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 HTC hepatoma cell line was used as an "in vitro" model to detect the cytotoxicity of eighteen chemicals, chosen on the basis of different biological activities and physicochemical characteristics. Two different cytotoxicity assays measuring cell lethality (CS) or inhibition of cell growth (CF) were applicated to confluent cell monolayers or to colony-forming cells, respectively. Cells were exposed to the chemicals at doses ranging from 10(-6) M to 10(-2) M for 24 h. The results indicated a wide range of IC 50 (the concentration resulting in 50% inhibition of toxicity parameters) from as low as 1 microM (Potassium dichromate) to as high as 407.5 mM (Ethanol), the sensitivity of the CF test being greater than that of the CS test. A battery of cytotoxicity tests could be established in order to offer simple, rapid and economic methods which can be complementary and, in part, alternative to the use of laboratory animals.
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PMID:Use of an established cell line in the evaluation of the cytotoxic effects of various chemicals. 180 10

Transcatheter chemo-embolization is an effective treatment for hepatocellular carcinoma, but some patients do not respond sufficiently. We have also percutaneous ethanol injection in patients who failed to respond to chemo-embolization alone, to improve the results of the treatment. Ten patients received the combined therapy; two had failed to retain Lipiodol in the lesions long enough after oily chemo-embolization, 3 had extrahepatic collateral blood supply, 2 had giant hepatocellular carcinomas 10 cm or more in diameter, which were supplied with blood from both the right and left hepatic arteries, 2 also had obstructive jaundice, and one had intraportal tumor thrombus as well. Ethanol was mixed with Lipiodol at 1/10 to 1/5 the volume of ethanol, and injected under ultrasonic or fluoroscopic control. Five to 10 ml of the mixture was injected until the tumors were filled with Lipiodol. It is difficult to discuss the effectiveness of the combined therapy, but it seemed to provide a safer and more effective treatment.
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PMID:[Combined therapy with transcatheter chemo-embolization and percutaneous ethanol injection]. 216 46

Hepatocellular carcinoma (HCC) with portal thrombosis is usually regarded as a contraindication for surgery and for percutaneous alcohol injection (PAI). For palliative purposes we used PAI in 4 patients with infiltrative HCC and segmental portal thrombosis. Ethanol, injected directly into the thrombus, diffused mostly along it. No complications emerged after 20 injections. In the first patient, who later received a liver transplant, the thrombus was completely necrotic. In the other patients, biopsies yielded only necrotic material: in two cases, progression of the thrombus was stopped at 4 and 12 months of follow-up, and in one case the thrombus shrank and remained as such 13 months later. This preliminary experience might broaden the scope of treatment for HCC.
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PMID:Percutaneous alcohol injection of portal thrombosis in hepatocellular carcinoma: a new possible treatment. 216 81

Although sonographically guided percutaneous ethanol injection therapy has been attracting a great deal of attention in the treatment of liver neoplasms, few reports regarding long-term results of this therapy have been published. We report here our 4-year experience, in which ethanol injection was performed 419 times on 108 lesions in 77 patients with hepatocellular carcinoma. Histopathologic examination performed in 14 cases after the therapy revealed that the lesion was completely necrotic in 10 cases, 90% necrotic in three cases, and 70% necrotic in the remaining case. Angiography performed after the therapy showed complete disappearance of tumor stain in 37 of 42 cases treated with ethanol injection. CT after the therapy showed no enhancement of the treated lesion in 55 of 56 cases. Elevated serum levels of alpha-fetoprotein decreased in 21 of 24 cases. Ethanol injection improved the long-term prognosis of the patients. Among the 50 patients in whom there were three or fewer lesions and all lesions were treated by ethanol injection, the 1-, 2-, 3-, and 4-year survival rates were 89%, 74%, 68%, and 60%, respectively. Factors that significantly affected the prognosis were the goal of the treatment, liver function, and size of the largest lesion. Serious complications rarely occurred even in patients with severe liver dysfunction. Percutaneous ethanol injection therapy appears to be valuable for treatment of hepatocellular carcinoma.
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PMID:Percutaneous ethanol injection therapy of hepatocellular carcinoma: analysis of 77 patients. 217 84

We have characterized the growth responses of HTC rat hepatoma sublines after exposure to clinically relevant concentrations of ethanol. These experiments demonstrate growth inhibition by ethanol, and both adaptive and non-adaptive growth responses after chronic exposure. Examination of the cell cycle compartmentation of HTC lines shows that a rapid accumulation of G0/G1 cells is induced by ethanol. Estimates of cellular G1 RNA content by flow cytometry reveal increases in mean G1 RNA and in late G1 cells in the line which growth adapts, and decreases in these parameters in a line which does not adapt to ethanol. Both the growth responses and the timing of cell cycle restriction by ethanol in the adapting line suggest parallels with the reported data for regenerating rat liver. Ethanol induced late G1 restriction appears to be of significant interest in the study of cellular mechanisms which are disturbed by ethanol in proliferating tissues.
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PMID:Ethanol induced growth inhibition and growth adaptation in vitro. Cell cycle delay in late G1. 233 94

For the treatment of small hepatocellular carcinoma, intratumor injection of absolute ethanol under ultrasound guidance was performed in 27 tumors in 23 patients, with a tumor diameter of between 1.0 and 3.3 cm. The initially elevated serum alpha-fetoprotein levels in 15 patients decreased during treatment, with 13 returning to normal after this regimen. In the 6 patients who finally received surgical resection, 4 had complete necrosis of the tumor, while the other 2 had a small peripheral residual cancer nest. In the remaining non-resected 17 cases, follow-up CT, multiple biopsies and angiography revealed evidence of viable tumor in only 3 cases. After additional ethanol injections, these 3 cases were successfully treated. Inhomogeneous distribution of the injected ethanol and difficulty in identifying the tumor after previous injections accounted for the incomplete necrosis of the tumor. To cope with these problems, a steel coil was implanted in the tumor before treatment, and a needle with multiple side holes was used in the last 3 cases, with satisfactory results. Ethanol injection is promising and may even be curative in the treatment of small hepatocellular carcinoma.
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PMID:Intratumor injection of absolute ethanol under ultrasound guidance for the treatment of small hepatocellular carcinoma. 244 15

Although hepatitis B virus (HBV) has been closely associated with the development of hepatocellular carcinoma (HCC), no serologic markers of HBV can be found in up to 11% of HCC patients in developing countries and up to 68% of HCC patients in industrialized countries. Despite the absence of HBV serologic markers in these HCC patients, HBV DNA sequences have been found to be integrated into HCC DNA in 13-100% of these patients, indicating a possible role of HBV in the etiology of their HCC. Although six patients with chronic non-A, non-B hepatitis virus infection who were followed have been documented to develop HCC, it is not known whether the non-A, non-B hepatitis viruses cause or contribute to the development of HCC in some HCC patients without HBV serologic markers. Ethanol, cigarette smoking, oral contraceptives, and aflatoxin also have been suggested as possible etiologies and should be studied further. Suggested etiologies that are not supported by the published data include alpha-1-antitrypsin deficiency and schistosomiasis.
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PMID:Hepatocellular carcinoma: possible etiologies in patients without serologic evidence of hepatitis B virus infection. 253 73

Spontaneous cell-mediated cytotoxicity (SCMC), antibody-dependent cellular cytotoxicity (ADCC) and proliferative lymphocyte stimulation in alcoholic liver disease (ALD) were investigated. Peripheral blood lymphocytes (PBL) from eight patients with advanced ALD and nine normal controls were tested against hepatoma cells (PLC/PRF/5) as targets. Target cells were grown in either normal culture medium or medium supplemented with 1 and 5% ethanol, respectively, for 24 to 48 h. Ethanol-exposed hepatoma cells exhibited profound and characteristic morphological alterations. Ethanol preincubation, however, proved to be without effect on immune reactions. Provided that hepatoma cells are an appropriate model, we assume that the proposed immune reactions in ALD are based on metabolic interactions operative only in vivo but do not parallel morphological alterations of liver cells directly induced by ethanol.
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PMID:Spontaneous and antibody-dependent cellular immune reactions to ethanol-altered hepatoma cells. 303 23

We have studied a short term effect (96 hr) of ethanol on hormone-stimulated DNA synthesis in a primary rat hepatocyte culture system. Studies were also performed with respect to total RNA and protein synthesis as well as albumin secretion measured by a solid-phase radioimmunoassay. We found that ethanol, when added to cultured hepatocytes, resulted in a substantial reduction in hormone-stimulated hepatocyte DNA synthesis and this effect was concentration dependent and occurred in serum-free medium. Ethanol also had an inhibitory effect on total RNA synthesis but protein synthesis and albumin secretion remained essentially unchanged. We determined that hepatocytes exposed to ethanol during the first 24 hr of culture were the most susceptible to inhibition of DNA synthesis. During the first 24 hr, alcohol dehydrogenase (ADH) activity was present in the cells at higher levels than at 48 and 72 hr. In human hepatoma cell lines and differentiated primary and secondary chick fibroblasts, no ADH activity was demonstrable; such cells were not inhibited by 100 mM ethanol additions and DNA synthesis rates were similar to untreated cultures. Other alcohols found to be metabolized by hepatocyte ADH were inhibitory towards hormone-stimulated DNA synthesis whereas those with less metabolism had little effect. Hepatocytes treated with 4-methylpyrazole, an inhibitor of ADH, were partially protected from ethanol effects. Taken together our results are consistent with the hypothesis that a major physiological effect of ethanol on the hepatocyte is a direct impairment of DNA synthesis and that alcohol metabolism is required.
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PMID:Ethanol-induced inhibition of liver cell function: I. Effect of ethanol on hormone stimulated hepatocyte DNA synthesis and the role of ethanol metabolism. 305 77

The conversion of alcoholic hepatitis into cirrhosis and the eventual development of hepatocellular carcinoma (HCC) has been documented by serial biopsies in patients with uncomplicated alcoholism. Ethanol toxicity, nutritional deficiency and immunological abnormalities in a genetically predisposed individual appear to account for this sequence which can be accelerated by the hepatitis B virus and other noxious agents. Immune deficiency in malnourished alcoholics with liver disease diminishes response to the hepatitis B vaccine and may contribute to the development of HCC. Antigenic moieties in Mallory bodies appear to contribute directly to cytotoxicity and fibrosis in alcoholics, and may act like proto-oncogens. Available Mallory-body-specific monoclonal antibodies will hopefully facilitate diagnosis and treatment. Studies of DNA and collagen synthesis by in vitro perfusion of percutaneous liver biopsies provide information on precursor lesions of HCC. Abstinence, nutrient therapy and drug-induced anabolism lead to repair of liver damage and correction of immunological abnormalities, both of which may contribute to development of HCC in alcoholics with cirrhosis.
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PMID:Hepatocellular carcinoma in the alcoholic. 610 Feb 66


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