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)

Antibodies against hepatitis C (HCV) in 512 patients were measured by an enzyme immunoassay (Ortho-HCV ELISA). The frequency of anti-HCV was 80%, 86%, 85% in nonB (NB) chronic hepatitis (CH), cirrhosis (LC), hepatocellular carcinoma (HCC), respectively; 70%, 90% in alcoholic (AL) LC, HCC; 15%, 33%, 58% in hepatitis B (HB) CH, LC, HCC, respectively. Anti-HCV positive cirrhotics had a shorter survival time and earlier development of HCC than anti-HCV negative cirrhotics. The findings suggest that HCV is a major cause of NB chronic liver diseases and may play a pathogenetic role in AL and HB liver diseases.
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PMID:Hepatitis C virus infection in patients with chronic liver diseases. 190 68

The recent discovery of an antigenic component of the causative agent of Non-A, Non-B hepatitis, has led to the characterization of this virus--Hepatitis C Virus (HCV)--and to the identification of an antibody present in infected subjects (anti-HCV) detected by means of the C-100 antigen derived from a nonstructural region of the viral genome. Using a commercial Kit (Ortho Diagnostic Inc.), the incidence of anti-HCV antibody was studied in the Military Hospital "Dr. Carlos Arvelo" of Caracas, Venezuela with the following results: Health personnel (doctors, nurses, laboratory staff): 102 persons studied, 2 positives (1.96%); 16 patients in chronic hemodialysis: 6 positives (33%); 20 subjects with antibodies against HIV virus, confirmed by Western Blot: 7 positives (35.4%). Of 10 patients with Surface Antigen negative Chronic Hepatitis, 7 (70%) positive for anti-HCV, of 25 patients with cirrhosis: 12 positive (48%), 2 patients with hepatocarcinoma 1 positive (50%). There was also a high incidence of total anti-core antibodies in the patients studied. The results suggest that the hepatitis C virus could be playing an important role as a causative factor of liver diseases in our Country.
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PMID:[Antibodies against hepatitis C virus in patients with liver diseases and in risk subjects. Preliminary report]. 196 87

One of the critical issues in risk assessment for chemical carcinogens is the evaluation of dose-response relationships for tumor promoters. In the studies reported here we have systematically investigated dose-response relationships for the liver tumor-promoting actions of 17 alpha-Ethinylestradiol (EE2) following a single injection of diethylnitrosamine (200 mg/kg) to ovariectomized female rats. Parameters measured included tumor incidence, gamma-glutamyltranspeptidase (GGT) positive foci, serum prolactin and serum EE2. The length of tumor promotion ranged from 30 to 60 wk. Results showed a linear increase in GGT-positive foci between doses of 16 and 90 micrograms EE2 kg/d for 30 wk. This was associated with corresponding increases in liver tumor incidence at 60 wk. Seventy-five percent of the animals had either hepatocellular adenoma or hepatocellular carcinoma in the group promoted with 90 micrograms EE2/kg for 60 wk. No liver tumors were evident in either controls or animals receiving estrogen only. Serum prolactin concentrations were elevated in all estrogen-treated groups. In summary, our studies have evaluated dose-response relationships for GGT-positive foci and tumor incidence in a two-stage model for hepatocarcinogenesis using EE2 as the promoting agent.
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PMID:Dose-response relationships in promotion of rat hepatocarcinogenesis by 17 alpha-ethinylestradiol. 196 81

Antibodies against a possible causative agent of non-A, non-B hepatitis, hepatitis C virus (HCV), in Japanese patients with hepatocellular carcinoma were analyzed using the enzyme-linked immunosorbent assay (ELISA) system from Ortho Diagnostic Systems, Japan. Fifty of 58 cases of hepatitis B virus surface antigen (HBsAg)-negative hepatocellular carcinoma were positive for the antibody (86%) and 8 of 42 cases of HBsAg-positive hepatocellular carcinoma were positive (19%). Among patients with HBsAg-negative hepatocellular carcinoma, the prevalence of the antibody was greater among those who had received a blood transfusion (97%) than among those with no history of transfusion (70%). Only 3 of 54 patients with cancers other than hepatocellular carcinoma were found to be antibody-positive (5.6%) and all three patients had a history of blood transfusion. These results show a close relationship between the presence of anti-HCV antibody and HBsAg-negative hepatocellular carcinoma in Japan.
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PMID:Prevalence of antibody against non-A, non-B hepatitis virus in Japanese patients with hepatocellular carcinoma. 216 69

Both estrogens and androgens have been shown to stimulate sex hormone binding globulin (SHBG) secretion in vitro in the hepatocellular carcinoma cell line, Hep G2, in contrast to the expected inhibition by androgens from in vivo studies. However, such in vitro stimulation was only demonstrated at high steroid doses, generally in serum-containing medium, with added Phenol Red. In the present study, Hep G2 cells were grown in serum-free medium, without Phenol Red, under the influence of testosterone (T) (0, 0.5-500 nM) and ethinyl estradiol (EE2) (0, 50 pM-500 nM). Levels of secreted SHBG and albumin were correlated with androgen receptors in cytosolic (ARc) and nuclear (ARn) fractions and with DNA levels. In the presence of increasing T levels, SHBG levels fell to 39% of control values at 5 nM T (P = 0.047), rising to 97% of control at 500 nM. Conversely, incubation with EE2 produced a rise in SHBG secretion of more than 100% at 0.5 nM (P less than 0.02) which was sustained to 50 nM (P less than 0.005). DNA levels did not change with the addition of testosterone or EE2, with the exception of a 15% reduction at 5 nM EE2 (P less than 0.05). Albumin levels in the medium were not significantly altered by either steroid. However, in response to T, androgen receptor (AR) levels were reduced in cytosolic (42% of control) and nuclear (22%) fractions at 5 nM, and these changes in ARc and ARn correlated with SHBG levels over the range of T concentrations (P = 0.04 and P = 0.017, respectively). Nuclear estrogen receptor (ER) increased over 10-fold at 5 and 50 pM EE2 (P less than 0.001) and maintained 50 nM (P less than 0.001). Cytosolic ER was reduced at 0.5 and 5 nM but recovered at 50 nM, correlating with SHBG levels (P less than 0.001). These findings are consistent with the hypothesis that estrogens and androgens regulate SHBG synthesis in man by direct, specific, probably receptor-mediated effects on hepatocytes. Hep G2 cells grown in serum-free medium are a suitable experimental system for further study of this phenomenon.
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PMID:Estrogen and androgen regulation of sex hormone binding globulin secretion by a human liver cell line. 227 57

Unlike the proven causal association between oral contraceptive (OC) use and hepatic cell adenoma, the link between OCs and hepatocellular carcinoma remains speculative. The case history of a 53-year-old US woman suggests, however, that hepatic cell adenomas may transform into hepatocellular carcinoma. The patient, who had used Ovral continuously since 1966, presented in 1985 with vague abdominal pain and a palpable right upper quadrant mass. Computed tomography revealed a 12 x 8 cm mass in the right hepatic lobe and 2 small lesions in the left lobe. Serum alpha-fetoprotein and ferritin levels were normal and tests for hepatitis B were negative. A needle biopsy of the right lobe mass indicated benign hepatic adenoma. OC use was discontinued and the patient was examined at bimonthly intervals. Although she continued to report vague pain, there were no significant changes in radiologic findings or levels of alpha-fetoprotein over the next 18 months. At the 18-month follow-up visit, the alpha-fetoprotein level showed an increase to 227 mcg/L and had risen to 2300 mcg/L by the 30-month follow-up visit. At this time, computed tomography showed slight enlargement of the right lobe mass and inhomogeneity, while biopsy revealed sclerosing hepatocellular carcinoma. This is the 3rd case reported in the literature in which there is evidence of a transformation of hepatic cell adenomas into hepatocellular carcinoma in longterm OC users. Thus, the premalignant potential of hepatic cell carcinomas in OC users should be considered by physicians who follow such cases.
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PMID:Transformation of hepatic cell adenoma to hepatocellular carcinoma due to oral contraceptive use. 253 93

Serum levels of estrogens and testosterone were measured in 25 male patients with hepatocellular carcinoma and associated cirrhosis of the liver and in another 25 male patients with cirrhosis only. The two groups were statistically comparable in terms of age distribution, duration of liver disease, incidence of alcohol abuse, incidence of hepatitis B surface antigenemia, and grade of hepatic dysfunction. Estrone was significantly elevated in both groups of patients. Estradiol concentrations were above normal in 10 patients with hepatocellular carcinoma and in 11 with cirrhosis only. All patients had normal concentrations of estriol. There were no statistical differences between the two groups in either individual or total estrogen levels (estrone 0.05 less than p less than 0.1). Eight of the patients with hepatocellular carcinoma and 5 of the cirrhotics had lower testosterone levels than normal, but this difference was not significant. However, the estrone to testosterone ratios were significantly higher in the hepatocellular carcinoma group than in the cirrhosis group (p less than 0.05). The present study seems to indicate that hyperestrogenemia commonly seen in male patients with liver cirrhosis may play some role in hepatic carcinogenesis of cirrhotic livers. Further studies are needed to determine if the estrone to testosterone ratio is implicated in hepatocarcinogenesis in cirrhotic men.
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PMID:Serum levels of estrogens and testosterone in cirrhotic men with and without hepatocellular carcinoma. 298 53

7 case reports of women with benign hepatic adenoma suggest that, since all of the women were taking oral contraceptives (OCs), there may be an association between ingestion of exogenous hormones and development of benign hepatoma of the liver. The cases were rapidly diagnosed by using hepatic arteriography; prompt, precise diagnosis is emphasized because, though the tumors are benign, they may cause serious, if not fatal, hemorrhage if left unchecked. Case 1 was a 26-year-old woman who had taken Enovid for 2 years, who presented with acute abdomen and impending shock. Coliotomy was performed, in which a left-lobe hepatic tumor was found; she underwent left hepatectomy and cholecystectomy and no evidence of recurrence was found 1 year later. Case 2 had been taking Oracon for a unknown time. Case 3, on OCs for 6 years, had a pedunculated mobile tumor removed. Case 4, 25 years old, had been taking Ovral for 6 months before diagnosis and excision of a right lobe liver tumor. Case 5, 5 years on combined OCs, required surgical intervention for a hypervascular mass. Case 6, taking a total of 8 years of OC therapy, was operated on for an hepatic mass which was a white-to-yellow hemorrhagic mass. Case 7, taking Enovid for 7 years, yielded a surgical specimen that was hemorrhagic, partly necrotic, and yellow-tan, about 10 cm in diameter.
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PMID:Possible association between benign hepatomas and oral contraceptives. 412 57

A 21-year-old woman presented with a 12-month history of epigastric pain, and for 3 months she had noticed a mass in the right hypochondrium. She had taken 'Norinyl-1' (norethisterone 1 mg and mestranol 50 mcg) for 5 years. She smoked 20 cigarettes a day but drank little alcohol. Physical examination revealed irregular hard hepatomegaly 10 cm below the right costal margin. Hepatitis B surface antigen was not detected in the serum and alpha fetoprotein levels were normal ( 10 M.R.C. units). A liver scan showed a large space-occupying lesion in the right lobe of the liver, and liver biopsy revealed a cholangicarcinoma with striking fibrous reaction. Multiple shadows consistent with metastases were present on chest X-ray, but no bony deposits were found on radiological skeletal survey or bone scan. The serum calcium was persistently high (2.74-2.92 mmol/l) but fell on prednisolone therapy. Serum parathyroid hormone levels were normal. A causal relation between oral contraceptives and hepatic adenoma is now generally accepted, and several patients with hepatocellular carcinoma have also been reported. We have been able to find only 1 previous report of cholangiocarcinoma in a young female taking oral contraceptives, and there is 1 report of this tumor in a man taking high doses of anabolic steroids for refractory anemia. This tumor has its peak incidence in the 6th decade and is very rare in the 3rd decade. The association with hypercalcemia due to pseudohyperparathyroidism is well recognized. In only some cases are parathyroid hormone levels raised, and the cause of the pseudohypercalcemia in our patient is unknown.
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PMID:Cholangiocarcinoma and oral contraceptives. 610 61

Estrogen binding protein activities were determined in the cytosol from adult male Buffalo rat liver and Morris hepatoma 7777. Estrogen receptors were prepared using the protamine sulfate precipitation technique of Chamness. The ability of various unlabeled steroids competing with [3H]estradiol was examined to establish the binding specificity. Estradiol binding in Morris hepatoma 7777 cytosol was greatly decreased compared with that present in hepatic cytosol prepared from normal rat liver. The receptor concentration expressed as femtomoles per milligram of cytoplasmic protein was 31.1 +/- 2.9 SD for normal rat liver and 0.41 +/- 0.88 SD for the hepatoma. Gel filtration chromatography revealed the presence of an estrogen binder in hepatoma cytosol which was not present in either normal liver or in the protamine sulfate precipitates of hepatoma cytosol. The molecular weight, binding specificity, and precipitation of this protein by specific antiserum suggests that it is alpha-fetoprotein.
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PMID:Estrogen binding protein activity in Morris hepatoma 7777 compared with normal rat liver. 620 12


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