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1. 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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  • [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

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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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2. 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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3. 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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4. 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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5. 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


6. 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
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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

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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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7. 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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8. 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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9. 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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10. 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

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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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11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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. 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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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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