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 yields of immediate DNA single-strand breaks in normal tumour tissues of irradiated animals were measured by a viscosimetric method of determination of high-polymer single-strand DNA molecular weight in alkaline nuclear lysates. It has been shown that in irradiated thymus, bone marrow leukocytes, Ehrlich ascitic carcinoma and Zaidel hepatoma cells (first group by tissues) in vivo the yields of DNA single-strand breaks were characterized by 80 to 130 eV per break. In in vivo irradiated liver, lymph node, spleen, and sarcoma 180 cells (second group of tissues) the yields of DNA single-strand breaks have been characterized by 30 to 40 eV per break. DNA single-strand breaks of the first group of tissues have rejoined 1 hour after the irradiation in vivo; DNA single-strand breaks of the second group have not done so.
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PMID:Viscosimetric analysis of the occurrence and repair of DNA single-strand breaks in irradiated animal tissues. 697 61

As an extension of the previous finding that radioactivity of 14C-labeled D-amino acids after injection is localized preferentially in the tumor and the pancreas of tumor-bearing animals as compared with the corresponding L-amino acids tested, the results of similar uptake experiments using other tumors araa reported here. The present studies show high radioactivity uptake by human colon cancer, human thyroid cancer, and human leiomyosarcoma transplanted into nude mice, and by solid leukemia L1210 and solid sarcoma 180, but not by Morris hepatoma 7316A or 3'-methyl-4-(dimethylamino)azobenzene-induced rat hepatoma. The results suggest the potential utility of 11C-labeled D-amino acids for the detection of some cancers.
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PMID:High uptake of 14C-labeled D-amino acids by various tumors. 711 46

Tetrocarcin A, isolated from a Micromonospora culture showed activity against experimental i.p. inoculated tumors such as Ehrlich carcinoma, MH134 hepatoma, B16 melanoma. But it was not active against solid tumors such as sarcoma 180 and Ehrlich carcinoma. It was marginally active against the growth of solid Lewis lung carcinoma without prolonging the life span of the tumor-bearing mice. It was active against P388 leukemia (i.v.-i.v. system). It did not show myelosuppression and nephrotoxicity in mice. DNA and protein synthesis of P388 cells in culture were more significantly suppressed than RNA synthesis by tetrocarcin A.
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PMID:Tetrocarcins, new antitumor antibiotics. 3. Antitumor activity of tetrocarcin A. 714 4

A lipolytic substance in the ascites fluid of mice with Sarcoma 180, called toxohormone-L, was purified and characterized. The lipolytic activity of toxohormone-L was measured in vitro using rat adipose tissue slices. Toxohormone-L, purified approximately 90-fold from the ammonium sulfate fraction, gave a single band on polyacrylamide gel electrophoresis. Its molecular weight was about 75,000, and its isoelectric point was 4.7. Toxohormone-L is heat labile and nondialyzable, but, on its digestion with trypsin, an active fragment that was heat stable and dialyzable was produced. Toxohormone-L is a protein and is also present in the ascites fluid of patients with hepatoma and Grawitz's tumor.
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PMID:Purification and characterization of a lipolytic factor (toxohormone-L) from cell-free fluid of ascites sarcoma 180. 744 67

Zinostatin stimalamer (ZSS) is a new anticancer agent derived from neocarzinostatin (NCS), which is synthesized by conjugation of one molecule of NCS and two molecules of poly(styrene-co-maleic acid). ZSS exhibited potent in vitro and in vivo antitumor activity in preclinical experiments, and a clinical trial of the intra-arterial administration of ZSS with iodized oil on hepatocellular carcinoma showed potent antitumor activity. We investigated the effect of ZSS and NCS on antitumor resistance and found that pretreatment with either drug suppressed the growth of MethA tumors in Balb/c mice and induced tumor eradication when given separately by single administration at therapeutic doses between 1 day and 4 weeks before tumor transplantation. The findings that the cytocidal activity of these drugs was not detected in vivo at the time of tumor transplantation and that tumor regression was preceded by a period of transient growth suggested that tumor regression was due to host-mediated antitumor activity induced by these drugs. Pretreatment with ZSS or NCS also suppressed the growth of Colon 26 carcinoma and Sarcoma 180. The finding that NCS showed the same effect as ZSS suggests that poly(styrene-comaleic acid) is not essential for the induction of host-mediated antitumor activity. Furthermore, apo-ZSS, which lacks cytocidal activity, did not induce antitumor activity. From this, it is suggested that the cytocidal effect of ZSS involves the induction of host-mediated antitumor resistance. In athymic Balb/c nu/nu mice, pretreatment with ZSS or NCS did not induce tumor eradication, suggesting that mature T lymphocytes play an important role in tumor eradication. Challenging MethA was rejected without transient growth in mice that had been cured of MethA, but challenging Colon 26 was not, showing that anti-MethA resistance was augmented selectively in the MethA-eradicated mice. Splenocytes from MethA-bearing mice pretreated with the drug showed tumor-neutralizing activity beginning 14 days after tumor transplantation. Tumor-neutralizing activity was only induced after MethA transplantation. The effector cells of this tumor-neutralizing activity were Thy1.2+ T lymphocytes that had been passed through a nylon-wool column, but no significant augmentation of cell-mediated cytotoxic activity of splenocytes from MethA-eradicated mice was observed in vitro.
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PMID:Antitumor resistance induced by zinostatin stimalamer (ZSS), a polymer-conjugated neocarzinostatin (NCS) derivative. I. Meth A tumor eradication and tumor-neutralizing activity in mice pretreated with ZSS or NCS. 760 May 66

IMR-90 human embryonic lung fibroblasts secrete a tumor cytotoxic factor. This factor, termed F-TCF, is moderately cytotoxic in human tumor cell lines (KB, MCF-7, BG-1) and is very cytotoxic in mouse tumor cell lines (Sarcoma 180, Meth A sarcoma, P388). The cytotoxicity depends on the initial target cell number and is due to cytostasis rather than cytolysis. F-TCF was purified from conditioned medium by a combination of UF-concentration, CM sephadex C-50, Con A sepharose, Mono S cation-exchange and heparin sepharose chromatography and exhibited a molecular mass (M(r)) of 76 to 80 kD on SDS-PAGE under non-reducing conditions. F-TCF is a heterodimer composed of a large alpha-subunit with M(r) 52 to 56 kD and a small beta-subunit with M(r) 30 to 34 kD. F-TCF is a heparin-binding, heat-labile, basic glycoprotein (pI 7.4-8.6). Its activity is stable over the pH range of 6.0 to 9.0, but is completely lost after reduction with 2-mercaptoethanol. Protein sequencing indicates that the alpha-subunit is blocked at the aminoterminus. The primary amino acid sequences deduced from hepatocyte growth factor (HGF) cDNAs cloned from human placenta and liver cDNA libraries indicate that F-TCF is identical to the placenta type HGF in the aminoterminal sequence of the beta-subunit, but differs at two sites from the liver type HGF. Two forms of F-TCF cDNA were found in an IMR-90 human fibroblast cDNA library. One form was identical to placenta type HGF cDNA and the other was a variant with a 15 base pair deletion in the coding region. In addition, mRNA corresponding to the deleted form of cDNA was present in total RNA prepared from IMR-90 cells. F-TCF was thus identified as placenta type HGFs including a variant. The deleted form of recombinant HGF (rHGF) expressed in CHO cells had slightly lower heparin-binding affinity than did the intact form. Both rHGFs had almost the same dose-response curves for cytotoxicity in Sarcoma 180 or Meth A sarcoma cells. Moreover, rHGF (the deleted form) was cytotoxic in hepatocellular carcinoma cells (HepG2, Hep3B, H35). Dose-response curves for the stimulation of DNA synthesis in rat hepatocytes by HGFs were very similar up to about 12.5 ng/ml, but differed significantly at higher concentrations. The deleted form gave maximal activity in a dose range of 12.5 to 100 ng/ml and had about 1.4- to 1.9-fold higher specific activity in that range than the intact form did.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tumor cytotoxic activity of HGF-SF. 838 Jul 42

We performed an experimental study on slow releasing anticancer drug implantation treatment as a new therapy for hepatocellular carcinoma. Hydroxyapatite (HAP) was chosen for the carrier material and doxorubicin hydrochloride (DOX) for anticancer agent. DOX-HAP was produced by adsorbing DOX to porous HAP particles of 1375 +/- 125 microns diameter using the freeze drying method. In vitro experiments showed slow release of the drug resulting in the steady release of DOX from HAP for 1 month duration. In healthy white rabbits with DOX-HAP implantation in the liver, serum DOX was not detectable, and DOX release rate was stable at the implanted region after 7, 14, and 21 days. When DOX-HAP (DOX; 100 mg kg-1) was administered to mice with sarcoma 180, an improved survival rate was observed without acute toxicity. We also found that VX2 liver tumour growth on white rabbit was inhibited by implantation of DOX-HAP, without acute toxicity. We hope that DOX-HAP implantation therapy will open up new avenues for the treatment of hepatoma.
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PMID:Implantation treatment method of slow release anticancer doxorubicin containing hydroxyapatite (DOX-HAP) complex. A basic study of a new treatment for hepatic cancer. 847 23

RPSP, a refined polysaccharide peptide fraction isolated by fast performance liquid chromatography (FPLC) from the crude powder of total peptide-bound polysaccharides of cultivated Coriolus versicolor Cov-1 dose-dependently inhibited the proliferation of a human hepatoma cell line (HEPG2). The effective dose causing 50% inhibition following 3-day exposure to RPSP was 243 +/- 36 micrograms/ml for HEPG2. However, little or no inhibitory effects were detected in normal human foetal hepatocytes. On the other hand, in the pretreatment group, in which RPSP was administered i.p. for two weeks before sarcoma 180 inoculation in nude mice, the incidence of tumor growth was less (2 out of 5 mice) than that of the control group (all 5 mice). The tumor size of the control group was about 3-5 times bigger than that of the pretreatment group. In tumor-bearing nude mice, 5 days after sarcoma 180 inoculation, i.v. administration of RPSP significantly suppressed the growth of tumor mass. The inhibition rate was 93.6% on day 13. Furthermore, administration of RPSP did not cause any pathological lesions in vital organs of rabbits such as heart, liver, spleen, lung and kidney. In conclusion, these results indicate that RPSP acts by directly suppressing tumor cell growth in vitro and the prevention of in vivo growth of tumor mass is probably mediated also via its immunomodulating effects.
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PMID:Antitumor effects of a refined polysaccharide peptide fraction isolated from Coriolus versicolor: in vitro and in vivo studies. 877 67

Bardanae Furctus (Goboshi) extract showed potent in vitro cytotoxicity and in vivo antitumor activity against human hepatoma HepG2 cells and mouse sarcoma 180 cells, respectively. In this study, the cytotoxicities of four fractions and three major components (arctiin, arctigenin, and chlorogenic acid) isolated from Goboshi extract were examined. Arctiin and arctigenin, which were contained in the ethylacetate fraction and n-butanol fraction, respectively, showed strong cytotoxicity against HepG2 cells, but little toxicity against Chang liver cells. Chlorogenic acid isolated from the water fraction did not affect the viability of these cells. The cytotoxicity of arctigenin against Chang liver cells was markedly potentiated by treatment with glutathione (GSH) synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO). On the other hand, in HepG2 cells, the cytotoxicity of arctigenin was hardly changed by BSO. The cytotoxicity of arctigenin against HepG2 cells increased in an exposure-time dependent manner. These characteristics of arctigenin were similar to those of Goboshi extract, as previously observed. We therefore conclude that the principal cytotoxic components of Goboshi extract are arctiin and its aglycone arctigenin.
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PMID:Cytotoxic components of bardanae fructus (goboshi). 895 Nov 77

Physarumin, a carbohydrate-binding protein (hemagglutinin or lectin), was isolated from the plasmodium of Physarum polycephalum. Physarumin agglutinated not only several species of erythrocytes but also tumor cells such as AH109A ascites hepatoma cells, sarcoma 180 ascites cells and mouse leukemia P388 cell lines. Physarumin had tumor cell growth-inhibitory activity, and induced the apoptosis of P388 cell lines. Physarumin-induced apoptosis required binding to a 68 kDa counter-receptor on the P388 cell surface. Since the agglutinating and antiproliferative activities of physarumin were inhibited by asialofetuin and thyroglobulin, respectively, it is suggested that physarumin reacts with the galactose moiety of carbohydrate chains of physarumin receptor.
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PMID:Apoptotic cell death induced by physarumin (hemagglutinin from myxomycete, Physarum polycephalum). 955 47


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