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)

Serum beta2-microglobulin levels were measured by radioimmunoassay in patients with various malignant neoplasms, ascitic patients, and also patients with definite or suspected hepatoma showing variable levels of serum alpha-fetoprotein. Elevated serum beta2-microglobulin levels greater than 2.5 mg/liter were found in various malignant neoplasms, especially in multiple myeloma (66.6%) and hepatoma (60.4%) The ascites/serum ratio of beta2-microglobulin levels in the patients with malignant ascites is significantly higher than in those with non-malignant ascites. However, ascites/serum ratios of total protein, IgG, albumin, creatinine levels were not significantly different between the two groups. Levels of serum beta2-microglobulin were correlated well with those of alpha-fetoprotein in the patients with definite or suspected hepatoma (r=0.72, P less than 0.001). From these results it was concluded that (1) high levels of serum beta2-microglobulin in these patients could be attributed to its hyperproduction by tumor cells or by the cells which had been infiltrated and activated, (2) it is useful to estimate the ascites/serum ratio of beta2-microglobulin levels in differentiating malignant from non-malignant ascites, and (3) it might suggest that a function of beta2-microglobulin is in some way related to that of alpha-fetoprotein, and the alpha-fetoprotein-synthesizing cells secrete a great deal of beta2-microglobulin, although its function remains unclear.
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PMID:Beta2-microglobulin levels of serum and ascites in malignant diseases. 8 Mar 42

Plasma and 24-hour urinary cyclic AMP and cyclic GMP levels were determined by saturation analysis in specimens from normal subjects and from 101 patients with tumours of the gastrointestinal tract, breast, lung, bladder or prostate, or with cirrhosis of the liver. Relative to 46 control subjects, plasma cyclic GMP concentrations were significantly elevated in seven patients with gastric tumours, 20 patients with cancer of the breast, six patients with lung cancer, and 12 patients with cirrhosis of the liver. Urinary cyclic GMP/creatinine ratios were significantly increased in cirrhotic patients and in the lung and oesophageal cancer groups. In no cancer group were increases in plasma or urine cyclic GMP levels sufficiently consistent to be of value in the diagnosis of human malignant disease. Changes in extracellular fluid cyclic nucleotide levels in the cirrhotic group were very similar to those that have been reported for primary hepatoma patients.
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PMID:Plasma and urine cyclic nucleotide levels in malignant disease and cirrhosis of the liver. 23 Feb 5

The acute form of tyrosinemia type I usually causes severe hepatocellular dysfunction. We report a 4-month-old infant with hepatosplenomegaly, ascites, and multiple intrahepatic mass lesions mimicking hepatoma. A marked increase of serum alpha-fetoprotein (97.6 micrograms/ml) and multiple small low-density lesions in the liver demonstrated by computed tomography suggested the presence of hepatoma. The liver specimens obtained at laparatomy showed mixed nodular cirrhosis with fatty metamorphosis. Serum levels of tyrosine (6.6 mg/100 ml) and methionine (5.9 mg/100 ml) were increased. Urinary organic acid analyses disclosed increased excretions of succinylacetone (1,330 mg/g creatinine) and delta-amino-levulinic acid (113.6 mg/g creatinine). Histological abnormalities and biochemical evidences led to the correct diagnosis. This case emphasizes the need for complete investigations of puzzling cases and warns against undue reliance on noninvasive imaging techniques.
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PMID:An acute form of tyrosinemia type I with multiple intrahepatic mass lesions. 169 41

Subacute doses (1/20 LD50) of aflatoxin B1 and ochratoxin A were fed to weanling albino rats individually and in combination for 36 weeks and then rats were maintained on toxin free normal diet for a period of 24 weeks. Livers of rats were fatty, wherever aflatoxin was administered but the enzyme activity did not show significant differences among various groups. However, in a few individuals whose livers were severely affected, higher concentrations of urine creatinine, liver RNA and DNA, and ALT enzyme activity were recorded. Histopathological examination showed various stages of hepatoma and hepatocarcinoma including nodular hyperplasia, hypertrophy, vacuolisation, degeneration, pseudolobulation, cellular infiltration and fibrosis of liver of rats fed with aflatoxin individually and in combination. Few anaplastic cells in the corticomedullary region and nuclear enlargement of proximal tubular epithelium of kidney were found wherever combined toxin and ochratoxin alone were administered. Liver tumor expression was time dependent.
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PMID:Effect of long term feeding and withdrawal of aflatoxin B1 and ochratoxin A on kidney cell transformation in albino rats. 179 62

A multi-institutional prospective study for the analysis of prognostic factors for patients with osseous metastasis was performed. From February 1986 through June 1988, a total of 216 patients were included in this study. Cox's regression model made it clear that the most significant overall prognostic factor was primary site (p = 0.0002). In the lung cancer group, performance status (p = 0.0036) and metastasis of organs than bone (p = 0.0105) were also significant prognostic factors. In the breast cancer group, no significant factors were obtained. In the hepatoma group, the values for alkaline phosphatase (ALP) (p = 0.0021), lactate dehydrogenase (LDH) (p = 0.0195), and sex (p = 0.0264) proved significant. In the group of other cases, the most significant prognostic factor was the value for urinary hydroxyproline/creatinine ratio (p = 0.0001), followed by the pain score of RTOG (p = 0.0018). These factors and actual survival periods obtained in this study will be useful for the future stratification of patients for individualized optimal radiation schedules.
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PMID:Prognostic factors for patients with osseous metastasis: a multi-institutional prospective study. 219 3

Experience with high-dose cytosine arabinoside (HDAC) in pediatric solid tumors is limited. Sixteen children with solid tumors resistant to conventional therapies were registered in a pilot Pediatric Oncology Group (POG) study that required the administration of HDAC at 3 g/m2 every 12 hours for four doses. There were four cases of rhabdomyosarcoma, two cases of fibrosarcoma, four cases of neuroblastoma, and one case each of germ cell tumor, Wilm's tumor, retinoblastoma, hepatocellular carcinoma, Ewing's sarcoma, and Burkitt's lymphoma. All eligible patients had advanced diseases and had previously received extensive chemotherapy. Thirteen patients received one course of HDAC and three patients received two courses of HDAC. Due to prior treatments, patients had less than normal marrow reserves. Short-term toxicity included nausea, vomiting, suppression of hemopoiesis, drug fever, and increased blood urea nitrogen (BUN), creatinine, and liver enzymes. All evaluable patients recovered from their toxicities. There were no drug-related deaths. None of the patients had neurologic problems, including the only patient with prior irradiation to the skull. With the above schedule, HDAC appears to have manageable toxicity.
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PMID:Toxicity of high-dose cytosine arabinoside in the treatment of advanced childhood tumors resistant to conventional therapy. A Pediatric Oncology Group study. 222 60

Three patients with hereditary tyrosinemia type 1, two brothers and one girl, studied at the age of 5, 12 and 15 years, respectively, had neither generalized hyperaminoaciduria, glucosuria nor clinical symptoms of rickets. Untreated the elder brother had only slightly elevated plasma tyrosine level (141 mumol/l, normal less than 80), and low excretion of p-hydroxyphenyllactate. He presented with pronounced thrombocytopenia (3 X 10(9)/l). At 13 years of age he contracted hepatocellular carcinoma. The younger brother presented with serum tyrosine of 318 mumol/l and thrombocyte count 48 X 10(9)/l. Succinylacetone in urine was elevated in both, 30 and 79 mumol/mmol creatinine, respectively. The female patient was investigated for hepatomegaly in infancy, atypical tyrosinemia being considered, but afterwards developed normally without diet or any other treatment until she contracted hepatoma at the age of 15 years. Her plasma tyrosine level was 600-700 mumol/l, and she excreted large amounts of p-hydroxyphenyllactate. Succinylacetone in urine was low but elevated (8 mumol/mmol creatinine). The fumarylacetoacetase activity in fibroblasts from the brothers and in lymphocytes from the girl was less than 5% and 10% of control levels, respectively. In conclusion, the chronic form of hereditary tyrosinemia may occur without evidence of renal tubular dysfunction.
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PMID:Hereditary tyrosinemia of chronic course without rickets and renal tubular dysfunction. 226 24

A radioimmunoassay for transforming growth factor alpha (TGF-alpha) using synthetic rat sarcoma transforming growth factor and its rabbit polyclonal antibody has been developed. Using radioimmunoassays, the urinary TGF-alpha and epidermal growth factor (EGF) concentrations in 31 patients with hepatocellular carcinoma (HCC), 15 probable HCC, four metastatic liver cancer, and 33 age, sex-matched healthy controls were determined. For the first time, we have shown that the average TGF-alpha concentration for HCC patients was 21.5 +/- 20.3 micrograms per g creatinine, significantly higher than that of healthy subjects, 4.9 +/- 2.8 micrograms per g creatinine (P less than 0.001). There was no statistical difference in the level of EGF between HCC patients and controls (40.9 +/- 29.3 versus 46.2 +/- 16.6 micrograms per g creatinine; P greater than 0.05). The ratio of EGF/TGF-alpha between HCC patients (3.37 +/- 4.42) and controls (15.5 +/- 13.0) was significantly different (P less than 0.001). Among patients, 65% (20 of 31) of HCC cases and 87% (13 of 15) of probable HCC cases showed a marked elevation of TGF-alpha levels. We found only 16% (five of 31) of HCC cases with increased EGF level. EGF excretion was inversely age related. Serum total protein concentration and alkaline phosphatase activity were positively correlated to EGF concentration (r = 0.522, P less than 0.01 and rt = 0.393, P less than 0.05, respectively). There was no correlation between biochemical functions of liver and TGF-alpha concentration in HCC patients. Our results also suggested that TGF-alpha may be a useful complementary tumor marker for management of patients with clinical manifestation of HCC who have low alpha-fetoprotein levels.
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PMID:Elevation of transforming growth factor alpha and its relationship to the epidermal growth factor and alpha-fetoprotein levels in patients with hepatocellular carcinoma. 243 30

The urinary level of pseudouridine, primarily a degradation product of transfer ribonucleic acid (tRNA), was determined in 38 patients with primary hepatocellular carcinoma, 18 with liver cirrhosis, 12 with chronic hepatitis, nine with acute hepatitis, and 28 healthy subjects. The mean urinary pseudouridine concentration was significantly higher in the patients with hepatoma [38.2 +/- 12.8 (SD) nmol/mumol creatinine] than in those with liver cirrhosis (20.3 +/- 6.8), chronic hepatitis (24.4 +/- 8.2), and acute hepatitis (21.7 +/- 8.2), and in healthy subjects (23.8 +/- 4.9). Urinary pseudouridine level was elevated above the mean value plus 2 SD for the healthy subjects (33.6 nmol/mumol creatinine) in 71% of our hepatoma cases. Serum alpha-fetoprotein levels correlated poorly with urinary pseudouridine levels, thus, the combination assay for urinary pseudouridine and serum alpha-fetoprotein could detect 79% of the patients with hepatoma. Moreover, urinary pseudouridine level was reduced after effective transcatheter arterial embolization therapy.
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PMID:Urinary pseudouridine as a biochemical marker in the diagnosis and monitoring of primary hepatocellular carcinoma. 245 10

Ten patients with hepatocellular carcinoma, three of whom had pulmonary metastasis, were treated with adoptive immunotherapy using autologous lymphokine-activated killer cells plus recombinant interleukin 2. Patients received 15 micrograms per day of recombinant interleukin 2 consecutively (for 14 to 64 days), from Day 7 prior to the first leukapheresis, and received 10(9) to 10(10) lymphokine-activated killer cells once or twice per week intravenously; the lymphokine-activated killer cells had been generated from mononuclear cells obtained through leukapheresis. Preadministration of recombinant interleukin 2 prior to the first leukapheresis resulted in a remarkable increase of lymphokine-activated killer activity in seven of nine cases in whom lymphokine-activated killer activity had been poorly inducible even at high concentrations of recombinant interleukin 2. At the end of the treatment, liver tumor regression (34 and 63%, respectively, of two-dimensional size) was observed in two of two patients with a solitary tumor; no increase of liver tumor size was observed in seven patients with massive or multiple tumors, and no changes in the size or number of pulmonary metastatic tumors in any patients were observed. More than a 35% decrease in serum alpha-fetoprotein level was noted in four of nine alpha-fetoprotein-positive patients. However, Child's grades, performance status and lymphokine-activated killer activity on entry into the study could not be used as parameters to predict therapy responsiveness. Neither serious side effects nor significant changes of serum bilirubin, ALT and creatinine were noted. Thus, this treatment seems to be well tolerated even in advanced hepatocellular carcinoma with poor liver function reserve, and tumor regression could be expected in small-burden hepatocellular carcinoma. The assessment of the therapeutic effects and application in hepatocellular carcinoma awaits the development of this trial.
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PMID:Adoptive immunotherapy with lymphokine-activated killer cells plus recombinant interleukin 2 in patients with unresectable hepatocellular carcinoma. 247 81


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