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)

This report presents a review of tumors, except those of pituitary, that have been reported to occur in women taking combined oral contraceptive preparations. Pathologic features, both gross and microscopic, and differential diagnosis are emphasized. Particular attention is given to tumors of the liver: focal nodular hyperplasia (hepatic hamartoma) and liver cell adenoma (benign hepatoma). The characteristic features of these usually distinctive lesions are illustrated, and an attempt is made to evaluate the significance of each with respect to oral contraceptives. Tumorigenic aspects relating to the uterus and the breast are briefly discussed.
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PMID:Tumorigenic aspects. 3 11

Antiserum against yolk-sac carcinoma of rat was prepared in rabbits. After appropriate absorption in vitro or in vivo this antiserum was examined on different tumors and normal tissues or rat, hamster and mouse. The methods used were indirect immunofluorescence and indirect immunoperoxidase staining and cytotoxicity tests. The immune serum was found to react with the cell membrane of different rat and hamster yolk-sac carcinomas. It reacted also with the cell surface of rat hepatoma cells. By absorption on hyalin and blocking with amniotic fluid it was shown that the antigen was neither a basement membrane component nor alpha-fetoprotein. The antiserum was cytotoxic to yolk-sac carcinoma and hepatoma cells. The immune reaction was limited to the cell membrane, as observed in immunofluorescence and in immunoperoxidase staining. The specificity of the antiserum was proved by cross-absorptions with various tumor lines and by removing its activity with the soluble fraction of yolk-sac carcinoma cells. Non-endodermal rat and hamster tumor lines did not react with the anti-yolk-sac carcinoma immune serum. Most normal adult tissues, including spermatozoa, were negative, but a positive reaction was observed in ovaries and on glandular cells of the uterus. In embryonal tissues this surface antigen(s) was detected in the endoderm of 8-day-old rat embryos 7-day-old mouse embryos and in yolk-sac endoderm of both species. The data indicate that the antigen(s) is associated with endodermal differentiation.
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PMID:Presence of common surface antigens(s) on endodermal tumors and embryonal tissues of rats, hamsters and mice. 7 14

Myosin has been purified from the following cultured cell lines: normal rat kidney fibroblast (NRK), HeLa-Rhino (HeLa), human choriocarcinoma, human acute lymphoblastic leukemia, rat hepatoma (HTC), monkey kidney (VERO), pigmented mouse melanoma, Y-1 rat adrenal cortex, and growth hormone-secreting GH-1. Myosin constitutes 0.5-5.4% of the protein of these cells. It was not detected in washed human erythrocytes or in two types of mouse plasmacytoma cells. Two methods for the purification of myosin from cultured cells have been employed. With Method I highly purified myosin was prepared by Sepharose 4B and DEAE-cellulose chromatography from 10(10) L-929 cells as well as from mouse uterus. Those myosins have similar molecular and subunit weights as well as ATPase activity but are immunologically distinct. Method II involving ultracentrifugation and Sepharose 4B chromatography, is suitable for the production of moderately pure myosin in good yield from as few as 5-10(7) cells (five 100-mm Petrie dishes).
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PMID:The purification and quantitation of myosin from cultured cells. 13 88

Thymidine kinase-deficient OTT6050 mouse teratocarcinoma cells were fused with hypoxanthine phosphoribosyltransferase-deficient Fu5AH rat hepatoma cells by means of inactivated Sendai virus. The resulting hybrid cells, which were selected in hypoxanthine/aminopterin/thymidine medium, retained almost all of the mouse chromosomes and various numbers of rat chromosomes, and showed many chromosomal rearrangements. The hybrid cells, as well as both parental lines, formed tumors after subcutaneous injection into athymic nude mice. Single rat--mouse hybrid cells from a clonally established subline were transplanted into C57BL6/J mouse blastocysts carrying many genetic markers suitable for the detection of hybrid cell-derived tissue contributions. From 144 blastocysts, each of which was injected with a hybrid cell and then surgically transferred to the uterus of a pseudopregnant foster mother, 62 adult mice developed without any visible coat mosaicism. However, three of these mice showed internal hybrid-cell participation in their livers and a limited number of organs of endomesodermal origin. A tumor classifiable as hemangio endothelioma was found in the liver, the only mosaic tissue, of one of the chimeric mice. Nine different rat-specific enzyme variants were detected in the mosaic organs. A considerable number of variations concerning the presence and quantitative activity of the foreign gene products probably resulted from chromosomal segregation, tissue-specific gene activity, or dosage compensation during differentiation in vivo. Our results demonstrate that cultured malignant rat--mouse hybrid cells differentiate normally and become functionally integrated during development. The appearacne in vivo of certain rat-specific gene products that are not found in the hybrid cells under conditions in vitro indicates differential gene expression of the introduced xenogeneic chromosomes.
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PMID:Xenogeneic gene expression in chimeric mice derived from rat--mouse hybrid cells. 28 11

In order to estimate end effects of chronic prolonged gammairradiation of dogs, an exposure of 80 animals to irradiation was terminated and they were followed up closely. Out of 80 animals 30 dogs (1st series) were irradiated for 3 years and 50 dogs (II series) for 6 years. The dogs were exposed to irradiation at doses of 21 to 190 rad per year. Out of the total number of animals 22 dogs died. Post-mortem examinations showed neoformations in 13 animals (7 malignant and 12 benign neoformations). The highest number of tumors developed in dogs of the II series (10 out of 11) one-two years after irradiation (6 malignant tumors--malignant pheochromocytoma of adrenals; malignant adenoma of the hypophysis: polymorphocellular sarcoma of the liver; leucomyosarcoma of the uterus; bladder cancer; breast cancer; and 10 benign tumors--pancreatic adenoma; liver angioma; 2 papillary adenomas of the prostate; 3 renal adenomas; lipoma; polyps of the gall-bladder). Animals of the 1st series displayed 3 neoformations (1 malignant tumor--bladder tumor and 2 benign tumorsliver hepatoma and spleen angioma) 4--5 years after irradiation.
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PMID:[Formation of neoplasms in dogs after chronic gamma irradiation at a low-intensity dose]. 64 24

1. A protein which binds retinol in vitro with high affinity and specificity was detected by sucrose gradient centrifugation or by gel filtration after preincubating rat tissue cytosols with all-trans-[3H]retinol. This protein sediments in the 2 S region of sucrose gradients. Molecular size determination by gel filtration indicates a molecular weight of 16 000. 2. Competition studies revealed that only all-trans-retinol, not retinal or retinoic acid, competes for binding. The binding of radioactive retinol is reversible. 3. This protein was detected in cytosols of rat liver, lung, spleen, brain, testis, ovaries, uterus and intestinal mucosa whereas heart or gastrocnemius muscle seem to lack this protein. 4. The cellular retinol binding protein was found in fetuses as early as day 12 of the gestation period and possessed the same specificity for the ligand as the one in adult tissues. 5. This binding component was not detected in cytosols prepared from Novikoff hepatoma, ascites hepatoma AS-30D, mouse Ehrlich ascites tumor and mouse pituitary tumor cell line AtT 20. 6. The cellular retinol binding protein seems to be different from that described to be present in the serum as suggested by difference in size and by the inability of the antisera against the serum retinol binding protein to remove the cellular binding protein from the cytosol preparations.
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PMID:Cellular retinol-binding protein. 81 Jan 77

DNA adduct formation in the liver, pancreas, kidneys and uterus in ethynylestradiol (EE)-induced carcinogenesis and the effect of tamoxifen (TAM) on DNA adduct formation were evaluated in female Wistar JCL rats using the 32P-postlabeling method. Hyperplastic nodules were noted in the liver of all rats 4 months after the first oral administration of 0.075 mg of EE, and hepatocellular carcinoma was detected in 8.1% of rats treated with EE for 12 months. DNA adducts increased in the liver for 4 months, reaching a level of 7.3 adducts/10(7) nucleotides and decreasing thereafter. Formation of DNA adducts was also noted in the pancreas and kidney, but the adduct levels were lower than those in the liver. TAM inhibited estrogen receptors (ER) in liver tissues and completely suppressed the development of hyperplastic nodules or hepatocellular carcinoma but did not affect DNA adduct formation in the liver. In this model, therefore, EE is considered to cause mutations of hepatocytes due to DNA adduct formation without mediation by ER and to induce initiated cells to develop into hepatocellular carcinoma in the presence of ER-mediated hormonal activities.
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PMID:32P-postlabeling analysis of DNA adducts in rats during estrogen-induced hepatocarcinogenesis and effect of tamoxifen on DNA adduct level. 131 83

We analyzed the expression of plasma glutathione peroxidase (GSHPx-P) messenger RNA (mRNA) in mouse, rat, and human tissues, using a human GSHPx-P cDNA clone as the probe. Unlike the classical cellular glutathione peroxidase (GSHPx-1), GSHPx-P expression appears to be tissue-specific. In the mouse and rat, kidney expresses an mRNA at a high level detected with the human probe. A signal is also detected in mRNA isolated from mouse and rat heart, rat cardiac myocytes, mouse lung, epididymis, and the mammary gland of midpregnant mice. No signal is detected in mRNA isolated from mouse and rat liver, mouse brain, uterus, and testis. In human tissues, an mRNA hybridizing to GSHPx-P cDNA is present in liver, as well as kidney, heart, lung, breast, and placenta. We have shown that human kidney expresses a GSHPx-P mRNA, and not a GSHPx-P-like message, by isolating a cDNA clone from a human kidney library in lambda gt11. From the 412-nucleotide partial sequence of the kidney cDNA, which codes for the 40-170 amino acids of GSHPx-P including the TGA codon for selenocysteine, we found complete sequence identity of the kidney cDNA with GSHPx-P isolated from placenta. The expression of GSHPx-P mRNA in cell lines was also studied. There is some correlation of the expression of GSHPx-P in these cell lines with that in normal tissues. Cell lines that expressed GSHPx-P mRNA or protein included the human hepatocarcinoma HepG2, Hep3B cells, human kidney carcinoma A498 cells, and the human breast cancer SK-BR-3, T47D, MDA-MB-231, and AdrrMCF-7 cells. Cell lines that did not express GSHPx-P included human choriocarcinoma BeWo cells, human breast cancer MCF-7, ZR-75-1, and Hs578T cells, and mouse hepatoma Hepa-1 cells.
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PMID:Expression of plasma glutathione peroxidase in human liver in addition to kidney, heart, lung, and breast in humans and rodents. 133

A case of quadruple cancer is reported. A 74-year-old female was admitted because of surgery for left breast cancer. Abdominal echography showed a mosaic patterned mass of the liver and a solid tumor with central necrosis at the left kidney. Echographic diagnosis was hepatoma and Grawitz's tumor. All the tumors were justified as being operable. Progressive cystorrhagia which was due to radiation cystitis after radiotherapy for uterine carcinoma could not be controlled. Autopsy diagnosis was a quadruple carcinoma composed of solid tubular carcinoma of left breast, left renal carcinoma, hepatocellular carcinoma and squamous cell carcinoma of the uterus.
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PMID:[A case of quadruple cancer composed of the breast, kidney, liver and uterus carcinomas]. 216

Sensitivity to phenylephrine, isoproterenol, serotonin, oxytocin, acetylcholine and barium chloride of vas deferens uterus und fundus strip was studied comparatively in hepatectomized and sarcoma-45, sarcoma-M1, Walker carcinosarcoma and Zajdela ascites hepatoma bearing rats. The contractile response to monoamines and oxytocin was considerably lower or absent at certain periods after hepatectomy or tumour grafting. Effects of biogenic amine antagonists were also substantially altered. The response to isoproterenol, acetylcholine and barium chloride remained unchanged. Apparently a selective alteration of a response of visceral smooth muscles mediated through alpha-adrenergic and D-serotonin receptors occurred not only during the tumour growth but also in the case of active (extensive) proliferation of the normal tissue.
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PMID:[The monoaminergic receptors of the internal organs in rats with a tumor and after partial hepatectomy]. 217 98


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