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)

Although alcohol is known to enhance hepatocarcinogenesis, the mechanism of this action remains to be explained. To test the hypothesis that ethanol depletes the liver of antitumor promoters such as retinoid, we measured the retinoid concentration in hepatocellular carcinoma tissues and noncancerous surrounding liver tissues in humans known to have a history of alcohol consumption. By high-performance liquid chromatography, the retinoid contents of 29 surgically resected hepatocellular carcinoma specimens and their noncancerous surrounding tissues were measured. Retinoid contents were decreased in both the cancerous and the surrounding noncancerous liver tissues of patients with a high intake of alcohol. The levels correlated inversely with the estimated cumulative lifetime ethanol consumption. The decrease in the retinoid content of hepatic parenchymal cells paralleled that in stellate cells. When compared with the surrounding liver tissues, the cancerous liver tissues were in the state of retinoid deficiency. In summary, alcohol abuse may help promote the hepatocarcinogenesis in man by depleting the liver of the antitumor promoter, retinoid.
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PMID:Reduced retinoid content in hepatocellular carcinoma with special reference to alcohol consumption. 165 53

Ethanol alters many metabolic processes within the liver. Both ethanol abuse and the inability to mount an acute phase response (APR) have been associated with an increased morbidity and mortality in critically ill patients. To determine if ethanol influences the hepatic APR, relative amounts of two different human acute phase protein mRNA's were examined in the human hepatoma cell line Hep 3B before and after exposure to ethanol. Hep 3B cells were treated with one or more of the following: ethanol ((E) 150 mM); interleukin-1 beta ((IL-1) 200 units/ml); or interleukin-6 ((IL-6) 50 units/ml). After a 12-20 hr incubation relative amounts of mRNA for a1-protease inhibitor (PI) or beta fibrinogen were determined by Northern blot hybridization. Both ethanol and IL-6 were found to induce a1-PI mRNA. Fibrinogen mRNA was induced by IL-6 but not by ethanol, and no induction of PI or fibrinogen mRNA was found with IL-1. This suggests that under certain conditions, ethanol may influence acute phase protein metabolism. To our knowledge, this is the first description of an ethanol induced alteration of acute phase protein mRNA.
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PMID:Ethanol induces a1-protease inhibitor mRNA in Hep 3B cells. 165 92

Percutaneous ethanol injection (PEI) under ultrasound guidance is a new therapeutic possibility for patients with small hepatocellular carcinoma (HCC). In our series, 51 patients with a total of 72 lesions were treated (tumor size 0.8-5.0 cm). No significant complications occurred after 745 treatments. Forty patients presented complete remission, as no evidence of residual HCC was revealed during the follow-up (mean 18 months). Ten patients with lesions larger than 3.5 cm and one with lesion less than 3 cm presented partial remission (80-90% of necrosis). The cumulative survival rates at 1, 2 and 3 years (Kaplan-Meier method) were 100%, 89% and 58%. The survival rates for patients carrier of single lesion were 100%, 94% and 71% respectively. In comparison with the survival curves of untreated and surgically treated patients, PEI seems to be the better treatment for operable HCC smaller than 3 cm, and for lesions smaller than 5 cm in patients with surgical risk.
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PMID:[Percutaneous alcoholization of the small hepatocarcinoma]. 165 73

Hepatoma cells in culture synthesized fatty acid ethyl esters when exposed to ethanol at concentrations known to occur in man. Unesterified fatty acids, potentially dangerous to cells, were produced by hydrolysis, and there was significant conversion to cholesterol esters.
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PMID:Synthesis and metabolism of fatty acid esters in cultured hepatoma cells exposed to ethanol. 165 78

We conducted interviews on 74 patients with histologically confirmed hepatocellular carcinoma. These patients, aged 18-74 years, were black or white residents of Los Angeles County. We also interviewed 162 population control subjects who were comparable to the case patients by age, sex, and race. Cigarette smoking was a significant risk factor for hepatocellular carcinoma [relative risk (RR) = 2.1; 95% confidence limits (CL) = 1.1, 4.0]; the effects were similar in men and in women. Heavy alcohol consumption was another risk factor for hepatocellular carcinoma in men; men who consumed 80 g or more of ethanol per day had an RR of 4.7 (95% CL = 1.4, 15.4) relative to those who had never drunk alcohol on a weekly basis. The level of alcohol intake was relatively low in women, and no significant effect on risk of hepatocellular carcinoma was observed. Use of oral contraceptives was significantly related to risk of hepatocellular carcinoma in women (RR = 3.0; 95% CL = 1.0, 8.8); those who were exposed for more than 5 years exhibited a 5.5-fold increased risk (95% CL = 1.2, 24.8). The effects of these three risk factors on hepatocellular carcinoma development were independent of each other and independent of serologically determined viral hepatitis. Our data suggest that cigarette smoking, alcohol consumption, and use of oral contraceptives are major risk factors for hepatocellular carcinoma among non-Asian residents of Los Angeles County. We also observed a significant association between a history of diabetes and hepatocellular carcinoma (RR = 3.3; 95% CL = 1.5, 7.2), especially among those who had received insulin treatment (RR = 18.5; 95% CL = 2.2, 156.0). This association may have etiological significance.
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PMID:Nonviral risk factors for hepatocellular carcinoma in a low-risk population, the non-Asians of Los Angeles County, California. 166 May 42

The serum activity of alcohol dehydrogenase was determined in healthy controls and in patients with liver diseases. The mean activity in hepatoma (6.4 +/- 1.0U/L) was significantly higher (P less than 0.05) than the mean values in liver cirrhosis (2.7 +/- 0.5U/L); hepatitis (4.3 +/- 1.0U/L), obstructive jaundice (2.9 +/- 0.5U/L) and healthy controls (0.7 +/- 0.1U/L). Alcohol dehydrogenase purified by CM-cellulose chromatography from the sera of patients with hepatoma had a higher affinity for butanol long chain saturated and unsaturated alcohols than the purified enzyme from healthy controls. Similarly, hepatoma alcohol dehydrogenase oxidized ethanol very poorly (KM = 154 microM) when compared with that from healthy controls (KM = 40.2 microM). Hepatoma alcohol dehydrogenase was inhibited by pyrazole while those of other liver diseases and the healthy controls were not. These properties of serum alcohol dehydrogenase may prove useful in the early diagnosis of hepatoma since biochemical changes occur before morphological changes in the development of cancer.
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PMID:Properties of serum alcohol dehydrogenase in Nigerians with primary hepatoma. 166 17

We examined the effect of alcohol ingestion on hepatocarcinogenesis induced by oral administration of synthetic female hormones, 0.075 mg of ethynylestradiol (EE) and 6.0 mg of norethindrone acetate (NA), every day for 12 months in female Wistar rats. Administration of 10% ethanol in drinking water for 5 days a week every week resulted in the development of hepatocellular carcinoma (HCC) in 38.4% of the hormone-treated rats at 12 months, which is approximately 5 times the incidence of HCC observed following EE and NA treatment alone. The number of hyperplastic nodules was significantly higher than the number observed in the case of EE and NA treatment alone after 4 months of the experimental period. The additional alcohol treatment also increased the value of unoccupied nuclear estrogen receptors (ERn) at months 6 and 8 of the experimental period, and increased the value of total ERn in the rat liver after 6 months of the experimental period. This indicates that additional alcohol treatment may increase occupied ERn (estrogen-ER complex) in the rat liver. A 32P-postlabeling analysis of liver DNA revealed that the maximum number of extra spots consisting of modified nucleotides induced by EE and NA appeared earlier when the additional alcohol treatment was imposed. Consequently, alcohol affects the hepatocarcinogenesis by EE and NA, promoting not only the change in kinetics of ER, but also DNA adduct formation induced by EE and NA in the rat liver.
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PMID:Effect of alcohol ingestion on carcinogenesis by synthetic estrogen and progestin in the rat liver. 167 55

The therapeutic effect of hepatocellular carcinoma (HCC) was assessed by the serial change of serum AFP value before and after treatment. Subjects were 56 therapies for HCCs in 48 cases, who were diagnosed as inoperative HCCs, and were performed chemotherapy, transcatheter hepatic arterial embolization (TAE) and percutaneous ethanol injection therapy (PEIT). As the indicator of therapeutic effect, the angle (supplement) alpha was used, that was formed by the cross of two lines based on several points of serum AFP value on the hemilogarithm graph before and after treatment respectively. The alpha were distributed from -34 degrees to 118 degrees, and its mean value was 32 +/- 38 degrees (+/-SD). The angle alpha value of cases evaluated as CR or PR was high, and that of PD was low. We could quantitatively assess the effects evaluated as NC by tumor size. The survival curve of group with high alpha value was significantly longer than that of group with low value. It was concluded that this method using angle alpha based on the serial change of serum AFP value was useful for clinical assessment of HCCs treatment.
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PMID:[An assessment of therapeutic effect of hepatocellular carcinoma by the serial changes in serum AFP value]. 169

The authors report a case of repeated brain metastases from hepatocellular carcinoma (HCC) in a 70-year-old male, who had underwent liver segmentectomy for HCC 5 years earlier. He developed intracerebral hemorrhage in the right parietal region, which was considered to be intratumoral because the metastatic tumor was detected in the same region. Total removal of the tumor and hepatic artery embolization followed by ethanol injection for recurrent HCC were performed. One month later, a metastatic tumor was discovered in the upper vermis and was totally removed. Both metastatic brain tumors were histologically verified as Edmondson grade 2 HCC. Four months later, multiple metastases to the left frontal region and the upper vermis occurred, and he died of pneumonia. Brain metastasis from HCC is rare; nine such cases have been reported in the literature, of which eight cases developed intracranial hemorrhage as in the present case.
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PMID:Intracranial hemorrhage due to brain metastasis from hepatocellular carcinoma--case report. 170 53

Fifty-seven magnetic resonance (MR) imaging examinations were obtained at 0.5 T in 19 patients before and after percutaneous ethanol injection (PEI) for 23 hepatocellular carcinoma (HCC) lesions less than 3.5 cm in diameter. Seventeen patients also underwent MR imaging 6 months after completion of therapy. In 11 patients, computed tomography was performed before and after treatment. After PEI, fine-needle biopsy specimens were obtained in all cases. Before treatment, HCC lesions had low signal intensity on T1-weighted images in 13 cases, had the same signal intensity as normal liver parenchyma in six, and had high signal intensity in four; all 23 tumors had high signal intensity on T2-weighted images. After treatment and at 6-month follow-up, all 21 lesions that contained no malignant cells at fine-needle biopsy had high signal intensity on T1-weighted images and had low signal intensity on T2-weighted images. The remaining two HCC lesions in which tumor necrosis was not achieved with PEI displayed a different MR pattern, since the residual neoplastic tissue showed no change in signal intensity on either T1- or T2-weighted images. The authors conclude that MR imaging may be useful for evaluating the effectiveness of PEI in achieving tumor regression.
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PMID:Small hepatocellular carcinoma treated with percutaneous ethanol injection: MR imaging findings. 171 99


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