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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although hepatic resection for hepatocellular carcinoma is the only known modality that offers an opportunity for cure, the practicing oncologist must be aware of alternative modes of therapy. A multidisciplinary approach between surgeon, medical oncologist, and invasive radiologist is necessary in exploring all potential therapeutic options. The oncologist must not only consider the stage of the tumor, but must also take into account the functional reserve of the nontumor-bearing liver in selecting appropriate therapy. More recently, hepatic transplantation has been recognized as a potential curative modality for specific tumor types and stages. Percutaneous ethanol injection and chemoembolization are excellent palliative measures. However, it remains clear that new and innovative techniques are necessary in the therapeutic, adjuvant, and palliative settings in the comprehensive care of the patient with hepatocellular carcinoma.
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PMID:Current strategies for the treatment of hepatocellular carcinoma. 138 Aug 39

The wild mushroom, Dermocybe sanguinea, contains several anthraquinone pigments, of which emodin (1,3,8-trihydroxy-6-methylanthraquinone) is quantitatively the most important. In our preliminary tests, Dermocybe sanguinea extracts were genotoxic without metabolic activation. The ethanol extract of Dermocybe sanguinea was fractionated by flash chromatography, and the emodin contents of the fractions were determined by HPLC. Their genotoxicities were assayed using a bacterial repair assay and sister-chromatid exchange analysis. The cytotoxicity of the fractions was assayed with mouse hepatoma cells using growth inhibition as the endpoint. The results of the biological tests were compared with those obtained with pure emodin. It was concluded that, in addition to emodin, Dermocybe sanguinea contains several other geno- and cytotoxic compounds.
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PMID:Directly acting geno- and cytotoxic agents from a wild mushroom Dermocybe sanguinea. 138 68

The formation of intracellular lumina with apical differentiation is observed in several cancerous epithelial cell lines including human hepatocarcinoma. This disorder of cell polarization can be induced by the inhibition of cell-cell communication, a known factor of carcinogenesis. This work was designed to study the effects of ethanol on the differentiation of hepatocytes in short-term culture. Isolated hepatocytes were plated on plastic culture dishes that were 35 mm in diameter (10(6) cells/dish). Three hours after plating, the hepatocytes were incubated in the presence of 20 mmol/L ethanol for 1 hr. Treated cells were compared with controls using morphometric methods after conventional treatment for ultramicroscopy and by measuring cellular dye coupling by the fluorescent Lucifer Yellow CH transfer method. Bile canaliculi formation decreased in alcohol-treated cells (6.5% vs. 9.9%, 2p less than 0.05), whereas intracellular lumina incidence increased (3.1% vs. 0.5%, 2p less than 0.01). In parallel, the dye-coupling capacity decreased significantly when hepatocytes were treated with alcohol (2p less than 0.01). This work shows that short-term ethanol treatment induces significant disturbances of cell polarization and inhibits the reestablishment of cell-cell communication in cultured hepatocytes. These disorders could, at least in part, explain the carcinogenic effects of ethanol.
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PMID:Effects of ethanol on intercellular communications and polarization of hepatocytes in short-term culture. 156 37

Glucocorticoids induced ADH activity and mRNA 2- to 4-fold in rat hepatoma cells (H4IIE and H4IIEC3), but were reported not to alter ADH activity in rat liver. The failure of corticosteroids to induce ADH may have been due to the short-term treatment of the rats or the dose of steroid used. To reevaluate the effect of glucocorticoids in vivo, we studied animals 4.5 weeks after adrenalectomy so that ADH activity and mRNA should have reached a new steady-state level; the dose of glucocorticoid used was estimated to provide physiological replacement. Male Wistar rats were injected with a single daily dose (10 mg/kg/day) of corticosterone-21-acetate or vehicle subcutaneously for 10 days. Liver extracts were assayed for ADH activity, ADH protein, and ADH mRNA. Nuclei were isolated for nuclear run-on assays. Adrenalectomy did not reduce the activity of ADH in liver. Subsequent corticosterone treatment did not alter ADH enzyme activity, nor did it affect ADH protein levels as analyzed on Western blots. However, Northern blot analysis of ADH mRNA indicated a 2-fold increase in ADH mRNA in the treated animals when the data were normalized to the level of the 28S ribosomal RNA or CHO-B mRNA. The rate of transcription of the ADH gene in nuclei isolated at the end of 10 days of treatment from corticosterone-treated adrenalectomized rats was not statistically different from that in the oil-treated adrenalectomized ones. The disparity between ADH activity and protein levels and the mRNA level may have resulted from other effects of corticosterone, e.g., stimulation of protein degradation or effects on translation.
Alcohol Clin Exp Res 1992 Jun
PMID:Corticosterone induces rat liver alcohol dehydrogenase mRNA but not enzyme protein or activity. 162 40

An autopsied case of well-differentiated hepatocellular carcinoma (HCC), showing neural invasion into the portal tract of the liver, a hitherto undescribed lesion, is reported. The patient, a 68-year-old man, had had treatment for HCC over nine years, comprising surgical resection, transcatheter arterial embolization, transportal venous embolization and percutaneous ethanol injection to nodules of the HCC. At autopsy, many HCC nodules (less than 7 cm in diameter) were found in the liver. In one of them, carcinoma cells infiltrated the medium-sized protal tract among the regenerative nodules and some of these carcinoma cells further invaded nerve fibers. Although the majority of the HCC nodules showed ischemic necrosis, the infiltrating carcinoma cells in the portal tract were viable, suggesting the biological behavior and/or blood supply of these infiltrating carcinoma cells to be different.
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PMID:Well-differentiated hepatocellular carcinoma showing intrahepatic neural invasion: autopsied case. 164 37

Despite the epidemiological evidence of a correlation between ethanol abuse and hepatocellular carcinoma, some of the results of experimental and clinical studies remain controversial. Apart from inducing cirrhosis, which may be viewed as a precancerous liver lesion, ethanol may act as a cocarcinogen. Most investigations on this topic have focused on two aspects: ethanol's capacity to induce the cytochrome P-450-dependent microsomal biotransformation system and its interference with at least one DNA repair mechanism. Ethanol exposure enhances the capacity of mixed function oxidases to activate many chemical carcinogens, such as dimethylnitrosamine (DMN). On the other hand, ethanol exposure fails to influence DMN-induced liver carcinogenesis. The capacity of alcohol to inhibit DMN-demethylase activity has not been clearly demonstrated in experiments carried out with human tissue. In conclusion, both the effects of ethanol and their underlying mechanisms as regards liver carcinogenesis are open to debate. The link between ethanol abuse and hepatocellular carcinoma appears to be mediated mainly by its capacity to induce cirrhosis.
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PMID:Hepatocellular carcinoma, alcohol, and cirrhosis: facts and hypotheses. 165 Jun 91

Two patients with recurrent hepatocellular carcinoma underwent reoperation following percutaneous ethanol injection therapy (PEIT) and transarterial embolization (TAE). In the first case, although the nodules where the accumulation of Lipiodol (LpD) was seen showed complete necrosis, viable cancer cells were seen in the areas with slight accumulation of LpD. One nodule with no accumulation of LpD where PEIT seemed to have been performed, developed necrosis. In the second case, the nodules with LpI) accumulation also showed almost complete necrosis. The area where PEIT was performed was mixed with necrosis and bleeding, where a small viable cancer nodule existed. The reason for incomplete anticancer effects by PEIT seemed to be the too small ethanol injection.
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PMID:[Percutaneous ethanol injection therapy (PEIT) and transarterial embolization (TAE) for recurrent hepatocellular carcinoma--report of 2 cases]. 165 29

The rates of oxidation of ethanol to acetate by human blood monocyte-derived macrophages and the two human hepatoma cell lines PLC/PRF/5 and Hep G2 were studied. The average rates obtained were, respectively, 621, 447 and 596 nmol/h/mg cellular protein. Cultures of these three cell types, containing known quantities of cellular protein per flask, were incubated with 0 or 2 mg ethanol/ml for 72 h and the culture supernatants subjected to affinity chromatography on blue sepharose CL-6B. Pure albumin fractions obtained in this way were adjusted to the same optical density and tested for cytotoxicity against A9 cells. The data showed that the albumin fractions obtained from ethanol-containing macrophage cultures were considerably more cytotoxic than those obtained from ethanol-containing cultures of PLC/PRF/5 and Hep G2 cells. It appeared that, for a given quantity of ethanol metabolised, considerably more acetaldehyde was released extracellularly by macrophages than by the two hepatoma cell lines and that this acetaldehyde bound to albumin to form cytotoxic acetaldehyde-albumin complexes. The data raise the possibility that macrophages are an important source of extracellular acetaldehyde and circulating acetaldehyde-albumin complexes in vivo.
Alcohol Alcohol 1991
PMID:Comparison of the generation of albumin-associated cytotoxic activity in supernatants from ethanol-containing cultures of human blood monocyte-derived macrophages and of two human hepatoma cell lines. 165 51

Histopathologic examination was done on 18 cases after percutaneous ethanol injection therapy (PEIT) for hepatocellular carcinoma. In eight cases, the lesion was treated by PEIT alone; in the other ten cases, PEIT was combined with transcatheter arterial embolization. The lesion was completely necrotic in 13 cases, 90% necrotic in four cases, and 70% necrotic in the rest. In addition, PEIT seemed to be effective against intercapsular, extracapsular, and vascular invasions. In the four cases of incomplete necrosis, the viable cancer tissue remained in small tumor nodules around the main tumor, in portions isolated by septa, or along the edge of the lesion. Therefore, ethanol should be injected not only into the center of the lesion, but also into sites close to its edge. Ethanol did not damage noncancerous liver parenchyma distant from injected sites. Local dissemination of the cancer cells was not found in any case. Therefore, PEIT seems to be a valuable therapy and may be an alternative to surgery in some cases.
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PMID:Percutaneous ethanol injection therapy for hepatocellular carcinoma. A histopathologic study. 165 96

The results of hepatectomy, percutaneous ethanol injection therapy and transcatheter arterial embolization for small hepatocellular carcinoma (HCC) of 3 cm or less in diameter from the published literature were compared with the authors' experiences with surgical treatment. The survival rates for those treated by hepatectomy and ethanol injection were almost the same, being more than 90% at 1 year and 70% at 3 years. The overall results achieved by embolization were inferior to those achieved by the other two therapeutic modalities, although the 1 year survival rate was not worse. The cancer-free survival rates after hepatectomy and ethanol injection were also similar. Most of the patients with small HCC had associated liver cirrhosis or chronic active hepatitis, but the degree of liver dysfunction and the level of hepatic reserve varied. Anatomically, the number, size, and location of the cancer also varies. Choice of treatment for small HCC should be made based upon the degree of liver function and the anatomic status of the cancer. For example, a patient with multiple (more than four) cancer nodules is a good candidate for embolization. Ethanol injection is indicated for a small HCC, deeply seated in a severely diseased liver. Hepatectomy is the first choice for a small HCC situated near the surface of a liver with relatively good liver function.
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PMID:Choice of treatments for small hepatocellular carcinoma: hepatectomy, embolization or ethanol injection. 165


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