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1. Otrocka M, Verschueren H, Malicka-Błaszkiewicz M: The effect of methotrexate on actin and invasiveness of hepatoma Morris 5123 cells in culture. Acta Biochim Pol; 2001;48(4):1051-60
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of methotrexate on actin and invasiveness of hepatoma Morris 5123 cells in culture.
  • Monomeric (G), total (T) and filamentous (F) actin and the state of actin polymerisation (F:G) were determined and actin filaments were visualized in hepatoma Morris 5123 cells cultured in the presence of methotrexate (MTX) at various concentration.
  • The exposure of the cells to this drug resulted in a decrease of total and polymerised actin in cytoplasm and in some changes in actin filament organization.
  • [MeSH-major] Actins / metabolism. Carcinoma, Hepatocellular / drug therapy. Methotrexate / pharmacology
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / pharmacology. Biocompatible Materials / chemistry. Cell Movement. Collagen / pharmacology. Cytoplasm / metabolism. Cytosol / metabolism. Dose-Response Relationship, Drug. Drug Combinations. Laminin / pharmacology. Microscopy, Fluorescence. Neoplasm Invasiveness. Proteoglycans / pharmacology. Rats. Tumor Cells, Cultured

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  • (PMID = 11995967.001).
  • [ISSN] 0001-527X
  • [Journal-full-title] Acta biochimica Polonica
  • [ISO-abbreviation] Acta Biochim. Pol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Actins; 0 / Antimetabolites, Antineoplastic; 0 / Biocompatible Materials; 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; YL5FZ2Y5U1 / Methotrexate
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2. Sebzda T, Hanczyc P, Saleh Y, Akinpelumi BF, Siewinski M, Rudnicki J: Effect of vitamin E and human placenta cysteine peptidase inhibitor on expression of cathepsins B and L in implanted hepatoma Morris 5123 tumor model in Wistar rats. World J Gastroenterol; 2005 Jan 28;11(4):587-92
MedlinePlus Health Information. consumer health - Vitamin E.

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  • [Title] Effect of vitamin E and human placenta cysteine peptidase inhibitor on expression of cathepsins B and L in implanted hepatoma Morris 5123 tumor model in Wistar rats.
  • AIM: To examine the effectiveness of human placental inhibitors, by injecting vitamin E to rats with transplanted Morris-5123 hepatoma, on the expression of cathepsins B and L in tumor, liver, lung and blood sera after transplantation of Morris 5123 hepatoma.
  • Effectiveness of treatment was evaluated with regard to survival time, tumor response and determination of the activities of proteolytic enzymes and their inhibitors using flurogenic substrates.
  • RESULTS: Cathepsins B and L activities were elevated by 16-fold in comparison with negative control tissues, and their endogenous inhibitor activity decreased by 1.2-fold before treatment.
  • Cathepsins B and L were expressed significantly in tumor, liver, lung tissues and sera in parallel to the increasing of the endogenous inhibitor activity compared with the controls after treatment (P<0.0001).
  • CONCLUSION: The data indicate formation of metastasis significantly reduced in treated rats, which might provide a therapeutic basis for anti-cancer therapy.
  • [MeSH-major] Antioxidants / pharmacology. Cathepsin B / metabolism. Cathepsins / metabolism. Cysteine Proteinase Inhibitors / pharmacology. Liver Neoplasms, Experimental / drug therapy. Vitamin E / pharmacology

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  • (PMID = 15641152.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cysteine Proteinase Inhibitors; 1406-18-4 / Vitamin E; EC 3.4.- / Cathepsins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / CTSL1 protein, human; EC 3.4.22.15 / Cathepsin L; EC 3.4.22.15 / Ctsl protein, rat
  • [Other-IDs] NLM/ PMC4250817
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3. Pfab T, Stoltenburg-Didinger G, Trautner C, Godes M, Bauer C, Hocher B: The endothelin system in Morris hepatoma-7777: an endothelin receptor antagonist inhibits growth in vitro and in vivo. Br J Pharmacol; 2004 Jan;141(2):215-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The endothelin system in Morris hepatoma-7777: an endothelin receptor antagonist inhibits growth in vitro and in vivo.
  • 2. We thus analyzed the endothelin system in a rat hepatoma model (Morris hepatoma 7777) in vitro and in vivo.
  • 3. Our study revealed that tissue concentrations of endothelin-1 (ET-1) and big-ET-1, the precursor of ET-1, were significantly elevated in Morris hepatoma 7777 as compared to normal liver.
  • The ETA receptor density was significantly elevated, whereas the density of the ETB receptor was decreased in Morris hepatoma 7777.
  • 4. We could also demonstrate that hepatoma cells secrete ET-1.
  • 5. Exogenously added ET-1 enhances hepatoma cell growth in a dose-dependent manner.
  • Since the combined ETA/ETB receptor antagonist was more effective in vitro, we used this compound also for in vivo studies and could demonstrate that a combined ETA/ETB receptor antagonist is able to reduce hepatoma growth in vivo.
  • 6. In conclusion, the endothelin system is activated in Morris hepatoma 7777 and contributes to hepatoma growth.
  • Since endothelin receptor antagonists are well-tolerated upcoming clinically used drugs without major side effects, our data might provide a new pharmacological approach to reduce hepatoma growth in vivo.
  • [MeSH-major] Endothelin Receptor Antagonists. Growth Inhibitors / therapeutic use. Liver Neoplasms, Experimental / drug therapy. Liver Neoplasms, Experimental / pathology
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Endothelin-1 / metabolism. Endothelin-1 / pharmacology. Male. Propionates / pharmacology. Propionates / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. Rats. Rats, Inbred BUF. Receptors, Endothelin / metabolism. Xenograft Model Antitumor Assays / methods

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  • (PMID = 14662722.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endothelin Receptor Antagonists; 0 / Endothelin-1; 0 / Growth Inhibitors; 0 / LU 224332; 0 / Propionates; 0 / Pyrimidines; 0 / Receptors, Endothelin
  • [Other-IDs] NLM/ PMC1574189
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4. Bukietyńska K, Podsiadly H, Karwecka Z: Complexes of vanadium(III) with L-alanine and L-aspartic acid. J Inorg Biochem; 2003 Apr 1;94(4):317-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complexes of vanadium(III) with L-alanine and L-aspartic acid.
  • The equilibria of the complexation processes of V(3+) with L-alanine and L-aspartic acid in aqueous solution over a wide pH range (2-10) were studied by potentiometric and spectroscopic (UV-Vis, CD) methods.
  • The results show that alanine forms complexes with V(3+) in the metal ion concentration range and at the ligand-to-metal ratios investigated, giving mononuclear species only.
  • Both V(III)-L-aspartic acid and V(III)-L-alanine complexes have a significant apoptotic effect on Hepatoma Morris 5123 cells.
  • [MeSH-minor] Animals. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Circular Dichroism. Hydrogen-Ion Concentration. Hydroxides / chemistry. Ligands. Liver Neoplasms, Experimental / drug therapy. Models, Molecular. Potentiometry. Rats. Spectrophotometry / methods. Spectrophotometry, Ultraviolet. Tumor Cells, Cultured. Water / chemistry

  • Hazardous Substances Data Bank. (L)-ALANINE .
  • Hazardous Substances Data Bank. (L)-ASPARTIC ACID .
  • Hazardous Substances Data Bank. VANADIUM, ELEMENTAL .
  • Hazardous Substances Data Bank. Water .
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  • [Copyright] Copyright 2003 Elsevier Science Inc.
  • (PMID = 12667702.001).
  • [ISSN] 0162-0134
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxides; 0 / Ligands; 0 / Organometallic Compounds; 00J9J9XKDE / Vanadium; 059QF0KO0R / Water; 30KYC7MIAI / Aspartic Acid; 9159UV381P / hydroxide ion; OF5P57N2ZX / Alanine
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5. Dziegiel P, Surowiak P, Rabczyński J, Zabel M: Effect of melatonin on cytotoxic effects of daunorubicin on myocardium and on transplantable Morris hepatoma in rats. Pol J Pathol; 2002;53(4):201-4
Hazardous Substances Data Bank. MELATONIN .

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  • [Title] Effect of melatonin on cytotoxic effects of daunorubicin on myocardium and on transplantable Morris hepatoma in rats.
  • The present study aimed at corroborating cytostatic effectiveness of daunorubicin, applied in parallel with melatonin, in rats with transplanted Morris hepatoma.
  • [MeSH-major] Antibiotics, Antineoplastic / toxicity. Antioxidants / pharmacology. Daunorubicin / toxicity. Heart / drug effects. Liver Neoplasms, Experimental / drug therapy. Melatonin / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. In Situ Nick-End Labeling. Myocardium / pathology. Necrosis. Rats. Tumor Cells, Cultured / transplantation

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  • Hazardous Substances Data Bank. DAUNORUBICIN .
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  • (PMID = 12597337.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antioxidants; JL5DK93RCL / Melatonin; ZS7284E0ZP / Daunorubicin
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6. Jaromin A, Kozubek A, Suchoszek-Lukaniuk K, Malicka-Blaszkiewicz M, Peczynska-Czoch W, Kaczmarek L: Liposomal formulation of DIMIQ, potential antitumor indolo[2,3-b]quinoline agent and its cytotoxicity on hepatoma Morris 5123 cells. Drug Deliv; 2008 Jan;15(1):49-56

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liposomal formulation of DIMIQ, potential antitumor indolo[2,3-b]quinoline agent and its cytotoxicity on hepatoma Morris 5123 cells.
  • Treatment of hepatoma Morris 5123 cells for 24 hr with different concentrations of both free and its liposomal formulation of DIMIQ.HCl resulted in significant changes in cell morphology accompanied by reduction of cell viability.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carbolines / pharmacology. Glycerophospholipids / chemistry. Liposomes. Liver Neoplasms, Experimental / drug therapy
  • [MeSH-minor] 1,2-Dipalmitoylphosphatidylcholine / chemistry. Animals. Cell Shape / drug effects. Cell Survival / drug effects. Chemistry, Pharmaceutical. Dimyristoylphosphatidylcholine / chemistry. Dose-Response Relationship, Drug. Drug Compounding. Hemolysis / drug effects. Hydrogen-Ion Concentration. Particle Size. Phosphatidylglycerols / chemistry. Rats. Rats, Inbred BUF. Sheep. Tumor Cells, Cultured

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  • (PMID = 18197524.001).
  • [ISSN] 1071-7544
  • [Journal-full-title] Drug delivery
  • [ISO-abbreviation] Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbolines; 0 / Glycerophospholipids; 0 / Liposomes; 0 / Phosphatidylglycerols; 114414-79-8 / 5,11-dimethyl-5H-indolo(2,3-b)quinoline; 2644-64-6 / 1,2-Dipalmitoylphosphatidylcholine; U86ZGC74V5 / Dimyristoylphosphatidylcholine; VA9U6BR3SB / 1,2-dipalmitoylphosphatidylglycerol
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7. Evans SM, Kachur AV, Shiue CY, Hustinx R, Jenkins WT, Shive GG, Karp JS, Alavi A, Lord EM, Dolbier WR Jr, Koch CJ: Noninvasive detection of tumor hypoxia using the 2-nitroimidazole [18F]EF1. J Nucl Med; 2000 Feb;41(2):327-36
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  • [Title] Noninvasive detection of tumor hypoxia using the 2-nitroimidazole [18F]EF1.
  • The noninvasive assessment of tumor hypoxia in vivo is under active investigation because hypoxia has been shown to be an important prognostic factor for therapy resistance.
  • EF1 is a 3-monofluoro analog of the well-characterized hypoxia marker EF5, 2(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl)acetami de, which has been used to detect hypoxia in tumor and nontumor systems using immunohistochemical methods.
  • METHODS: We have studied 2 rat tumor types: the hypoxic Morris 7777 (Q7) hepatoma and the oxic 9LF glioma tumor, each grown in subcutaneous sites.
  • PET studies were performed using a pharmacological dose of nonradioactive carrier in addition to [18F]EF1 to optimize and assess drug biodistribution.
  • After PET imaging of the tumor-bearing rats, tissues were obtained for gamma-counting of the 18F in various tissues and immunohistochemical detection of intracellular drug adducts in tumors.
  • The tumor-to-muscle (T/M) ratio of [18F]EF1 in the Q7 tumors was 2.7 and 2.4 based on PET studies and 2.1, 2.5, and 3.0 based on gamma-counting of the tissues (n = 3).
  • In contrast, the T/M ratio of [18F]EF1 in the 9LF glioma tumor was 0.8 and 0.5 based on PET studies and 1.0, 1.2, and 1.4 based on gamma-counting of the tissues (n = 3).
  • Immunohistochemical analysis of drug adducts for the two tumor types agreed with the radioactivity analysis.
  • [MeSH-minor] Animals. Cell Hypoxia. Glioma / radionuclide imaging. Liver Neoplasms, Experimental / radionuclide imaging. Mice. Mice, Inbred BALB C. Rats. Rats, Inbred BUF. Rats, Inbred F344. Tomography, Emission-Computed

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  • (PMID = 10688119.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA28332; United States / NCI NIH HHS / CA / CA74071
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 0 / Nitroimidazoles
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8. Osińska-Królicka I, Podsiadły H, Bukietyńska K, Zemanek-Zboch M, Nowak D, Suchoszek-Łukaniuk K, Malicka-Błaszkiewicz M: Vanadium(III) complexes with L-cysteine--stability, speciation and the effect on actin in hepatoma Morris 5123 cells. J Inorg Biochem; 2004 Dec;98(12):2087-98
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  • [Title] Vanadium(III) complexes with L-cysteine--stability, speciation and the effect on actin in hepatoma Morris 5123 cells.
  • The complexation processes of vanadium(III) with L-cysteinate and s-methyl-L-cysteinate ligands have been studied in aqueous solutions in the pH range 2-7 by the pH-potentiometric, UV-Vis absorption and CD spectroscopy methods.
  • Solution of vanadium(III) with L-cysteine (pH approximately 7, L/M=20) was administrated to the culture medium of hepatoma Morris 5123 growing cells.
  • [MeSH-major] Actins / drug effects. Cysteine / chemistry. Organometallic Compounds / chemistry. Vanadium / chemistry
  • [MeSH-minor] Animals. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Cell Fractionation. Cell Survival. Cells, Cultured. Circular Dichroism. Cytosol / chemistry. Fluorescent Dyes. Hydrogen-Ion Concentration. Ligands. Liver Neoplasms, Experimental / drug therapy. Microscopy, Fluorescence. Phalloidine. Potentiometry. Rats. Spectrophotometry, Ultraviolet. Water / chemistry

  • Hazardous Substances Data Bank. PHALLOIDIN .
  • Hazardous Substances Data Bank. CYSTEINE .
  • Hazardous Substances Data Bank. VANADIUM, ELEMENTAL .
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  • (PMID = 15541498.001).
  • [ISSN] 0162-0134
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Antineoplastic Agents; 0 / Fluorescent Dyes; 0 / Ligands; 0 / Organometallic Compounds; 00J9J9XKDE / Vanadium; 059QF0KO0R / Water; 17466-45-4 / Phalloidine; K848JZ4886 / Cysteine
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9. Dziegiel P, Podhorska-Okolow M, Surowiak P, Ciesielska U, Rabczynski J, Zabel M: Influence of exogenous melatonin on doxorubicin-evoked effects in myocardium and in transplantable Morris hepatoma in rats. In Vivo; 2003 Jul-Aug;17(4):325-8
Hazardous Substances Data Bank. MELATONIN .

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  • [Title] Influence of exogenous melatonin on doxorubicin-evoked effects in myocardium and in transplantable Morris hepatoma in rats.
  • The present study aimed at examining the cytostatic efficiency of doxorubicin (DOX) applied together with melatonin to rats with transplantable Morris hepatoma.
  • CONCLUSION: Melatonin weakens the cytotoxic activity of DOX by the decreased proportions of necrotic and apoptotic cells of transplantable Morris hepatoma.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Free Radical Scavengers / therapeutic use. Liver Neoplasms, Experimental / drug therapy. Melatonin / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Count. Drug Therapy, Combination. In Situ Nick-End Labeling. Myocytes, Cardiac / drug effects. Myocytes, Cardiac / pathology. Necrosis. Neoplasm Transplantation. Rats

  • Hazardous Substances Data Bank. DOXORUBICIN .
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  • (PMID = 12929587.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Free Radical Scavengers; 80168379AG / Doxorubicin; JL5DK93RCL / Melatonin
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10. Haberkorn U, Bellemann ME, Brix G, Kamencic H, Morr I, Traut U, Altmann A, Doll J, Blatter J, Kinscherf R: Apoptosis and changes in glucose transport early after treatment of Morris hepatoma with gemcitabine. Eur J Nucl Med; 2001 Apr;28(4):418-25
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  • [Title] Apoptosis and changes in glucose transport early after treatment of Morris hepatoma with gemcitabine.
  • Dynamic positron emission tomography (PET) measurements of fluorine-18 fluorodeoxyglucose (FDG) uptake were done in rats bearing Morris hepatoma prior to and after therapy with 90 mg gemcitabine/kg b.w.
  • In vitro measurements of FDG and TdR uptake were performed immediately and 24 h after the end of gemcitabine treatment, and the amount of apoptotic cells was determined using the TUNEL reaction.
  • In vivo an increase in FDG transport and phosphorylation occurred early after gemcitabine treatment, although TdR incorporation into the DNA of the tumours declined.
  • In vitro, an enhanced glucose transport, an increase in TdR uptake in the cytoplasm and a decrease in TdR incorporation in the nucleic acid fraction early after treatment occurred.
  • The increase in glucose uptake and TdR metabolism early after therapy is interpreted as a stress reaction of the tumour cells, protecting the cells from apoptosis during this early period after exposure to cytotoxic drugs like gemcitabine.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Apoptosis / drug effects. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Glucose / metabolism. Liver Neoplasms, Experimental / drug therapy
  • [MeSH-minor] 3-O-Methylglucose / metabolism. Animals. DNA, Neoplasm / drug effects. Fluorodeoxyglucose F18. Immunohistochemistry. Neoplasm Transplantation. Phosphorylation. Radiopharmaceuticals. Rats. Rats, Inbred Strains. Thymidine / metabolism. Tomography, Emission-Computed. Tumor Cells, Cultured

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  • (PMID = 11357491.001).
  • [ISSN] 0340-6997
  • [Journal-full-title] European journal of nuclear medicine
  • [ISO-abbreviation] Eur J Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / Radiopharmaceuticals; 0W860991D6 / Deoxycytidine; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 146-72-5 / 3-O-Methylglucose; B76N6SBZ8R / gemcitabine; IY9XDZ35W2 / Glucose; VC2W18DGKR / Thymidine
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11. Simile MM, De Miglio MR, Muroni MR, Frau M, Asara G, Serra S, Muntoni MD, Seddaiu MA, Daino L, Feo F, Pascale RM: Down-regulation of c-myc and Cyclin D1 genes by antisense oligodeoxy nucleotides inhibits the expression of E2F1 and in vitro growth of HepG2 and Morris 5123 liver cancer cells. Carcinogenesis; 2004 Mar;25(3):333-41
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  • [Title] Down-regulation of c-myc and Cyclin D1 genes by antisense oligodeoxy nucleotides inhibits the expression of E2F1 and in vitro growth of HepG2 and Morris 5123 liver cancer cells.
  • The knowledge of the behavior of these interactions in hepatocellular carcinoma, could optimize preventive and therapeutic strategies based on cell cycle restraint.
  • We studied downstream events following c-MYC and CYCLIN D1 gene inhibition, by lipoplex-delivered MYC and CYCLIN D1 antisense oligodeoxy nucleotides (aODNM, aODND1), in in vitro cultured human HepG2 and rat Morris 5123 hepatoma cells.
  • 0.5-20 micro M aODN(M) and aODND1 inhibited in vitro growth of both cell types.
  • Treatment of the cells with aODNM plus aODND1 had no additive effect on growth and apoptosis. aODNM and aODND1 induced >50% decrease in c-MYC and CYCLIN D1 gene expression, respectively, at both mRNA and protein level.
  • These results suggest the involvement of both c-MYC and CYCLIN D1 on E2F1 gene function, and indicate that aODNM and aODND1 may inhibit hepatoma cell growth through down-regulation of the E2F1 gene.
  • Thus, interactions of c-MYC and CYCLIN D1 with E2F1 gene are essential for cell cycle activity in hepatoma cells, and their inhibition may have a therapeutic effect.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Cycle Proteins. DNA-Binding Proteins. Genes, bcl-1 / drug effects. Genes, myc / drug effects. Liver Neoplasms / drug therapy. Oligodeoxyribonucleotides, Antisense / pharmacology. Transcription Factors / drug effects
  • [MeSH-minor] Animals. Down-Regulation / drug effects. E2F Transcription Factors. E2F1 Transcription Factor. Humans. Precipitin Tests. Rats. Tumor Cells, Cultured

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  • (PMID = 14604889.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / E2F Transcription Factors; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / E2f1 protein, rat; 0 / Oligodeoxyribonucleotides, Antisense; 0 / Transcription Factors
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12. Seigers R, Pourtau L, Schagen SB, van Dam FS, Koolhaas JM, Konsman JP, Buwalda B: Inhibition of hippocampal cell proliferation by methotrexate in rats is not potentiated by the presence of a tumor. Brain Res Bull; 2010 Mar 16;81(4-5):472-6
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  • Methotrexate is a widely used cytostatic in chemotherapy cocktails for the treatment of cancer but is associated with cognitive impairment.
  • However, clinical studies have shown that cognitive impairment can also be noticed in some cancer patients before any systemic treatment is initiated.
  • Buffalo rats were subcutaneously injected with PBS or Morris Hepatoma 7777 cells to induce a tumor.
  • Treatment with Morris Hepatoma 7777 cells decreased the number of proliferating cells as compared to control animals.
  • An overall tumor effect was absent mainly because methotrexate treatment significantly decreased cell proliferation with no differences between animals with or without a tumor.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Brain Neoplasms / drug therapy. Cell Proliferation / drug effects. Hippocampus / drug effects. Methotrexate / pharmacology
  • [MeSH-minor] Animals. Body Weight / drug effects. Body Weight / physiology. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / physiopathology. Cell Line, Tumor. Feeding Behavior / drug effects. Feeding Behavior / physiology. Immunohistochemistry. Liver Neoplasms / drug therapy. Liver Neoplasms / physiopathology. Male. Neoplasm Transplantation. Pica / chemically induced. Pica / physiopathology. Rats. Rats, Inbred BUF

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  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • (PMID = 19828128.001).
  • [ISSN] 1873-2747
  • [Journal-full-title] Brain research bulletin
  • [ISO-abbreviation] Brain Res. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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13. Ganslmayer M, Ocker M, Kraemer G, Zopf S, Hahn EG, Schuppan D, Herold C: The combination of tamoxifen and 9cis retinoic acid exerts overadditive anti-tumoral efficacy in rat hepatocellular carcinoma. J Hepatol; 2004 Jun;40(6):952-6
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  • BACKGROUND/AIMS: Medical treatment for hepatocellular carcinoma (HCC) remains elusive.
  • While an acyclic retinoid improved tumor-free survival after hepatoma resection, tamoxifen finally proved ineffective.
  • Combination therapy of both agents has not been investigated in vitro and in vivo.
  • METHODS: MH7777A hepatoma cells were incubated with tamoxifen (TAM) and 9-cis retinoic acid (CRA) alone or in combination.
  • In vivo efficacy was studied using the Morris hepatoma model in immunocompetent rats.
  • Combination therapy significantly enhanced apoptosis rate and growth inhibition in hepatoma cells.
  • This combination could be a promising adjunctive therapy of HCC.
  • [MeSH-major] Liver Neoplasms / drug therapy. Liver Neoplasms, Experimental / drug therapy. Tamoxifen / therapeutic use. Tretinoin / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Cell Division / drug effects. Cell Line, Tumor. DNA Replication / drug effects. In Situ Nick-End Labeling. Rats. Rats, Inbred BUF

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  • (PMID = 15158335.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin
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14. Wolf M, Bauder-Wüst U, Haberkorn U, Mier W, Eisenhut M: Alkylating benzamides with melanoma cytotoxicity: role of melanin, tyrosinase, intracellular pH and DNA interaction. Melanoma Res; 2005 Oct;15(5):383-91
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  • Therefore, this class of compound has previously been evaluated as a transporter for cytostatic drugs.
  • In order to identify mechanistic reasons for this effect, we investigated the DNA and melanin binding affinities of a selection of four benzamide-drug conjugates, together with their parental cytostatics.
  • An investigation of the influence of the melanin content on the cytotoxicity of these substances in B16 melanoma and Morris hepatoma (MH3924A) cells was performed, together with their influence on melanosomal pH and tyrosinase activity.
  • The consequence of this reaction chain is an amplification of the scavenging effect for the benzamide-drug conjugates.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Benzamides / pharmacology. DNA / metabolism. Melanins / metabolism. Melanoma, Experimental / drug therapy. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / metabolism
  • [MeSH-minor] Animals. Cell Survival / drug effects. Chlorambucil / administration & dosage. Chlorambucil / pharmacokinetics. Drug Carriers. Enzyme Activation. Liver Neoplasms, Experimental / drug therapy. Liver Neoplasms, Experimental / enzymology. Liver Neoplasms, Experimental / metabolism. Mice

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  • (PMID = 16179865.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Benzamides; 0 / Drug Carriers; 0 / Melanins; 18D0SL7309 / Chlorambucil; 9007-49-2 / DNA; EC 1.14.18.1 / Monophenol Monooxygenase
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15. Haberkorn U, Kinscherf R, Krammer PH, Mier W, Eisenhut M: Investigation of a potential scintigraphic marker of apoptosis: radioiodinated Z-Val-Ala-DL-Asp(O-methyl)-fluoromethyl ketone. Nucl Med Biol; 2001 Oct;28(7):793-8
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  • The imaging of apoptosis represents an attractive diagnostic goal in the area of tumor therapy, degenerative diseases and organ transplantation.
  • Uptake measurements were performed with Morris hepatoma cells (MH3924Atk8) which showed expression of the Herpes Simplex Virus thymidine kinase (HSVtk) gene.
  • Apoptosis was induced by treatment of the cells with 25 microM ganciclovir.
  • The TUNEL assay revealed 1.3 +/-0.3 and 23 +/-1.1% apoptotic cells immediately and 24 h after therapy, respectively.
  • A two-fold increase of [131I]IZ-VAD-fmk uptake was found at the end of treatment with the HSVtk/suicide system which constantly remained elevated for the following 4 hours.
  • [MeSH-major] Amino Acid Chloromethyl Ketones. Apoptosis / drug effects. Neuroprotective Agents. Radiopharmaceuticals
  • [MeSH-minor] Animals. Chromatography, High Pressure Liquid. DNA Fragmentation / drug effects. Genetic Therapy. Humans. In Situ Nick-End Labeling. Iodine Radioisotopes. Isotope Labeling. Liver Neoplasms, Experimental / genetics. Liver Neoplasms, Experimental / radionuclide imaging. Liver Neoplasms, Experimental / therapy. Tumor Cells, Cultured

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  • (PMID = 11578900.001).
  • [ISSN] 0969-8051
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Iodine Radioisotopes; 0 / Neuroprotective Agents; 0 / Radiopharmaceuticals; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
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16. Piguet AC, Semela D, Keogh A, Wilkens L, Stroka D, Stoupis C, St-Pierre MV, Dufour JF: Inhibition of mTOR in combination with doxorubicin in an experimental model of hepatocellular carcinoma. J Hepatol; 2008 Jul;49(1):78-87
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  • BACKGROUND/AIMS: Hepatocellular carcinoma (HCC) is resistant to chemotherapy.
  • Since antiangiogenic therapy may enhance chemotherapy effects, we tested the antitumorigenic properties of sirolimus combined with doxorubicin in experimental HCC.
  • METHODS: Morris Hepatoma (MH) cells were implanted into livers of syngeneic rats.
  • RESULTS: Animals treated with the combination developed smaller tumors with decreased tumor microvessel density compared to animals that received monotherapies.
  • These findings offer a rationale for combining mTOR inhibitors with chemotherapy in HCC treatment.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Carcinoma, Hepatocellular / drug therapy. Doxorubicin / analogs & derivatives. Liver Neoplasms, Experimental / drug therapy. Polyethylene Glycols / pharmacology. Sirolimus / analogs & derivatives. Transcription Factors / antagonists & inhibitors
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Aorta / cytology. Apoptosis / drug effects. Cells, Cultured. Disease Models, Animal. Endothelial Cells / cytology. Intracellular Signaling Peptides and Proteins / metabolism. Male. Neoplasm Transplantation. Oncogene Protein p21(ras) / metabolism. Phosphorylation / drug effects. Protein-Serine-Threonine Kinases / metabolism. Rats. Rats, Inbred ACI

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  • (PMID = 18486258.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Crtc1 protein, rat; 0 / Intracellular Signaling Peptides and Proteins; 0 / Transcription Factors; 0 / liposomal doxorubicin; 30IQX730WE / Polyethylene Glycols; 624KN6GM2T / temsirolimus; 80168379AG / Doxorubicin; EC 2.7.1.- / MAP-kinase-activated kinase 2; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.6.5.2 / Oncogene Protein p21(ras); W36ZG6FT64 / Sirolimus
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17. Bekeredjian R, Kroll RD, Fein E, Tinkov S, Coester C, Winter G, Katus HA, Kulaksiz H: Ultrasound targeted microbubble destruction increases capillary permeability in hepatomas. Ultrasound Med Biol; 2007 Oct;33(10):1592-8
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  • [Title] Ultrasound targeted microbubble destruction increases capillary permeability in hepatomas.
  • Ultrasound-targeted microbubble destruction (UTMD) has evolved as a promising tool for organ-specific gene and drug delivery.
  • Taking advantage of high local concentrations of therapeutic substances and transiently increased capillary permeability, UTMD could be used for the treatment of ultrasound accessible tumors.
  • The aim of this study was to evaluate if UTMD can locally increase capillary permeability in a hepatoma model of the rat.
  • Subcutaneous Morris hepatomas were induced in both hind limbs of ACI rats by cell injection.
  • In conclusion, ultrasound targeted microbubble destruction is able to transiently increase capillary permeability in hepatomas.
  • Using naked DNA, this technique does not seem to be feasible for noninvasive transfection of hepatomas.
  • [MeSH-minor] Animals. Contrast Media / pharmacokinetics. DNA / administration & dosage. Drug Delivery Systems. Evans Blue / pharmacokinetics. Extravasation of Diagnostic and Therapeutic Materials. Gene Expression. Genetic Therapy / methods. Hindlimb. Luciferases / genetics. Male. Microbubbles. Neoplasm Transplantation. Rats. Rats, Inbred Strains. Transfection / methods

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  • (PMID = 17618040.001).
  • [ISSN] 0301-5629
  • [Journal-full-title] Ultrasound in medicine & biology
  • [ISO-abbreviation] Ultrasound Med Biol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contrast Media; 45PG892GO1 / Evans Blue; 9007-49-2 / DNA; EC 1.13.12.- / Luciferases
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18. Haberkorn U, Altmann A, Kamencic H, Morr I, Traut U, Henze M, Jiang S, Metz J, Kinscherf R: Glucose transport and apoptosis after gene therapy with HSV thymidine kinase. Eur J Nucl Med; 2001 Nov;28(11):1690-6
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  • [Title] Glucose transport and apoptosis after gene therapy with HSV thymidine kinase.
  • The relation between tumour metabolism and induction of apoptosis by gene therapy was investigated in a rat Morris hepatoma (MH3924A) model expressing the HSV thymidine kinase (HSVtk) gene.
  • In vitro uptake studies with 2-fluoro-2-deoxy-D-glucose (FDG), 3-O-methylglucose and thymidine (TdR) and a TUNEL (TdT-mediated dUTP nick end labelling) assay for the assessment of apoptosis were done immediately and 24 h after treatment of the recombinant cells with different doses of ganciclovir (GCV).
  • The uptake of TdR, which was determined simultaneously, decreased in the acid-insoluble fraction of the cells to 27% and 11%, respectively, immediately and 24 h after therapy, while in the acid-soluble fraction it increased to 229% and to 167%, respectively.
  • Employing the TUNEL technique, 25% of cells were found to be apoptotic 24 h after the termination of GCV treatment.
  • Inhibition of glucose transport by cytochalasin B or competition with deoxyglucose resulted in a 78% (cytochalasin B) and 88% (deoxyglucose) decrease in FDG uptake in the recombinant hepatoma cells and in an increase in the apoptotic cell fraction.
  • [MeSH-major] Apoptosis. Genetic Therapy. Glucose / metabolism. Liver Neoplasms, Experimental / therapy. Nerve Tissue Proteins. Thymidine Kinase / genetics
  • [MeSH-minor] 3-O-Methylglucose / metabolism. Animals. Antiviral Agents / pharmacology. Cytochalasin B / pharmacology. Excitatory Amino Acid Transporter 2 / metabolism. Fluorodeoxyglucose F18 / pharmacokinetics. Ganciclovir / pharmacology. Glucose Transporter Type 3. Immunohistochemistry. In Situ Nick-End Labeling. Male. Monosaccharide Transport Proteins / metabolism. Neoplasm Transplantation. Radiopharmaceuticals / pharmacokinetics. Rats. Rats, Inbred ACI. Simplexvirus / genetics. Thymidine / metabolism. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. Tumor Cells, Cultured / pathology

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  • (PMID = 11702112.001).
  • [ISSN] 0340-6997
  • [Journal-full-title] European journal of nuclear medicine
  • [ISO-abbreviation] Eur J Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Excitatory Amino Acid Transporter 2; 0 / Glucose Transporter Type 3; 0 / Monosaccharide Transport Proteins; 0 / Nerve Tissue Proteins; 0 / Radiopharmaceuticals; 0 / Slc2a3 protein, rat; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 146-72-5 / 3-O-Methylglucose; 3CHI920QS7 / Cytochalasin B; EC 2.7.1.21 / Thymidine Kinase; IY9XDZ35W2 / Glucose; P9G3CKZ4P5 / Ganciclovir; VC2W18DGKR / Thymidine
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19. Maggard M, Meng L, Ke B, Allen R, Devgan L, Imagawa DK: Antisense TGF-beta2 immunotherapy for hepatocellular carcinoma: treatment in a rat tumor model. Ann Surg Oncol; 2001 Jan-Feb;8(1):32-7
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  • [Title] Antisense TGF-beta2 immunotherapy for hepatocellular carcinoma: treatment in a rat tumor model.
  • METHODS: A rat HCC cell line, Morris hepatoma rat cell line (MRH)-7777 (MRH), was transfected with antisense TGF-beta2 in pCEP-4 vector and used as immunotherapy against the development of wild-type tumors.
  • An enzyme-linked immunosorbent assay (ELISA) confirmed that TGF-beta2 production was markedly lower for antisense modified cells as compared to wild-type tumor cells.
  • RESULTS: In the group that received irradiated MRH unmodified cells, 55% of rats died from tumor burden, and 36% developed tumor regression.
  • In animals treated with pCEP-4/TGF-beta antisense modified cells, none developed tumors.
  • CONCLUSIONS: These results demonstrate the successful treatment of HCC tumors in rats by a HCC vaccine genetically altered with antisense TGF-beta2.
  • Decreased production of TGF-beta in HCC vaccine enhances immunogenicity against wild-type HCC tumor cells.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. DNA, Antisense / therapeutic use. Immunotherapy / methods. Liver Neoplasms, Experimental / therapy. Transforming Growth Factor beta / biosynthesis. Transforming Growth Factor beta / genetics
  • [MeSH-minor] Animals. Cytotoxicity, Immunologic. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Gene Expression / drug effects. Genetic Vectors. Humans. Injections, Subcutaneous. Neoplasm Transplantation. Neoplasms / chemically induced. Plasmids. Rats. Rats, Inbred BUF. Retroviridae. Transforming Growth Factor beta2. Tumor Cells, Cultured. Vaccination

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  • (PMID = 11206222.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Antisense; 0 / TGFB2 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta2
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20. Haberkorn U, Altmann A, Jiang S, Morr I, Mahmut M, Eisenhut M: Iodide uptake in human anaplastic thyroid carcinoma cells after transfer of the human thyroid peroxidase gene. Eur J Nucl Med; 2001 May;28(5):633-8
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  • Human thyroperoxidase (hTPO) is critical for the accumulation of iodide in thyroid tissues.
  • Poorly differentiated and anaplastic thyroid tumours which lack thyroid-specific gene expression fail to accumulate iodide and, therefore, do not respond to iodine-131 therapy.
  • The human anaplastic thyroid carcinoma cell lines C643 and SW1736, the rat Morris hepatoma cell line MH3924A and the rat papillary thyroid carcinoma cell line L2 were used as in vitro model systems.
  • Genetically modified cell lines expressed up to 1,800 times more hTPO as compared to wild type tumour cells.
  • The transduction of the hTPO gene per se is not sufficient to restore iodide trapping in non-iodide-concentrating tumour cells.
  • [MeSH-minor] Animals. Drug Resistance / genetics. Genetic Vectors. Humans. Iodine Radioisotopes / therapeutic use. Liver Neoplasms, Experimental / metabolism. Neomycin / pharmacology. Rats. Retroviridae. Thyroglobulin / metabolism. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism

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  • (PMID = 11383870.001).
  • [ISSN] 0340-6997
  • [Journal-full-title] European journal of nuclear medicine
  • [ISO-abbreviation] Eur J Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 1404-04-2 / Neomycin; 9010-34-8 / Thyroglobulin; 9679TC07X4 / Iodine; EC 1.11.1.8 / Iodide Peroxidase
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21. Finlay IG, Stewart GJ, Pourgholami MH, Akhter J, Morris DL: The use of lipiodol and medium chain triglyceride as delivery agents for hepatic arterial administration of 1, 25-dihydroxyvitamin D3--a potential new treatment for hepatocellular carcinoma. Anticancer Res; 2000 Jul-Aug;20(4):2705-9
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  • [Title] The use of lipiodol and medium chain triglyceride as delivery agents for hepatic arterial administration of 1, 25-dihydroxyvitamin D3--a potential new treatment for hepatocellular carcinoma.
  • It is well established that 1, 25 dihydroxyvitamin D3 is capable of inhibiting the proliferation of a number of human cancer cell lines, including hepatoma cell lines.
  • However, clinical usage in the treatment of cancers has been limited by its hypercalaemic effects.
  • We hypothesised that by delivering 1, 25 dihydroxyvitamin D3 dissolved in a lipid based carrier agent as a hepatic arterial infusion it would be possible to achieve high local concentrations within hepatomas for prolonged periods, whilst avoiding high systemic concentrations and hypercalcaemia.
  • We examined this hypothesis by administering a hepatic arterial infusion of 1, 25 dihydroxyvitamin D3 in either Lipiodol, Medium Chain Triglyceride (MCT), or saline to hepatoma bearing rats.
  • Assay of serum and tissue concentrations revealed that this approach using lipiodol or triglyceride results in selective distribution of 1, 25-dihydroxyvitamin D3 into, and retention within hepatoma tissue and low initial systemic serum levels.
  • This method of administration has potential in the treatment of hepatoma.
  • [MeSH-major] Calcitriol / administration & dosage. Iodized Oil / administration & dosage. Liver Neoplasms, Experimental / drug therapy. Triglycerides / administration & dosage
  • [MeSH-minor] Animals. Drug Carriers. Infusions, Intra-Arterial. Liver / metabolism. Male. Rats. Rats, Sprague-Dawley. Tumor Cells, Cultured

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  • (PMID = 10953347.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Drug Carriers; 0 / Triglycerides; 8001-40-9 / Iodized Oil; FXC9231JVH / Calcitriol
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22. Finlay IG, Stewart GJ, Ahkter J, Morris DL: A phase one study of the hepatic arterial administration of 1,25-dihydroxyvitamin D3 for liver cancers. J Gastroenterol Hepatol; 2001 Mar;16(3):333-7
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  • BACKGROUND AND AIMS: It is well established that exposure to 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) inhibits the proliferation of human colorectal cancer and hepatoma cell lines, both in vitro and in vivo.
  • However, clinical trials of the administration of 1,25(OH)2D3 and analogs for the treatment of malignancy have been limited by the development of hypercalcemia.
  • This suggested the hypothesis that hepatic regional administration may allow high doses of 1,25(OH)2D3 to be administered for the treatment of liver cancers without producing hypercalcemia, caused by a clinically significant first pass effect.
  • No patient experienced any side-effects from the treatment.
  • This route of administration may allow the potential of 1,25(OH)2D3 in the treatment of hepatic cancers to be realized.
  • [MeSH-major] Calcitriol / administration & dosage. Calcium Channel Agonists / administration & dosage. Liver Neoplasms / drug therapy

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  • (PMID = 11339427.001).
  • [ISSN] 0815-9319
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Calcium Channel Agonists; FXC9231JVH / Calcitriol
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23. McCarthy-Beckett DO: Dietary supplementation with conjugated linoleic acid does not improve nutritional status of tumor-bearing rats. Res Nurs Health; 2002 Feb;25(1):49-57
Hazardous Substances Data Bank. LINOLEIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The purpose of the present study was to examine the effects of a diet supplemented with 0.5% CLA on the nutritional status of rats implanted with the Morris 7777 hepatoma.
  • [MeSH-major] Anorexia / drug therapy. Anorexia / etiology. Dietary Supplements. Disease Models, Animal. Linoleic Acid / therapeutic use. Liver Neoplasms, Experimental / complications. Nutritional Status / drug effects. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / metabolism. Wasting Syndrome / drug therapy. Wasting Syndrome / etiology
  • [MeSH-minor] Analysis of Variance. Animals. Body Weight / drug effects. Drug Evaluation, Preclinical. Energy Intake / drug effects. Insulin / blood. Insulin-Like Growth Factor I / drug effects. Insulin-Like Growth Factor I / metabolism. Male. Mice. Rats. Rats, Inbred BUF

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  • [Copyright] Copyright 2002 John Wiley & Sons,
  • (PMID = 11807919.001).
  • [ISSN] 0160-6891
  • [Journal-full-title] Research in nursing & health
  • [ISO-abbreviation] Res Nurs Health
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 0 / Tumor Necrosis Factor-alpha; 67763-96-6 / Insulin-Like Growth Factor I; 9KJL21T0QJ / Linoleic Acid
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24. Ziemer LS, Evans SM, Kachur AV, Shuman AL, Cardi CA, Jenkins WT, Karp JS, Alavi A, Dolbier WR Jr, Koch CJ: Noninvasive imaging of tumor hypoxia in rats using the 2-nitroimidazole 18F-EF5. Eur J Nucl Med Mol Imaging; 2003 Feb;30(2):259-66
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  • Tumor hypoxia is an important prognostic indicator for cancer therapy outcome.
  • Therefore, validation of the PET data was performed by gamma counting of the imaged tissue.
  • The tumor models studied were the Morris 7777 (Q7) hepatoma (n=5) and the 9L glioma (n=2) grown subcutaneously in rats.
  • The seven rats were imaged in the HEAD Penn-PET scanner at various time points after administration of 50-100 micro Ci (18)F-EF5 in 30 mg/kg carrier nonradioactive EF5.
  • The carrier was used to ensure drug biodistribution comparable to prior studies using immunohistochemical methods. (18)F-EF5 was excreted primarily via the urinary system.
  • Images obtained 10 min following drug administration demonstrated that the EF5 distributed evenly to all organ systems, including brain.
  • Liver uptake remained relatively constant over the same time periods.
  • [MeSH-minor] Animals. Cell Hypoxia. Feasibility Studies. Fluorine Radioisotopes. Male. Metabolic Clearance Rate. Organ Specificity. Radiopharmaceuticals / pharmacokinetics. Rats. Rats, Inbred F344. Rats, Sprague-Dawley. Sensitivity and Specificity. Tissue Distribution. Tomography, Emission-Computed / methods. Tumor Cells, Cultured

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  • (PMID = 12552344.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl)acetamide; 0 / Fluorine Radioisotopes; 0 / Hydrocarbons, Fluorinated; 0 / Radiopharmaceuticals; 30DKA3Q1HL / Etanidazole
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