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 Stilbestrol treatment of the female rats with the Morris hepatoma 5123 D resulted in decrease of the gamma-glutamyl-transpeptidase (GGTP) activity in serum and in hepatoma, but only during the treatment. Given to the male rats under the same conditions, Stilbestrol had no influence on the GGTP activity. Castration of males was the cause of the GGTP activity decay in hepatoma and in serum, but it was not the case with females. Sustanon diminished the GGTP activity in serum of the female rats with hepatoma.
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PMID:Influence of sex hormones on gamma-glutamyltranspeptidase activity in rats serum with Morris hepatoma 5123 D. 4 20

The activity of estrogen 16alpha-hydroxylase was measured for nine Morris hepatomas of different growth rates and host livers. Activity was measured in the microsomal fraction of the cell (100,000 X g). In the spectrum of hepatomas studied, 16alpha-hydroxylase activity was significantly decreased in parallel with the increase in hepatoma growth rate. The decrease in enzymic activity ranged from 16 to 19% for the slow-growing tumors (Hepatomas 44, 28A, and 9633), 2 to 9% for the intermediate-growing tumors (Hepatomas 38B, 7795, and 5123A), and 0% for the fast-growing tumors (Hepatomas 7288C, 7777, and 42A). Estrogen 16alpha-hydroxylase activity of the liver of tumor-bearing rats differed from that of liver of healthy animals. There was a decrease in enzymic activity ranging from 66% to 90% of normal control rats. The activity level of the host liver did not correlate with tumor growth rate. Stimulation of 16alpha-hydroxylase with phenobarbital showed a 4-fold increase in activity in normal liver and only a 2- to 3-fold increase in host livers. The slow- and intermediate-growing hepatomas showed a 1.2-to 1.4-fold increase in enzyme activity, and no activity or stimulation in the fast-growing hepatomas was observed.
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PMID:Metabolism of estrogens in hepatomas of different growth rates. 19 Nov 75

Estrogen regulates the expression of the yolk protein genes in the chicken liver during periods of egg laying. While all five of these genes, vitellogenins I, II, and III, very low density apolipoprotein II (apo VLDLII), and apolipoprotein B, respond to estrogen, individual controls are superimposed on their coordinate regulation with respect to the kinetics of induction, magnitude of response, and developmental expression. The estrogen-responsive Leghorn strain M hepatoma (LMH) cell line provides a model system for studying the molecular basis of the similarities and differences in the regulation of these genes. The apoVLDLII gene is regulated by estrogen in LMH cells in an appropriate time- and dose-dependent manner. Regulatory regions of the apoVLDLII gene have been identified by transient transfection studies in LMH cells. All four of the sequences previously shown to bind protein between the TAATA motif at -26 and proximal estrogen response element at -171 are essential in regulation of the apoVLDLII gene. Mutation of any single binding region reduces expression by more than 80%, indicating cooperative interactions of proteins across the entire region. While these sequences will direct assembly of a functional transcription complex, we demonstrate that addition of the first intron of the apoVLDLII gene to the promoter construct results in a 4-fold increase in estrogen-dependent expression following transient transfection into LMH cells. Results of deletion analyses indicate that two distinct regions of the intron contribute to this regulation.
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PMID:Functional analysis of regulatory regions upstream and in the first intron of the estrogen-responsive chicken very low density apolipoprotein II gene. 137 8

Estrogen (E) and epidermal growth factors (EGF) receptors were assayed in the liver of nine patients with hepatocellular carcinoma (HCC). Total E and nuclear E receptors were decreased significantly in neoplastic tissue as compared to the levels found in surrounding nonneoplastic tissue. The EGF receptor was decreased also in neoplastic tissue. On the basis of binding data, a decrease in the number but not in affinity of both the E and EGF receptors was found.
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PMID:Role of estrogens and epidermal growth factor in hepatocellular carcinoma (HCC). 165 42

Predisposing factors to cervical cancer development are age, smoking, socioeconomical status, parity, and number of sex partners. Long-term oral contraceptive (OC) use and less than 50 mg estrogen dose have been weakly linked to increased cancer risk. Regular examination and switching to other contraception in case of cervical intraepithelial neoplasia is recommended. Estrogen in sequential pills (Ovacon) increases the risks of uterine cancer by affecting the mucosa. Predisposing factors are: absence of pregnancy (nulliparity), postmenopause, hypertension, and diabetes. Parity reduces the risk. The risk is reduced in combined pills and after use of 1 year. Protection is offered by the progesterone component for 10-20 years after cessation of use. Ovarian cancer is prevented by parity and OC use even 10 years later. High estrogen levels inducing frequent ovulation damage the ovaries. Promoting factors are: old age, avoidance of breast feeding, and overweight. Breast cancer promoters are 1st pregnancy in older age, early menarche, and no pregnancy at all. OC use under age 25 and before 1st pregnancy are significant risk factors. High progesterone levels are associated with increased mitotic activity in the breast. Rare benign fibrocysts can develop into breast cancer. OC use is connected to hepatoma development mainly estrogen-induced. Liver cancer was found twice as high in OC users. Hepatoma often ruptures causing hemorrhage. 8% of liver tumors are malignant with a survival rate of 50% of patients to 4.8 years. The possible association of OCs to skin melanoma and hypophysial tumors could not be confirmed. OCs regulate menstruation, reduce bleeding, protect against uterine and ovarian cancer, but cervical and breast cancers have been influenced by them.
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PMID:[The contraceptive pill and cancer]. 207 68

We have used the human hepatoma cell line, Hep G2, to examine the ability of hormones and xenobiotics to modulate the hepatic induction of benzo(a)pyrene hydroxylase and epoxide hydrolase. Hep G2 cells were cultured in Eagle's Minimum Essential Medium supplemented with 10% fetal calf serum. 3-Methylcholanthrene, diethylstilbestrol, testosterone propionate, and combinations of 3-methylcholanthrene, and each of the hormones were added directly to the culture media. We subsequently studied the metabolism of benzo(a)pyrene using cell lysates of the Hep G2 cells. Metabolites were quantitated by high-performance liquid chromatography (HPLC) using fluorodetection. Exposure to 3-methylcholanthrene alone resulted in an eightfold increase in total benzo(a)pyrene metabolites with a change of the predominant metabolite from the 3-hydroxybenzo(a)pyrene to the carcinogenic pathway of the benzo(a)pyrene-7,8-diol. Diethylstilbestrol and testosterone propionate resulted in small, but significant, decreases in metabolism of benzo(a)pyrene. When exposed in combination with 3-methylcholanthrene, testosterone propionate antagonized and diethylstilbestrol potentiated the metabolism of benzo(a)pyrene. 3-Methylcholanthrene, diethylstilbestrol, and combinations of 3-methylcholanthrene and diethylstilbestrol or testosterone propionate resulted in increased epoxide hydrolase activity as compared to controls. These results, carried out in a human hepatoma cell line, lend support to a concern for potentiated toxicity and carcinogenicity following exposure to complex chemical mixtures.
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PMID:Diethylstilbestrol potentiates and testosterone antagonizes the action of 3-methylcholanthrene on benzo(a)pyrene metabolism in Hep G2 cells. 209 19

We have assayed both estrogen and androgen receptors in hepatocellular carcinomas, in the surrounding noncancerous liver tissue, and in normal liver tissue. Estrogen receptors (ERs) were detected in 5 out of 22 HCC tissues, 14 out of 22 surrounding noncancerous tissues, and in 5 out of 6 normal liver tissues. Androgen receptors (Ars) were detected in 4 out of 21 HCC tissues, in 7 out of 21 surrounding noncancerous tissues, and in 2 out of 5 normal liver tissues. These results suggest that the pathogenesis of some HCC may be dependent on estrogen or androgen. Hence, it may be beneficial to provide hormonal therapy for HCC, especially in cases that show high concentrations of ER and/or AR.
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PMID:[Estrogen and androgen receptors in hepatocellular carcinoma and in noncancerous liver tissue]. 255 Jun 81

Administration of estrogens in pharmacologic doses to rats and rabbits induces hepatic low-density lipoprotein (LDL) receptor activity. To determine if estrogens can regulate LDL receptor activity in human cells, 125I-LDL binding and ligand blotting studies were performed with the cell line Hep G2, well-differentiated cells derived from a human hepatoma, and with normal human fibroblasts. Addition of estradiol to Hep G2 cells growing in lipoprotein-deficient medium increased cell surface receptor activity by 141%, whereas fibroblast receptors were slightly reduced. Measurement of LDL internalization and degradation showed that estradiol induced the entire LDL receptor pathway and not simply surface receptors for LDL. Scatchard analysis of specific binding data in Hep G2 cells revealed that increased LDL receptor activity was due to high-affinity binding. When Hep G2 cells were incubated with LDL as well as estradiol, estradiol induction of LDL receptor activity did not occur. Estrogen treatment reduced Hep G2 free cholesterol content by 24% as determined by gas-liquid chromatography but had no significant effect on fibroblast free cholesterol, suggesting that estrogens may induce Hep G2 LDL receptor activity indirectly by lowering intracellular cholesterol. LDL receptor activity in Hep G2 cells grown in the absence of estradiol was resistant to down-regulation by LDL; incubation of cells with LDL for 48 h reduced receptor activity by only 25.8% in Hep G2 cells compared to 80.3% in fibroblasts. The Hep G2 LDL receptor was shown to be biochemically similar to the fibroblast receptor by ligand blotting and immunoblotting with IgG-C7, a monoclonal antibody to the extrahepatic LDL receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Estrogens induce low-density lipoprotein receptor activity and decrease intracellular cholesterol in human hepatoma cell line Hep G2. 282 2

The risk of contracting neoplastic liver disease after taking synthetic sex hormones, either estrogens or androgens, is discussed. Since the 1st reports that oral contraceptives were associated with liver neoplasms in the 1970s, tests on laboratory animals have suggested that sex steroids act as promoters of hepatocarcinogenesis in suitably initiated animals, and that some hormones act as weak complete carcinogens in certain lab hosts. It is known that oral contraceptives induce benign hepatic adenoma: hundreds of cases have been reported. These adenomas regress when women stop taking orals. The possible progression to malignant lesions is difficult to assess. Although a 1982 case review of women with hepatocellular carcinoma concluded that the association was a coincidence, 2 more recent epidemiological studies have proposed that there is a possible link between pills and hepatocarcinoma as well as cholangiosarcoma. In favor of the association is the finding that the histopathology of carcinoma in pill users differs from that in nonusers. Arguing against a causative role is the fact that natural cyclic estrogen levels are much higher than those found in pill users. Overall, the risk of developing liver cancer is far lower than the risk of other serious consequences of pill use, for example thromboembolism, and must be judged in the context of the many protective effects of the pill. The estrogen DES or diethylstilbestrol is no longer being used, but cases of clear-cell adenocarcinoma are still appearing in the daughters of its users. Anabolic androgens, prescribed therapeutically or abused, are known to cause liver neoplasms, primarily hepatocellular carcinoma, but also adenomas, focal nodular hyperplasia, cholangiosarcoma and angiosarcoma. The legitimate use of these steroids is on a much smaller scale, and for short periods of time, compared to oral contraceptives, so the causative role of androgens in neoplasia is less well known. With any of these drugs, especially in areas where potential cancer initiators such as oncogenes or viruses are endemic, careful screening is vital for safe use.
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PMID:Risk factors associated with the use of sex hormones. 282 3

The pathologic features, clinical presentation and natural history of hepatocellular carcinoma (HCC) developing in the noncirrhotic liver were studied in 61 patients against a background of 63 patients seen concurrently with HCC complicating cirrhosis. Noncirrhotic HCC had a bimodal age distribution, with females predominating the first age-clustering (10-50 years) and males predominating the second age-clustering (50-90 years). Cirrhotic HCC had a unimodal age distribution (40-90 years) with male dominance throughout. Estrogen exposure was noted in 57% of the noncirrhotic HCC women overall and in 80% of those in the younger age-clustering. The majority of noncirrhotic HCC presented with a single hepatic mass or a dominant primary with satellite lesions in contrast to the usual multinodular or diffuse disease seen with cirrhosis. Twenty-nine noncirrhotic patients survived complete resection of disease limited to the liver and exhibited a median survival of 2.7 years with a 5-year survival of 25%. Low histologic grade, minimal necrosis, and the absence of hemoperitoneum, hepatomegaly, and adjacent organ involvement were all favorable prognostic variable. Patients with metastatic or locally unresectable noncirrhotic HCC had a median survival of 9 months, and 24% survived in excess of 2 years. This survival experience is significantly more favorable than cirrhotic HCC patients, who had only a 1.2-month median and a 3% 2-year survival. Low histologic grade, mild mitotic activity and the presence of some fibrosis within the specimen were associated with a favorable outcome in advanced noncirrhotic HCC. The favorable prognosis and heterogeneous composition of the noncirrhotic, when compared to the cirrhotic HCC cohort, may be important considerations in the design and evaluation of future clinical trials.
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PMID:Hepatoma in the noncirrhotic liver. 284 80


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