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)

Metallothionein (MT) protein is readily induced in vivo in rat liver by adenosine and adenosine agonists (2-chloroadenosine, 5-(N-ethyl) carboxamido adenosine, and 5-chloro-5-deoxyadenosine). These presumably operate via AMP/adenosine receptors of the P1 (A2) type, which use the cAMP pathway. ATP was ineffective as an inducer for MT. 2-Chloroadenosine was the most effective inducer (7.27-fold at 11 hr). This induction was blockable by the adenosine antagonists, caffeine and theophylline. MT protein induction by 2-chloroadenosine in primary cultured rat hepatocytes was modest (1.55-fold), but this was also blocked by theophylline. MT mRNA induction was assessed using dot blot and Northern gel assays. Large inductions by 2-chloroadenosine (5.1- to 41-fold) were seen, and these were detectable as early as 2 hr in vivo. Two rat hepatoma cell lines (EC3 and 2M) were studied in vitro. Modest inductions of MT mRNA were seen: 2.10-fold for EC3 and 4.12-fold for 2M. Our studies implicate the potential role of the purinergic system in the modulation of transcription of MT genes in rat liver. The sources of adenosine in vivo that might cause induction of MT mRNA and protein are not well defined, but adenosine may be important as a signal in stress response situations involving tissue damage, such as ischemia, hypoxia, and hemorrhagic shock.
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PMID:Purinergic agonist induction of metallothionein. 152 9

Repeated hepatic dearterialization combined with intra-arterial infusion chemotherapy was performed in 29 patients with unresectable primary or secondary cancer of the liver. Partial Response (PR) was obtained in 4 cases (1 hepatocellular carcinoma and 3 gastric secondaries), when evaluated by measuring the regression rate radiologically. The most remarkable effect was found in those with metastases from gastric cancer. A satisfactory result was not obtained for hepatocellular carcinoma with liver cirrhosis because of frequent associated complications. A strategy to modulate the resistance of tumors to ischemia and anticancer drugs should be considered in order to obtain a better clinical result by this method.
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PMID:[Evaluation of repeated hepatic dearterialization combined with intra-arterial infusion chemotherapy of unresectable primary or secondary cancer of the liver]. 153 Mar 50

Three cases of bile duct necrosis owing to hepatic arterial infusion chemotherapy (HAI) were reported. Regarding HAI, transcatheter hepatic arterial embolization (TAE) was applied in two cases (hepatocellular carcinoma: 1; metastasis: 1) and 5-fluorouracil (continuous) combined with leucovorin (one shot) therapy (LV + 5-FU) was given to one metastatic case. In the data of blood biochemistry, serum alkaline phosphatase, gamma-glutamyl transpeptidase, and leucine aminopeptidase values characteristically elevated without the elevation of total bilirubin value. Hepatic tumors degenerated with necrosis in all cases and no viable cells were histologically recognized. Although the destruction of bile ducts was locally detected adjacent to these tumors in TAE cases and was more widespread in the LV + 5-FU case, these lesions were very similar in each case. Therefore, we concluded that both ischemia and drug toxicity induced bile duct necrosis and the necrosis around the bile duct was the secondary change due to the leaked bile juice.
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PMID:[Bile duct necrosis and hepatic necrosis following hepatic arterial infusion chemotherapy]. 165 26

The clinical experience following transplantation of livers obtained from non-heart-beating cadaver donors (NHBD) with the use of core cooling method is presented here. Six livers procured from such cadavers were transplanted into 6 recipients with hepatoma involving right and left lobes but without distant metastases. The first liver subjected to 75 minutes of warm ischemia had insufficient function after transplantation. The recipient died of graft failure 54 days later. The other 5 livers with 32 to 45 minutes of warm ischemia had a good or excellent immediate function. These 5 recipients died of tumor recurrence, acute rejection or septicemia 131 to 261 days after transplantation. The utilization of selected NHBD is suggested by our practice as a possible approach to help alleviate the acute organ shortage in the areas where heart-beating cadaver donors of brain death are not available.
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PMID:The results of transplant livers from selected non-heart-beating cadaver donors. 166 89

Major liver resections with complex vascular reconstruction require ischemia lasting from 2 h 30 to 5 h thus exceeding hepatic tolerance to warm ischemia. We describe a new technique of "ex situ-in vivo" liver surgery with prolonged ischemia with an intact hepatic pedicle. The surgical procedure encompasses complete mobilization of the liver and inferior vena cava, inferior mesenteric and femoral to axillary vein bypass, complete vascular exclusion of the liver, cold perfusion (U. W. solution), section of the hepatic veins allowing exteriorization of the liver ("ex situ") which remains connected by the hepatic pedicle ("in vivo"). The liver is placed on a heat exchanger at 4 degrees C. This procedure was performed in three patients: one each with hepatocellular carcinoma, huge metastasis of colorectal carcinoma and a "diffuse" hemangioma. Duration of ischemia was 225, 205, and 230 min respectively. The postoperative course was uneventful in all 3 cases and patients are alive at 15, 12, and 6 months. As it improves resecability rate of liver tumors and provides radical margins of resection, this procedure may be a beneficial alternative to liver transplantation for which poor results in cancer therapy with a high rate of recurrence are mainly due to immunosuppression.
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PMID:["Ex situ-in vivo" surgery of the liver: a new technique in liver surgery. Principles and preliminary results]. 166 68

The bilateral carotid occlusion model and a polyclonal antibody to the carboxyl terminus of the rat brain/human hepatoma glucose transporter were used to examine quantitatively changes in the transporter in gerbil hippocampal microvessels following 6-7.5 min of ischemia. The optical densities of immunocytochemically stained microvessels in the stratum lacunosum-moleculare (SLM) below the CA1 subfield were determined using image analysis of frozen sections from gerbils killed 2 h, 3 days, 6 days, 4 weeks, and 7 weeks after the ischemic episode. Microvessels were sparsely distributed in the stratum oriens, stratum pyramidale, and stratum radiatum. In contrast, the SLM was relatively well vascularized, and this distribution of microvessels persisted following ischemia. The SLM was identifiable based solely on microvessel distribution both in control gerbils and in gerbils that exhibited complete destruction of CA1 pyramidal cells. The abundance of the glucose transporter in SLM microvessels remained constant, suggesting that down-regulation of this protein cannot account for reported declines in brain glucose utilization and cell death following ischemia. Conversely, the presence and metabolic activity of CA1 pyramidal cells do not appear to be determinants of glucose transporter abundance in hippocampal microvessels. The brain/hepatoma glucose transporter was abundant in brain microvessels and the epithelial cells of the choroid plexus of gerbil and rat. Staining of hippocampal neuropil was less intense, poorly localized, and, at the light microscope level, not clearly associated with a particular cell type.
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PMID:Quantitative immunocytochemistry (image analysis) of glucose transporters in the normal and postischemic rodent hippocampus. 201 51

Starting from the assumption that tumor cells constantly experience transient ischemia and anoxia, and that this results in metabolic stress which is reflected above all, on the concentration of ATP, ADP and AMP, in other words, the adenine nucleotide pool (AdN), the aim of our research was to study the degradation and resynthesis kinetics of that pool on two types of malignant cells. All experiments were conducted in vitro with cells of the transplantable tumors of Ehrlich's ascitic carcinoma and the AS 30D hepatoma, and metabolite analyses were carried out enzymatically or by way of the HPLC chromatography method. It was found that immediately after the setting on of anoxia, there comes not only to a fall in ATP, but also to a fall in the complete adenine nucleotide pool for about 50%. The further maintenance of anaerobiosis does not have a significant influence on the AdN pool. The adenine nucleotide pool resynthesis is very rapid in the examined cells, and in the presence of glutamine and inosine, there comes to an occurrence of its significant growth. Evidence is given that the resynthesis in Ehrlich's ascitic carcinoma cells is made possible through the purine nucleotide cycle, which probably brings about the intensive glutamine oxidation and aspartate production, while in the AS 30D hepatoma cells it develops by means of adenosine kinase. The AS 30D hepatoma cells maintain a high ATP level in the absence of oxygen for a long time, provided that iodine-acetate is not added, which points to the fact that they have some other kind of energetic reserve aside from ATP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Kinetics of degradation and resynthesis of the adenine-nucleotide pool in tumor cells]. 209 81

An experimental study was conducted in the rat to evaluate the sensitivity of the liver to hyperthermia and ischemia. A 15-min asanguineous isolated hyperthermic in vivo perfusion of the liver was done in rats with a normal liver and in rats with an hepatocarcinoma induced by chronic 3'-diethylaminoazobenzene intoxication. The perfusion was made using various ranges of temperature of the perfusate. In normal rats, the in vivo perfusion was well tolerated as long as the mean intrahepatic temperature remained under 38 degrees C. Postoperative evolution of serum transaminase level was similar whatever the temperature of the perfusate. Histological lesions of the hepatic parenchyma were as severe as the temperature of the perfusate was elevated. In rats with tumors, the mortality rate was elevated in the animals with large tumors. A moderate decrease in the serum alpha-fetoprotein level was observed during the first days after liver perfusion. In all cases, death occurred apparently as a direct consequence of liver injury. This study defines the sensitivity of the normal or neoplastic rat liver to hyperthermia and ischemia using a model of isolated in vivo perfusion of the liver. It provides a basis for further investigations on the effect of hyperthermia on experimental liver tumors.
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PMID:Asanguineous isolated hyperthermic in vivo perfusion of the liver in the rat. 245 11

Partial resection of the liver is the only curative treatment for patients with hepatocellular carcinoma associated with severe cirrhosis of the liver. Surgical hemostasis on the cut surface of the cirrhotic liver appears very difficult because of the resultant deep cavity and the marked hemorrhagic diathesis. However, by using the microcrystalline collagen powder and the fibrinogen tissue adhesive, complete hemostasis and prevention of postoperative bleeding can be obtained, with minimal blood loss and hepatic ischemia.
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PMID:Use of microcrystalline collagen powder and fibrinogen tissue adhesive for hemostasis and prevention of rebleeding in patients with hepatocellular carcinoma associated with cirrhosis of the liver. 246 32

Transcatheter arterial embolization (TAE) has been widely used for treatment of hepatocellular carcinoma. Acute pancreatitis occasionally occurs as a complication of TAE. We have investigated the possible effects of TAE on the pancreas by monitoring serum pancreatic enzyme activities following TAE with various embolic materials. Serum amylase activity was increased very little in the patients treated with chemotherapy alone or plus TAE with lipiodol, slightly increased in many of the patients treated with chemotherapy plus TAE with gelatin sponge, and increased in all of the patients treated with chemotherapy plus TAE with gelfoam powder. The activity was increased to a level as high as 700 U/dl or more in most individuals of the last category. In one of them acute pancreatitis developed, probably because the gelfoam powder regurgitated into the pancreaticoduodenal artery, and occluded a very peripheral portion of the pancreatic vascular bed, leading to ischemia of the pancreas. These results suggest that choosing the correct particle size is important for prevention of acute pancreatitis.
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PMID:Acute pancreatitis after transcatheter arterial embolization (TAE) for hepatocellular carcinoma. 247 61


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