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)

A patient with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease), treated with ethinyl estradiol, multiple blood transfusions, and iron-dextran, developed hepatocellular carcinoma and acquired hepatocerebral degeneration. In addition to the carcinoma, the liver contained extensive arteriovenous maliformations, telangiectasis, and changes of Osler atypical cirrhosis. The carcinoma possibly had its genesis in the presence of an ocongenic serum hepatitis virus, or the cirrhosis, or both.
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PMID:Hereditary hemorrhagic telangiectasia. A case with hepatocellular carcinoma and acquired hepatocerebral degeneration. 16 31

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

Histological specimens from 150 women with liver tumors are discussed. Of the 150 patients under consideration, 85% had ingested contraceptive steroids, most for more than 3 years. Of these 64% had taken pills containing mestranol, and 18% had used ethinyl estradiol; 18% had taken both. Average age was about 30 years, and pain was the most common presenting symptom. 19 tumors were malignant (hepatoma), 57 were adenoma, 68 were focal nodular hyperplasia, and 6 were unclassified. To date, 12 of the 19 hepatoma patients have died. In addition to presenting numerous figures depicting the pathology material and a discussion of tumor differentiation difficulties, speculation between steroid ingestation and tumor appearance is considered. Since hepatomas are much more common than benign liver tumors, circumspection is in order before indicting steroids as causative. In this group of women studied, none had cirrhosis, for example, whereas cirrhosis is very common in the general population. The authors call for further investigation of estrogens and primary liver tumores.
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PMID:Relation of steroids to liver oncogenesis. 22 96

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

Well over 100,000,000 women have used the combined oral contraceptive (OC) pill. As a result of the population explosion in the 1970s and 1980s, there will be almost one third more women in fertile age in the year 2000 than in 1991. In the developing world outside China, the total number of contraceptive users could double in roughly 10 years. China, the total number of contraceptive users could double in roughly 10 years. The pill has a low failure rate, but one study in Egypt found that 90% of women made errors in moving from one packet to the next. Similarly, a 60% error rate was found among users in Colombia. The vaginal ring delivers combined progestogen and estrogen through a silastic wall. The device can be left in place for 21 days out of 28, and such delivery would virtually eliminate the low risk of hepatocellular carcinoma among OC users. A vaginal progestogen ring is being tested. Over 700,000 women have used Norplant, the subdermal implant method with an effectiveness rate of 99%. Depo-provera and norethindrone enanthate injections last 2 to 3 months. The Progestasert IUD, containing 38 mg progesterone released at a rate of 65 mcg per day, is effective. Progesterone-releasing IUDs lasting from 3 to 5 years could complement subdermal implants. Ethinyl estradiol (205 mg) and diethylstilbestrol (25-50 mg) have both been used as postcoital agents taken within 36 hours for 5 consecutive days after unprotected intercourse. In more than 3000 cases there were 17 pregnancies (.05%). These regimens are replaced by giving combined oral contraceptive tables (e.g., .25 mg d-norgestrel and 50 mg ethinyl estradiol), taken 2 at a time and repeated 12 hours later, within 72 hours of unprotected intercourse. Epidemiological studies have confirmed that the use of the combined oral contraceptive for 3 to 5 years halves a woman's risk of ovarian or endometrial cancer, and the protection persists for 10 to 18 years after cessation of use.
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PMID:The future of hormonal contraception. 168 5

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

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

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


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