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)

Radioimmunoassays specific for fructose-1, 6-diphosphate aldolase isozymes were developed for the quantification of human aldolase A, B and C. The method is a double-antibody radioimmunoassay using radioiodinated purified aldolase A, B and C as ligand, chicken antibodies to aldolase A, B and C, and rabbit antibodies to chicken IgG. The Iodogen method was used for the iodination of aldolase A, B and C in this study. Aldolase A was predominantly high in concentration in muscle, aldolase B was high in normal adult liver, and aldolase C was high in adult brain. Aldolase A was elevated in hepatoma tissue and hepatoma cell lines, where aldolase B was distinctly low. Normal serum levels for the three isozymes were determined. The aldolase A levels in serum obtained from 41 normal subjects were 170 +/- 39 ng/ml. Serum aldolase A levels were increased in many patients with cancer and muscle diseases, but were not increased in patients with hepatitis or other benign diseases. Serum aldolase B levels obtained from 11 normal subjects were 28.5 +/- 9.2 ng/ml. Serum aldolase B levels were increased in patients with hepatitis and correlated well with serum GPT levels. Serum aldolase C levels obtained from 12 normal subjects were 2.4 +/- 0.7 ng/ml. The determination of aldolase A, B and C by radioimmunoassay may be a valuable tool in biochemical and clinical studies of aldolase isozymes.
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PMID:Subunit-specific radioimmunoassay for aldolase A, B, and C subunits: clinical significance. 632 58

Isoelectric focusing and studies with 1-(2'-deoxy-beta-D-glucopyranosyl)thymine (GPT), a specific inhibitor of uridine phosphorylase activity, were used to determine the substrate specificities of mammalian pyrimidine nucleoside phosphorylases and their cleavage of 5-fluoro-2'-deoxyuridine (FdUrd). Isoelectric focusing profiles for the cytosol fractions from Ehrlich ascites cells and from Novikoff hepatoma cells each consisted essentially of one peak of nucleoside phosphorylase activity [isoelectric points (pl) 5.4 and 5.8, respectively] that cleaved both uridine and thymidine (dThd), as well as FdUrd. By contrast, cytosol fractions from HeLa (S3) cells, mouse liver, and normal human leukocytes each exhibited a major peak of activity (pl 4.6, 6.5, and 4.9, respectively) that cleaved only dThd and FdUrd, while mouse liver exhibited a second peak (pl 5.2) that cleaved primarily uridine. To distinguish clearly between (a) uridine phosphorylases that cleave primarily uridine and that are inhibited by GPT and (b)dThd phosphorylases that cleave only deoxynucleosides and that are not inhibited by GPT, we propose the term "uridine-deoxyuridine phosphorylases" to define those pyrimidine nucleoside phosphorylases that cleave both uridine and dThd and that are inhibited by GPT. On the basis of this definition and studies with GPT in nonfocused cytosol preparations, we conclude that FdUrd is cleaved to 5-fluorouracil by uridine-deoxyuridine phosphorylase activity in Ehrlich ascites cells and in Novikoff hepatoma cells, and by dThd phosphorylases in mouse liver, in normal human leukocytes, and in HeLa (S3) cells.
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PMID:Specificity of pyrimidine nucleoside phosphorylases and the phosphorolysis of 5-fluoro-2'-deoxyuridine. 645 Dec 86

In order to confirm the close association between chronic hepatitis B virus (HBV) infection and primary hepatocellular carcinoma (PHC) in Japan, 8,646 male hepatitis B surface antigen (HBs Ag)-positive blood donors (GPT less than or equal to 35 Karmen units) were followed up. Twenty liver cancer cases were observed during the follow-up period (average 6.2 years), the expected number calculated on the basis of age-specific incidence rates among the general population being 3.03. Therefore, the observed to expected ratio of liver cancer was 6.60, that is significantly higher than 1.0. During the same follow-up period, a total of 76 deaths were observed, of which 20 were due to liver cancers and 9 to liver cirrhoses, meaning that nearly 40% of deaths among the study subjects due to chronic liver diseases. Drinking and smoking habits in the liver cancer cases were compared with those observed in healthy male HBV carriers. A strong positive association between drinking habits and liver cancer was observed and there was a significant dose-response relationship after adjustment for cigarette smoking habits. A high risk of liver cancer was also observed among heavy smokers, but a significant dose-response relationship could not be found between smoking habits and liver cancer, partly because of the limited number of the study subjects. These findings suggest that HBV is a major etiologic agent of PHC in Japan where the HBs Ag prevalence rate is about 2%, and alcohol drinking and cigarette smoking may promote the process of HB viral hepato-carcinogenesis.
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PMID:Follow-up study of HBs Ag-positive blood donors with special reference to effect of drinking and smoking on development of liver cancer. 651 Nov 24

1. The expression of soluble GPT (E.C. 2. 6. 1. 2) was analysed in seventeen independent rat hepatoma/human somatic cell hybrids and in forty-one subclones derived from two of these hybrids. 2. As judged by electrophoretic mobility, twelve hybrid clones expressed rat GPT activity only and three expressed strong rat and weak human GPT activity but no heteromeric isozymes. In the remaining two hybrids, only human GPT was demonstrable. 3. The segregation of GPT and marker enzymes in the primary hybrid cells and the subclones suggests that the human structural GPT locus is on chromosome 8. 4. The re-expression of rat GPT in segregating subclones derived from two primary hybrids which had extinguished this function, could not be correlated with presence or absence of any particular human chromosome(s).
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PMID:Regulation of expression of liver-specific enzymes. II. Activation and chromosomal localization of soluble glutamate-pyruvate transaminase. 711 91

Lipiodolization--selective regional cancer chemotherapy using Lipiodol plus an anticancer drug (LPD)--can prolong survival time of patients with an unresectable hepatocellular carcinoma (HCC). To enhance understanding of LPD's influence on the cirrhotic liver, we carried out related studies. Forty-three cirrhotic patients with HCC were treated with LPD (epirubicin in a dose of 15-40 mg/m2 and Lipiodol of 0.02-0.25 ml/kg). Seven cirrhotic patients with HCC were subjected to hepatic angiography alone, and these subjects selected randomly served as controls. Among the 43 treated with LPD, 23 belonged to Child's class A, 15 to class B, and 5 to class C. Blood samples were taken before angiography (pre) and at 24 hours after angiography (post) from each patient. Post/pre ratio of the following parameters were compared between patients of the two groups: sGOT, sGPT, and LDH as a marker for hepatocyte injury; t. bilirubin and hepaplastin test (HPT) as hepatocyte function; alkaline phosphatase and gamma-GTP to examine bile duct injury; and serum hyaluronic acid level to determine an endothelial cell functions. Post/pre ratio of serum GOT, GPT, LDH levels, and HPT in patients treated with vs. without LPD were 1.32 +/- 0.59 vs. 0.92 +/- 0.09 (P < 0.001), 1.18 +/- 0.43 vs. 0.88 +/- 0.09 (P < 0.001), 1.11 +/- 0.20 vs. 1.00 +/- 0.07 (P < 0.05), and 0.95 +/- 0.10 vs. 1.09 +/- 0.12 (P < 0.01), respectively. There were no significant differences in post/pre LPD ratio of other parameters, rates of complications, and hospital stay after LPD for patients with Child's class A, B, and C. Hepatocytes are apparently the primary site of injury in cases of LPD. LPDs, using epirubicin in a dose of 15-40 mg/m2 and Lipiodol in a dose of 0.02-0.25 ml/kg, proved to be safe for cirrhotic patients with HCC.
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PMID:Influence of lipiodolization on a cirrhotic liver. 772 71

Family history of hepatocellular carcinoma (HCC) has been identified as a risk factor of HCC. The pathogenesis is still uncertain. In order to evaluate the risk factors and to detect the small HCC. 721 asymptomatic family members (419 males and 302 females with a mean age of 40.21 years) of the index cases of HCC received a series of examinations including: serum GOT, GPT, alpha-fetoprotein (AFP). HBsAg, Anti-HCV, and abdominal ultrasonography (US). Of the 18 patients with liver tumor detected by US. 6 were proved to be HCC, 8 were hemangioma, and the nature of the rest was undetermined. The US found 22 with cirrhosis, 24 with chronic liver disease, 133 with fatty liver, and 14 with a liver cyst. The incidence of HCC in our study was 0.96% in males (4 of 419 cases), and 0.66% in females (2 of 302 cases) which was much higher than that in the general population of Taiwan (0.025% in males and 0.01% in females). The positive rate of HBsAg in the participants, including all the newly detected HCC patients, was 46.5% (335 cases) which was also higher than the prevalence in Taiwan (15-20%). Male, sibling and liver cirrhosis seemed to have higher risk. These results suggest that family members of patients with HCC have a high risk of developing HCC. The hepatitis B virus may be the most important link. Early diagnosis is possible by screening the family members by means of AFP and abdominal US.
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PMID:Risk factors of hepatocellular carcinoma with familial tendency. 776 61

Hepatectomy was performed under in situ right lobar hypothermic perfusion combined with hepatoprotective agents in six patients who had hepatocellular carcinoma and coexisting liver disease. Following occlusion of the right hepatic vein and the right portal pedicle, in situ cold perfusion was initiated using chilled Ringer's lactate infused through a cannula placed in the right main portal vein. The right superior segments were resected in a bloodless field. The liver was cooled to 22-26 degrees C for 40 to 80 minutes with no significant changes in systemic hemodynamics or body temperature. Postoperative liver functions showed no marked derangement; the mean peak GPT was 221 U and the mean peak total bilirubin 2.3 mg d/l. Local cooling minimizes the risk of ischemia/reperfusion injury in this very vulnerable population, yet gives the surgeon adequate time to perform a challenging resection in a bloodless field.
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PMID:Hepatic resection under in situ hemihepatic hypothermic perfusion with hepatoprotective agents. 778 26

Clinically, acute hepatitis C is an asymptomatic disease in up to 90% of cases. Transaminases fluctuate characteristically. Anti-HCV (RIBA-II) and HCV-RNA (PCR) are diagnostic early in the course of the disease. The risk of chronification is high, exceeding 50% of cases, irrespective of disease transmission (parenterally or sporadic). Alpha-interferon is applicated in pilot-studies to reduce the risk of chronification, with varying results. Chronic hepatitis C is an insidious disease. Again, most cases are asymptomatic. Bilirubin is normal. GPT-activity tends to fluctuate during the course. Anti-HCV and HCV-RNA can be detected in serum. About 20% of cases progress to cirrhosis (and HCC) after a long-lasting disease (20 to 30 years after infection). Alpha-Interferon therapy is successful in about 25% of patients.
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PMID:[Hepatitis C: clinical aspects, course and therapy]. 793 55

Epirubicin (EPIR), an anticancer agent, has recently been used with increasing frequency in transcatheter oily chemoembolization (TOCE) of hepatocellular carcinoma. We conducted a dose-finding study of EPIR with regard to its safety. One hundred thirty-four patients were divided into five groups according to the EPIR doses (mg/m2), Group A (< 30 mg/m2), Group B (> or = 30 - < 40 mg/m2), Group C (> or = 40 - < 50 mg/m2), Group D (> or = 50 - < 60 mg/m2), and Group E (> or = 60 mg/m2). The number of leukocytes decreased at 2 weeks but recovered at 4 weeks with no significant differences among the groups. However, there were significantly fewer leukocytes in Group E than in Groups A to D. There were no significant differences among the groups in either the number of erythrocytes or platelets. The number of platelets tended to remain at increased levels even at 4 weeks. Liver function as represented by GOT, GPT, LDH, and total bilirubin was not aggravated, but tended to improve. GOT and LDH in Groups D and E, in particular, improved significantly at 4 weeks, probably because of the antitumor effect of TOCE. These results suggest that EPIR can be administered up to 50 mg/m2 for TOCE.
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PMID:[Doses of epirubicin used in oily chemoembolization of hepatocellular carcinoma]. 794 44

We studied the alteration of aldolase isozymes in the serum and tissues of patients with cancer and other diseases using radioimmunoassays specific for aldolase A, B, and C subunits. Aldolase B was predominantly found in adult liver, where aldolase A and C were distinctly low. Aldolase A and B showed almost the same concentration in fetal liver, while in neonatal liver aldolase B protein concentrations were much higher than aldolase A. In contrast, aldolase A was the predominant isozyme found in hepatoma and gastric cancer tissues, whereas aldolase B was distinctly low in hepatoma tissues, and extremely low in gastric cancer tissues. These results suggest that the aldolase A is a more fetal type of liver isozyme than the aldolase B and C, and aldolase B is a more differentiated type of liver isozyme than aldolase A and C. Serum FDP aldolase activities were elevated in half of patients with liver diseases, all patients with muscle diseases and a few patients with cancer. Serum aldolase A levels were elevated in patients with muscle diseases and cancer, but not elevated in patients with liver diseases. In contrast, serum aldolase B levels were elevated in patients with liver disease, but not elevated in patients with muscle diseases and other diseases without liver injury. Serum aldolase B levels showed a trend to decrease in cancer patients with normal GPT levels. Serum aldolase A/B ratios were significantly increased in cancer patients with normal GPT levels, whereas they showed the decreased levels in patients with liver diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alteration of aldolase isozymes in serum and tissues of patients with cancer and other diseases. 804 42


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