole body protein flux, breakdown, synthesis, and oxidation rates in 8 adults with HCC, 4 patients with massive hepatomegaly due to metastatic adenocarcinoma from bowel, 6 patients with chronic liver disease, and 10 controls. Endogenous protein breakdown and oxidation were similar between patients with chronic liver disease (breakdown, 4.4 +/- 1.2 g/kg/day; oxidation, 0.8 +/- 0.4 g/kg/day) and controls but were significantly (P less than 0.002) higher in patients with liver tumors, the highest rates being observed in those with HCC (breakdown, 8.5 +/- 4.3 g/kg/day; oxidation, 1.4 +/- 0.5 g/kg/day). Protein turnover was generally higher in the HCC group, with increased rates of reincorporation of amino acids into protein synthesis (P less than 0.05). In one HCC patient a synchronized diagnostic liver biopsy demonstrated high fractional synthesis of rates of HCC proteins of 86%/day. In addition, the incorporation rates of labeled amino acid into fibrinogen, immunoglobulin G, and transferrin were also highest (P less than 0.03) in HCC patients. In order to assess the relative importance of diet in weight loss, dietary intake levels were assessed from hospital records of HCC patients and by dietary recall during the week prior to study. Intakes ranged from 30 to 70% of calculated requirement levels. In conclusion, our results suggest that the rapid wasting seen in patients with HCC is due to an imbalance between the metabolic demands, which can be elevated in some patients, and inadequate dietary replenishment.
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PMID:Contribution of elevated protein turnover and anorexia to cachexia in patients with hepatocellular carcinoma. 215 53

The intraperitoneal implantation of the ascitic hepatoma cells, AH-130 to rats induced marked atrophy of the systemic organs within 2 weeks, resulting in the animal death. By the method of Feulgen hydrolysis curve analysis, the amount of single-stranded DNA and the degree of DNA instability were shown to be increased in these atrophic organs. In keeping pace with the progression of the cachectic multi-organ damage (MOD), the amount of lipidperoxide and the activity of superoxide dismutase (SOD) as measured by electron spin resonance (ESR) were increased in the ascites toward the end stage of chachexia. The increased lipidperoxide and SOD induction reflect the increased production of active oxygens, especially superoxide. The marked systemic organ damage induced in cancer cachexia seems to be due to DNA damage by active oxygens.
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PMID:Multi-organ damage (MOD) induced by cancer cachexia and its pathogenesis. 262 6

Two rat tumors, Morris hepatoma 7777 (MH) and Yoshida ascites hepatoma AH130 (YAH) were compared, and the influence of systemic inhibition of prostaglandin (PG) synthesis on muscle protein metabolism was evaluated. Tumor-bearing rats were compared with ad libitum- and pair-fed controls. Rats were also treated with naproxen, an inhibitor of PG synthesis. Tumors caused progressive anorexia and weight loss and resulted in decreased weight and/or protein content of the soleus, extensor digitorum longus, and epitrochlearis muscles. The extent of this wasting varied with muscle and tumor type. Muscle wasting induced by the tumors appeared to result from increased protein degradation and/or decreased protein synthesis, as determined in isolated epitrochlearis muscle. In YAH, reduced feed intake did not appear to be responsible for muscle wasting; however, in MH, it accounted for a significant proportion of the muscle loss. YAH produced large amounts of PGE2. Treatment of rats with naproxen inhibited tumor PGE2 production and muscle protein loss in rats bearing YAH. Naproxen had no effect on muscle weight or protein degradation in rats bearing MH. These results would appear to implicate PGE2 in the development of cachexia in the laboratory rat.
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PMID:Effects of systemic inhibition of prostaglandin production on protein metabolism in tumor-bearing rats. 239 72

Liver cancer is the most common of all malignancies worldwide, its incidence reaching almost epidemic proportions in some countries. However, its significance in North America has generally been underemphasized. In a 5 year period, hepatocellular carcinoma was diagnosed in 35 adult patients in our institution. Preexisting liver inflammation was present in 27 of the patients (77 percent). Although most patients had symptoms, they included only poorly defined pain or cachexia in most cases, and 10 patients (29 percent) were totally asymptomatic at the time of diagnosis. Five patients presented with hemoperitoneum due to intraabdominal tumor rupture. Examinations useful in confirming the diagnosis included alpha-fetoprotein determination, liver scan, and computerized tomographic scanning. Eight patients (23 percent) had associated visceral or other malignancies. The outlook was poor, with a mean survival of 5 months, and only two patients survived more than 1 year. Hepatocellular carcinoma is uncommon but not at all rare in the Pacific Northwest. It arises from chronic liver inflammation, is diagnosed late, and has a grim prognosis. Prevention of various forms of chronic liver inflammation, and mass serial screening of populations at high risk for the development of hepatocellular malignancy will probably have the greatest role in reducing the lethality of this disease.
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PMID:Hepatocellular carcinoma. A 5 year institutional experience. 298 72

Twenty-two patients with hepatocellular carcinoma were treated with transcatheter arterial embolization therapy. In the six who died within about a month, serum albumin and Ch-E were lower, and total bilirubin and ICG R15 were higher than in the other cases. In four of them, more than 50% of the liver was occupied by tumor, and tumor thrombosis were found in the portal trunk or bilateral first portal branch. Five patients died of hepatic failure followed by upper gastrointestinal bleeding. One died of cachexia. The causes of short survival were 1) severe liver cirrhosis, 2) portal obstruction, 3) large tumor, 4) widespread TAE, 5) retrograde flow of gelfoam.
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PMID:[Retrospective study of short survival cases in hepatocellular carcinoma after transcatheter arterial embolization therapy]. 298 79

H 615, the first transplantable mouse liver carcinoma model established in China, was derived from a spontaneous hepatocellular carcinoma of an inbred 615 mouse and has been successfully propagated for 52 generations during the past 7 years and more. Its biologic and pathologic features are relatively stable. H 615 was a syngenic transplantable tumor model of 615-strain mice with a successful transplantation rate of 85.6% without spontaneous regression. The course of tumor growth after subcutaneous inoculation was divided into 4 stages: latent, slowly growing, rapidly growing and terminal stages. Cancer metastasis was rare. The tumor-bearing host would die of cachexia finally. The mean survival time was 62.2 +/- 11.0 days regardless of sex or age. Histologically and ultrastructurally, H 615 was a well-differentiated hepatocellular carcinoma, rather resembling human liver carcinoma. The short-term primary passage culture of H 615 showed that, in vitro, tumor tissue could easily grow into monolayer, the majority of which appeared as epithelioid cells in cytomorphology. Therapeutic tests of 15 anticancer drugs showed that H 615 was sensitive, in varying degrees, to 5 drugs, i. e. MMC, Thio-Tepa, 5FU, CPT and DACT. The inhibition rate of MMC and Thio-Tepa could be as high as 100%. These experimental results are similar to those of the human liver cancer chemotherapy. Hence, the authors believe that H 615 may be a useful model in experimental study of the liver cancer and screening of anticancer drugs.
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PMID:[Establishment and experimental study of a transplantable hepatocellular carcinoma model in 615-strain mice (H 615)]. 344 59


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