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1. Viglianti BL, Ponce AM, Michelich CR, Yu D, Abraham SA, Sanders L, Yarmolenko PS, Schroeder T, MacFall JR, Barboriak DP, Colvin OM, Bally MB, Dewhirst MW: Chemodosimetry of in vivo tumor liposomal drug concentration using MRI. Magn Reson Med; 2006 Nov;56(5):1011-8
Hazardous Substances Data Bank. MANGANESE SULFATE .

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  • [Title] Chemodosimetry of in vivo tumor liposomal drug concentration using MRI.
  • Effective cancer chemotherapy depends on the delivery of therapeutic drugs to cancer cells at cytotoxic concentrations.
  • Efforts to improve drug delivery have been limited by the lack of noninvasive tools to evaluate intratumoral drug concentration and distribution.
  • Here we demonstrate that tumor drug concentration can be measured in vivo using T(1)-weighted MRI, following systemic administration of liposomes containing both drug (doxorubicin (DOX)) and contrast agent (manganese (Mn)).
  • Mn and DOX concentrations were calculated using T(1) relaxation times and Mn:DOX loading ratios, as previously described.
  • Two independent validations by high-performance liquid chromatography (HPLC) and histologic fluorescence in a rat fibrosarcoma (FSA) model indicate a concordant linear relationship between DOX concentrations determined using T(1) and those measured invasively.
  • This method of imaging exhibits potential for real-time evaluation of chemotherapeutic protocols and prediction of tumor response on an individual patient basis.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacokinetics. Doxorubicin / pharmacokinetics. Fibrosarcoma / metabolism. Image Processing, Computer-Assisted / methods. Liposomes / pharmacokinetics. Magnetic Resonance Imaging / methods. Manganese Compounds / pharmacokinetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Hyperthermia, Induced. Neoplasm Transplantation. Rats. Rats, Inbred F344. Sulfates. Temperature. Tissue Distribution

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17029236.001).
  • [ISSN] 0740-3194
  • [Journal-full-title] Magnetic resonance in medicine
  • [ISO-abbreviation] Magn Reson Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA042745-20; United States / NCRR NIH HHS / RR / P41 RR005959; United States / NCI NIH HHS / CA / R24 CA092656
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Liposomes; 0 / Manganese Compounds; 0 / Sulfates; 7785-87-7 / manganese sulfate; 80168379AG / Doxorubicin
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2. Kleiter MM, Yu D, Mohammadian LA, Niehaus N, Spasojevic I, Sanders L, Viglianti BL, Yarmolenko PS, Hauck M, Petry NA, Wong TZ, Dewhirst MW, Thrall DE: A tracer dose of technetium-99m-labeled liposomes can estimate the effect of hyperthermia on intratumoral doxil extravasation. Clin Cancer Res; 2006 Nov 15;12(22):6800-7
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  • PURPOSE: A noninvasive method to monitor intratumoral Doxil delivery in individual patients during targeted tumor therapy is important to predict treatment response.
  • EXPERIMENTAL DESIGN: Experiments were carried out in a rat fibrosarcoma model with transplanted thigh tumors.
  • Eight treatment groups received either Doxil, a tracer dose or a large dose of 99mTc-labeled liposomes, or a combination of tracer and Doxil, with or without hyperthermia.
  • However, there was a significant positive correlation of intratumoral doxorubicin concentration and intratumoral uptake of the radiolabeled tracer (expressed as percentage of the injected dose per gram of tissue).
  • Coadministration of radiolabeled liposomes did not negatively influence the amount of drug delivered with Doxil.
  • CONCLUSIONS: The use of a radiolabeled tracer has potential value to monitor drug delivery and estimate the effect of an intervention aimed to increase liposomal accumulation, such as local hyperthermia.
  • [MeSH-major] Doxorubicin / pharmacokinetics. Doxorubicin / therapeutic use. Fibrosarcoma / therapy. Hyperthermia, Induced / methods. Liposomes / administration & dosage. Technetium Tc 99m Exametazime / administration & dosage
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / pharmacokinetics. Antibiotics, Antineoplastic / therapeutic use. Combined Modality Therapy / methods. Diagnostic Imaging / methods. Dose-Response Relationship, Drug. Drug Carriers / administration & dosage. Feasibility Studies. Female. Radioactive Tracers. Rats. Thigh / radiation effects. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 17121901.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA42745
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Drug Carriers; 0 / Liposomes; 0 / Radioactive Tracers; 3B744AG22N / Technetium Tc 99m Exametazime; 80168379AG / Doxorubicin
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3. Ying H, Biroc SL, Li WW, Alicke B, Xuan JA, Pagila R, Ohashi Y, Okada T, Kamata Y, Dinter H: The Rho kinase inhibitor fasudil inhibits tumor progression in human and rat tumor models. Mol Cancer Ther; 2006 Sep;5(9):2158-64
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  • [Title] The Rho kinase inhibitor fasudil inhibits tumor progression in human and rat tumor models.
  • Fasudil has been approved for the treatment of cerebral vasospasm and associated cerebral ischemic symptoms.
  • Therefore, the concept of Rho kinase inhibition as an antimetastatic therapy for cancer can now be clinically explored.
  • [MeSH-major] 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / analogs & derivatives. Breast Neoplasms / drug therapy. Fibrosarcoma / drug therapy. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Protein Kinase Inhibitors / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. rho-Associated Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Adhesion / physiology. Cell Growth Processes / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Disease Progression. Female. Humans. Male. Mice. Mice, Nude. Rats. Xenograft Model Antitumor Assays

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  • (PMID = 16985048.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Protein Kinase Inhibitors; 0 / ROCK1 protein, human; 0 / ROCK2 protein, human; 0 / Rock1 protein, mouse; 0 / Rock2 protein, mouse; 103745-39-7 / fasudil; 84477-87-2 / 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / ROCK2 protein, rat; EC 2.7.11.1 / rho-Associated Kinases
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4. Jho DH, Babcock TA, Tevar R, Helton WS, Espat NJ: Eicosapentaenoic acid supplementation reduces tumor volume and attenuates cachexia in a rat model of progressive non-metastasizing malignancy. JPEN J Parenter Enteral Nutr; 2002 Sep-Oct;26(5):291-7

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  • [Title] Eicosapentaenoic acid supplementation reduces tumor volume and attenuates cachexia in a rat model of progressive non-metastasizing malignancy.
  • As the liver plays a central role in modulating nutritional status and the cachexia syndrome, we examined the liver and nutritional parameters indicative of cachexia along with the tumor volume in response to oral EPA supplementation in a rat model of progressive non-metastasizing malignancy.
  • METHODS: Fischer 344 rats implanted with the methylcholanthrene-induced fibrosarcoma (MCA) were trained to meal-feed with access to food from 8:00 PM to 8:00 AM and water ad libitum.
  • The treatment was delivered via oral gavage twice daily.
  • The animals were killed on day 29, and serum plus tissues (ie, liver and lung) were collected and frozen for analysis.
  • EPA- and corn oil-treated rats received more calories than the saline group because of the dietary fat treatments (p < .01) and had elevated lipid content in their livers (p = .05 and p = .04, respectively) compared with saline rats.
  • Serum albumin (a marker of liver function) and MIP-2 levels (a marker of the hepatic acute phase response) were not different between treatment groups.
  • Regression analyses showed that the weight and protein differences between treatment groups were not correlated with individual tumor volumes.
  • To our knowledge, this is the first study to demonstrate the effects of EPA in the MCA fibrosarcoma model and is also novel in its evaluation of EPA as an anticachexiogenic therapy in progressive non-metastasizing malignancy.
  • Further studies may identify the protein(s) elevated in the liver and the mechanisms for the development of EPA nutritional therapies for the treatment of progressive malignancies.
  • [MeSH-major] Cachexia / drug therapy. Eicosapentaenoic Acid / therapeutic use. Fibrosarcoma / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Cell Division / drug effects. Chemokine CXCL2. Disease Models, Animal. Lipids / analysis. Liver / chemistry. Liver / drug effects. Liver / pathology. Lung / chemistry. Lung / drug effects. Lung / pathology. Monokines / analysis. Organ Size / drug effects. Proteins / metabolism. Random Allocation. Rats. Rats, Inbred F344. Weight Loss / drug effects

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  • (PMID = 12216709.001).
  • [ISSN] 0148-6071
  • [Journal-full-title] JPEN. Journal of parenteral and enteral nutrition
  • [ISO-abbreviation] JPEN J Parenter Enteral Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CXCL2; 0 / Lipids; 0 / Monokines; 0 / Proteins; AAN7QOV9EA / Eicosapentaenoic Acid
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5. Blackwell KL, Haroon ZA, Shan S, Saito W, Broadwater G, Greenberg CS, Dewhirst MW: Tamoxifen inhibits angiogenesis in estrogen receptor-negative animal models. Clin Cancer Res; 2000 Nov;6(11):4359-64
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  • Inhibition of tumor angiogenesis is a therapeutic strategy that can inhibit tumor growth and metastases.
  • The aim of this study was to determine whether the estrogen receptor (ER) ligand drug tamoxifen has antiangiogenic effects.
  • ER-negative fibrosarcoma tumors in tamoxifen-treated ovariectomized rats had significantly less vessel formation compared with untreated animals (median microvessel density, 53.6 versus 94.3 counts/per x 200 field; P = 0.002).
  • Rat aortic rings treated with tamoxifen at several different concentrations demonstrated significantly less vascular sprouting than control rings (P = 0.0001).
  • These three animal models all showed significant inhibition of angiogenesis by tamoxifen and suggest a possible contributory mechanism of ER-independent manipulation by tamoxifen in the treatment and prevention of breast cancer.
  • These studies raise the question as to whether or not newer ER ligand drugs might possess even more potent antiangiogenic effects, which in turn could lead to the broadening of the clinical usefulness of these compounds in a number of diseases.
  • [MeSH-minor] Animals. Aorta / drug effects. Breast Neoplasms / drug therapy. Cornea / drug effects. Female. Fibrosarcoma / blood supply. In Vitro Techniques. Models, Animal. Rats. Rats, Inbred F344

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  • (PMID = 11106254.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-68438; United States / NHLBI NIH HHS / HL / HL-26309; United States / NHLBI NIH HHS / HL / HL-38245
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Estrogen Receptor Modulators; 0 / Receptors, Estrogen; 094ZI81Y45 / Tamoxifen
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6. Ponce AM, Viglianti BL, Yu D, Yarmolenko PS, Michelich CR, Woo J, Bally MB, Dewhirst MW: Magnetic resonance imaging of temperature-sensitive liposome release: drug dose painting and antitumor effects. J Natl Cancer Inst; 2007 Jan 3;99(1):53-63
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  • [Title] Magnetic resonance imaging of temperature-sensitive liposome release: drug dose painting and antitumor effects.
  • BACKGROUND: In preclinical studies, lysolipid-based temperature-sensitive liposomes (LTSLs) containing chemotherapy drugs administered in combination with local hyperthermia have been found to increase tumor drug concentrations and improve antitumor efficacy of the drugs.
  • We used a novel magnetic resonance imaging (MRI) method to measure the temporal and spatial patterns of drug delivery in a rat fibrosarcoma model during treatment with LTSLs containing doxorubicin and an MRI contrast agent (manganese) (Dox/Mn-LTSLs) administered at different times with respect to hyperthermia.
  • Drug distribution was monitored continuously via MRI.
  • Magnetic resonance changes were used to calculate intratumoral doxorubicin concentrations throughout treatment.
  • Tumors were monitored until they reached five times their volume on the day of treatment or 60 days.
  • Doxorubicin concentrations and times for tumors to reach five times their volume on the day of treatment were analyzed using the Kruskal-Wallis test and the Kaplan-Meier product-limit method, respectively.
  • RESULTS: Administration of Dox/Mn-LTSLs before, during, and both before and during hyperthermia yielded central, peripheral, and uniform drug distributions, respectively.
  • LTSL administered during hyperthermia also yielded the greatest antitumor effect, with a median time for tumors to reach five times their volume on the day of treatment of 34 days (95% CI = 30 days to infinity) compared with 18.5 days (95% CI = 16 to 23 days) for LTSL before hyperthermia and 22.5 days (95% CI = 15 to 25 days) for LTSL before and during hyperthermia.
  • CONCLUSIONS: In this rat fibrosarcoma model, LTSLs were most effective when delivered during hyperthermia, which resulted in a peripheral drug distribution.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / pharmacokinetics. Doxorubicin / administration & dosage. Doxorubicin / pharmacokinetics. Fibrosarcoma / drug therapy. Hyperthermia, Induced. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Animals. Chromatography, High Pressure Liquid. Contrast Media / administration & dosage. Disease Models, Animal. Female. Liposomes. Manganese Compounds / administration & dosage. Rats. Rats, Inbred F344. Time Factors

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  • (PMID = 17202113.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA42745; United States / PHS HHS / / P4105959; United States / NCI NIH HHS / CA / R24 CA092656
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Contrast Media; 0 / Liposomes; 0 / Manganese Compounds; 80168379AG / Doxorubicin
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7. Carriero MV, Longanesi-Cattani I, Bifulco K, Maglio O, Lista L, Barbieri A, Votta G, Masucci MT, Arra C, Franco R, De Rosa M, Stoppelli MP, Pavone V: Structure-based design of an urokinase-type plasminogen activator receptor-derived peptide inhibiting cell migration and lung metastasis. Mol Cancer Ther; 2009 Sep;8(9):2708-17
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  • [Title] Structure-based design of an urokinase-type plasminogen activator receptor-derived peptide inhibiting cell migration and lung metastasis.
  • The urokinase-type plasminogen activator receptor (uPAR) plays a central role in sustaining the malignant phenotype and promoting tumor metastasis.
  • Here, we describe the generation of new peptide inhibitors of cell migration and invasion derived from SRSRY by a drug design approach.
  • Fluorescein-RERF associates with very high affinity to RBL-2H3 rat basophilic leukemia cells expressing the human formyl peptide receptor (FPR).
  • Furthermore, RERF reduces the speed of wound closure and the extent of Matrigel invasion by human fibrosarcoma HT1080 cells without affecting cell proliferation.
  • Our findings indicate that RERF effectively prevents malignant cell invasion in vivo with no signs of toxicity and may represent a promising prototype drug for anticancer therapy.
  • [MeSH-major] Cell Movement / drug effects. Lung Neoplasms / secondary. Neoplasm Metastasis / prevention & control. Peptide Fragments / pharmacology. Receptors, Urokinase Plasminogen Activator / chemistry
  • [MeSH-minor] Animals. Female. Fibrosarcoma / pathology. Humans. Immunoprecipitation. Mice. Mice, Nude. Microscopy, Fluorescence. Models, Molecular. Nuclear Magnetic Resonance, Biomolecular. Protein Conformation. Rats

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  • (PMID = 19706734.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptide Fragments; 0 / Receptors, Urokinase Plasminogen Activator
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8. Wakai Y, Matsui J, Koizumi K, Tsunoda S, Makimoto H, Ohizumi I, Taniguchi K, Kaiho S, Saito H, Utoguchi N, Tsutsumi Y, Nakagawa S, Ohsugi Y, Mayumi T: Effective cancer targeting using an anti-tumor tissue vascular endothelium-specific monoclonal antibody (TES-23). Jpn J Cancer Res; 2000 Dec;91(12):1319-25
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  • [Title] Effective cancer targeting using an anti-tumor tissue vascular endothelium-specific monoclonal antibody (TES-23).
  • In the present study, we attempted to achieve tumor vascular targeting with an anti-tumor tissue endothelium-specific monoclonal antibody (TES-23).
  • TES-23, an IgG1 monoclonal antibody raised against rat KMT-17 fibrosarcoma-derived endothelial cells, was covalently conjugated with neocarzinostatin (NCS) in a previous study.
  • The TES-23-NCS conjugate induced tumor hemorrhagic necrosis, and showed marked anti-tumor effects against rat KMT-17 fibrosarcoma.
  • This result prompted us to investigate whether this approach would be applicable to various other types of solid tumors.
  • One hour after injection of (125)I-labeled TES-23 into BALB / c mice bearing Meth-A fibrosarcoma and Colon 26 adenocarcinoma, the tumor accumulation of TES-23 was greater than that of the control IgG.
  • In the present study, we report the anti-tumor effects of this monoclonal antibody in mice bearing Meth-A fibrosarcoma.
  • [MeSH-major] Antibodies, Monoclonal / pharmacokinetics. Endothelium, Vascular / immunology. Fibrosarcoma / drug therapy. Fibrosarcoma / radiotherapy. Iodine Radioisotopes / therapeutic use. Zinostatin / therapeutic use
  • [MeSH-minor] Animals. Antibody Specificity. Body Weight. Female. Hemorrhage. Immunoglobulin G. Mice. Mice, Inbred BALB C. Necrosis. Radioimmunotherapy / methods. Rats. Tissue Distribution

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  • (PMID = 11123432.001).
  • [ISSN] 0910-5050
  • [Journal-full-title] Japanese journal of cancer research : Gann
  • [ISO-abbreviation] Jpn. J. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 0 / Iodine Radioisotopes; 9014-02-2 / Zinostatin
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9. Miller SD, Mohiuddin I, Cao XX, Ozvaran MK, Daniel JC, Roy Smythe W: Gene therapy for sarcoma utilizing adenoviral transfer of the beta-glucuronidase and bax genes and an anthracyline prodrug. J Surg Res; 2004 Oct;121(2):153-8
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  • [Title] Gene therapy for sarcoma utilizing adenoviral transfer of the beta-glucuronidase and bax genes and an anthracyline prodrug.
  • Use of this prodrug with adenoviral transfer of beta-glucuronidase (AdBG) is limited by the drug's inability to enter cells and intracellular retention of BG after transduction.
  • MATERIALS AND METHODS: Fibrosarcoma cells were treated with AdBG alone, AdBG plus HMR1826, AdBG followed by beta-galactosidase (AdLacZ) plus HMR1826, and AdBG followed by AdBax with no prodrug.
  • [MeSH-major] Doxorubicin / analogs & derivatives. Doxorubicin / therapeutic use. Fibrosarcoma / therapy. Genetic Therapy. Glucuronates / therapeutic use. Glucuronidase / genetics. Prodrugs / therapeutic use. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Adenoviridae / genetics. Animals. Anthracyclines / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Apoptosis / genetics. Cell Line, Tumor. Combined Modality Therapy. Drug Screening Assays, Antitumor. Gene Transfer Techniques. Genetic Vectors. Intracellular Membranes / metabolism. Rats. Rats, Inbred F344. bcl-2-Associated X Protein

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  • [Copyright] Copyright 2004 Elsevier Inc.
  • (PMID = 15501454.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0 / Bax protein, rat; 0 / Glucuronates; 0 / N-(4-glucuronyl-3-nitrobenzyloxycarbonyl)doxorubicin; 0 / Prodrugs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 80168379AG / Doxorubicin; EC 3.2.1.31 / Glucuronidase
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10. Murugesan S, Shetty SJ, Srivastava TS, Samuel AM, Noronha OP: Preparation and biological evaluation of the new chlorin photosensitizer T3,4BCPC for detection and treatment of tumors. J Photochem Photobiol B; 2002 Aug;68(1):33-8
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  • [Title] Preparation and biological evaluation of the new chlorin photosensitizer T3,4BCPC for detection and treatment of tumors.
  • The radiotracer was evaluated for tissue distribution in Wistar rats.
  • In N-nitrosomethylurea (NMU)-induced rat mammary tumors, the labeled ligand showed a five-fold tumor to muscle (T/M) ratio compared to 99mTc(V)-DMSA (3-fold) and 201TlCl (3-fold).
  • However, in the transplanted rat C(6)-glioma, the T/M ratio of the labeled compound was appreciably higher (four-fold) than that noted with 99mTc(V)-DMSA (two-fold), 201TlCl (three-fold) and 99mTc-citrate (more than three-fold).
  • These findings suggest that the radiolabeled T3,4BCPC may have potential for the detection of cancer.
  • In order to ascertain the efficacy of the compound for photodynamic therapy applications, a preclinical PDT study was carried out in fibrosarcoma-bearing mice after injecting 5.0 mg/kg body weight of the T3,4BCPC.
  • The labeled agent could also be useful in monitoring the progression/regression of tumors before, during, and after chemotherapy, radiation therapy or PDT.
  • [MeSH-major] Anthracenes / pharmacokinetics. Anthracenes / therapeutic use. Glioma / drug therapy. Mammary Neoplasms, Experimental / drug therapy. Neoplasms / drug therapy. Photosensitizing Agents / pharmacokinetics. Photosensitizing Agents / therapeutic use. Porphyrins / therapeutic use. Technetium
  • [MeSH-minor] Animals. Female. Isotope Labeling / methods. Male. Methylnitrosourea. Radiopharmaceuticals / chemical synthesis. Radiopharmaceuticals / therapeutic use. Rats. Rats, Wistar. Time Factors. Tissue Distribution

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  • [Copyright] Copyright 2002 Elsevier Science B.V.
  • (PMID = 12208034.001).
  • [ISSN] 1011-1344
  • [Journal-full-title] Journal of photochemistry and photobiology. B, Biology
  • [ISO-abbreviation] J. Photochem. Photobiol. B, Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / 5,10,15,20-tetrakis(3,4-bis(carboxymethyleneoxy)phenyl)chlorin; 0 / Anthracenes; 0 / Photosensitizing Agents; 0 / Porphyrins; 0 / Radiopharmaceuticals; 684-93-5 / Methylnitrosourea; 7440-26-8 / Technetium
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11. Cole PD, Kamen BA, Gorlick R, Banerjee D, Smith AK, Magill E, Bertino JR: Effects of overexpression of gamma-Glutamyl hydrolase on methotrexate metabolism and resistance. Cancer Res; 2001 Jun 1;61(11):4599-604
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  • Increased expression of GGH has been shown to be associated with resistance to MTX in human sarcoma cell lines and a rat hepatoma cell line.
  • To clarify the specific role of GGH in determining MTX sensitivity, we investigated the phenotype produced by forced GGH overexpression in two cell types.
  • The full-length cDNA for GGH, subcloned into a constitutive expression vector, was transfected into a human fibrosarcoma (HT-1080) and a human breast carcinoma (MCF-7) cell line.
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Drug Resistance, Neoplasm. Fibrosarcoma / drug therapy. Fibrosarcoma / enzymology. Folic Acid / physiology. Humans. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tetrahydrofolates / pharmacokinetics. Transfection. Tumor Cells, Cultured

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  • (PMID = 11389096.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09512; United States / NCI NIH HHS / CA / CA25933; United States / NCI NIH HHS / CA / CA82425
  • [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 / Antimetabolites, Antineoplastic; 0 / RNA, Messenger; 0 / Tetrahydrofolates; 134-35-0 / 5-methyltetrahydrofolate; 935E97BOY8 / Folic Acid; EC 3.4.19.9 / gamma-Glutamyl Hydrolase; YL5FZ2Y5U1 / Methotrexate
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12. Jones HJ, Vernon DI, Brown SB: Photodynamic therapy effect of m-THPC (Foscan) in vivo: correlation with pharmacokinetics. Br J Cancer; 2003 Jul 21;89(2):398-404
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  • [Title] Photodynamic therapy effect of m-THPC (Foscan) in vivo: correlation with pharmacokinetics.
  • The pharmacokinetics of m-THPC in a rat tumour model was determined using (14)C m-THPC in an LSBD(1) fibrosarcoma implanted into BDIX rats.
  • The photodynamic therapy (PDT) efficacy was determined at different drug administrations to light intervals and correlated with the tumour and plasma pharmacokinetic data.
  • Tissues of the reticuloendothelial system showed high accumulation of m-THPC, particularly the liver.
  • PDT efficacy of m-THPC over the same time course seemed to exhibit two peaks of activity (2 and 24 h), in terms of tumour growth delay with the peak at 24 h postinjection correlating to the maximum tumour concentration.
  • [MeSH-minor] Animals. Disease Models, Animal. Drug Administration Schedule. Fibrosarcoma / drug therapy. Half-Life. Kinetics. Male. Neoplasms, Experimental. Photochemotherapy. Rats

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  • (PMID = 12865935.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mesoporphyrins; 0 / Photosensitizing Agents; FU21S769PF / temoporfin
  • [Other-IDs] NLM/ PMC2394256
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13. Ciocca DR, Rozados VR, Cuello Carrión FD, Gervasoni SI, Matar P, Scharovsky OG: Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin. Cell Stress Chaperones; 2003;8(1):26-36
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  • Heat shock protein 27 (Hsp27) and Hsp70 have been involved in resistance to anticancer drugs in human breast cancer cells growing in vitro and in vivo.
  • In this study, we examined the expression of Hsp25 (the rodent homologue to human Hsp27) and Hsp70 in 3 different rodent tumors (a mouse breast carcinoma, a rat sarcoma, and a rat lymphoma maintained by subcutaneous passages) treated in vivo with doxorubicin (DOX) and lovastatin (LOV).
  • All tumors showed massive cell death under control untreated conditions, and this massive death increased after cytotoxic drug administration.
  • The tumor type that was more resistant to cell death was the sarcoma, and this was found in sarcomas growing both under control conditions and after cytotoxic drug administration.
  • After drug treatment, only sarcoma tumor cells showed a significant increase in Hsp70.
  • In sarcomas, Hsp25 and Hsp70 were found in viable tumor cells located around the blood vessels, and these areas showed the most resistant tumor cell phenotype after chemotherapy.
  • In conclusion, our study shows that each tumor type has unique features regarding the expression of Hsp25 and Hsp70 and that these proteins seem to be implicated in drug resistance mainly in sarcomas, making these model systems important to perform more mechanistic studies on the role of Hsps in resistance to certain cytotoxic drugs.
  • [MeSH-major] Adenocarcinoma / metabolism. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Fibrosarcoma / metabolism. HSP70 Heat-Shock Proteins / biosynthesis. Heat-Shock Proteins. Mammary Neoplasms, Animal / metabolism. Neoplasm Proteins / biosynthesis
  • [MeSH-minor] Animals. Apoptosis. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm. Endothelium, Vascular / metabolism. Female. HSP27 Heat-Shock Proteins. Lovastatin / administration & dosage. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred Strains. Rats. Rats, Inbred Strains

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  • (PMID = 12820652.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP27 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Hspb1 protein, mouse; 0 / Hspb1 protein, rat; 0 / Neoplasm Proteins; 80168379AG / Doxorubicin; 9LHU78OQFD / Lovastatin
  • [Other-IDs] NLM/ PMC514851
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14. Harhaji Trajković LM, Mijatović SA, Maksimović-Ivanić DD, Stojanović ID, Momcilović MB, Tufegdzić SJ, Maksimović VM, Marjanović ZS, Stosić-Grujicić SD: Anticancer properties of Ganoderma lucidum methanol extracts in vitro and in vivo. Nutr Cancer; 2009;61(5):696-707
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  • Furthermore, anticancer activity of GLme was demonstrated for the first time against two other rodent tumor cell lines, L929-mouse fibrosarcoma and C6-rat astrocytoma.
  • Thus, our results suggest that GLme might be a good candidate for treatment of diverse forms of cancers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drugs, Chinese Herbal / pharmacology. Melanoma, Experimental / drug therapy. Reishi / chemistry
  • [MeSH-minor] Animals. Apoptosis / drug effects. Astrocytes / pathology. Caspases / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Cells, Cultured. Gene Expression Regulation, Neoplastic. Mice. Mice, Inbred C57BL. Necrosis / chemically induced. Neoplasm Transplantation. Oxidative Stress / drug effects. Rats. Reactive Oxygen Species / analysis. Reactive Oxygen Species / antagonists & inhibitors. Serbia. Terpenes / analysis. Tumor Burden / drug effects

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  • (PMID = 19838944.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Chinese Herbal; 0 / Reactive Oxygen Species; 0 / Terpenes; EC 3.4.22.- / Caspases
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15. Grant DS, Williams TL, Zahaczewsky M, Dicker AP: Comparison of antiangiogenic activities using paclitaxel (taxol) and docetaxel (taxotere). Int J Cancer; 2003 Mar 10;104(1):121-9
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  • Tumor growth requires a competent vascular supply and angiogenesis has been considered as a potential target for the treatment of several cancers.
  • The purpose of our study was to examine and compare the effects of these drugs on angiogenic processes in vitro and in vivo.
  • These processes include: proliferation, migration and differentiation of cultured human umbilical vein endothelial cells (HUVEC) (in vitro), capillary sprouting of rat aortic ring explants (ex vivo) and HT1080 tumor growth in vivo.
  • Our results demonstrate that endothelial cells are 10-100-fold more sensitive to these drugs than tumor cells.
  • Additionally, comparison of the taxanes demonstrated that angiogenesis is blocked by both drugs primarily via inhibition of proliferation and differentiation (tube assay) and induction of cell death.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Endothelium, Vascular / drug effects. Paclitaxel / analogs & derivatives. Paclitaxel / pharmacology. Taxoids
  • [MeSH-minor] Animals. Aorta / cytology. Apoptosis / drug effects. Capillaries / drug effects. Capillaries / ultrastructure. Carcinoma, Non-Small-Cell Lung / pathology. Cell Differentiation / drug effects. Cell Division / drug effects. Cells, Cultured / drug effects. Chemotaxis / drug effects. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Fibrosarcoma / blood supply. Fibrosarcoma / drug therapy. Fibrosarcoma / pathology. Glioblastoma / pathology. Humans. Lung Neoplasms / pathology. Male. Melanoma / pathology. Mice. Mice, Nude. Neoplasm Transplantation. Rats. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / transplantation. Umbilical Veins / cytology. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12532428.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA 56036-03
  • [Publication-type] Comparative Study; 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 / Angiogenesis Inhibitors; 0 / Taxoids; 15H5577CQD / docetaxel; P88XT4IS4D / Paclitaxel
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16. Tsunoda S, Tsutsumi Y, Nakagawa S, Mayumi T: [Targeting therapy using a monoclonal antibody against tumor vascular endothelium]. Yakugaku Zasshi; 2000 Mar;120(3):256-64
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  • [Title] [Targeting therapy using a monoclonal antibody against tumor vascular endothelium].
  • Recent studies have revealed that the targeting therapy using monoclonal antibody against tumor associated antigens did not have a clinically satisfactory effect due to various physiological characters of tumor.
  • We propose a novel approach targeting tumor vascular endothelium to solve the inefficiency of common tumor missile therapy.
  • In this study, the tissue distribution of anti-tumor vascular endothelium monoclonal antibody (TES-23) produced by immunizing with plasma membrane vesicles obtained from isolated rat tumor-derived endothelial cells (TECs) was assessed in various tumor-bearing animals.
  • Radiolabeled TES-23 dramatically accumulated in KMT-17 fibrosarcoma, a source of isolated TECs after intravenous injection.
  • In Meth-A fibrosarcoma, Colon-26 adenocarcinoma in BALB/c mice and HT-1080 human tumor tissue in nude mice, radioactivities of 125I-TES-23 were also up to fifty times higher than those of control antibody with little distribution to normal tissues.
  • Furthermore, immunostaining of human tissue sections showed specific binding of TES-23 on endothelium in esophagus and colon cancers.
  • These results indicate that tumor vascular endothelial cells express a common antigen in different tumor types of various animal species.
  • In order to clarify the efficacy of TES-23 as a drug carrier, an immunoconjugate, composed of TES-23 and neocarzinostatin, was tested for its antitumor effect in vivo.
  • Thus, from a clinical view, TES-23 would be a novel drug carrier because of its high specificity to tumor vascular endothelium and its application to many types of cancer.
  • [MeSH-major] Drug Carriers. Drug Delivery Systems. Endothelium, Vascular / immunology. Immunoconjugates / therapeutic use. Neoplasms / blood supply. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / therapeutic use. Antibodies, Monoclonal / therapeutic use. Humans. Mice. Rats. Zinostatin / therapeutic use

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  • (PMID = 10723267.001).
  • [ISSN] 0031-6903
  • [Journal-full-title] Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
  • [ISO-abbreviation] Yakugaku Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Drug Carriers; 0 / Immunoconjugates; 9014-02-2 / Zinostatin
  • [Number-of-references] 44
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17. Mirshafiey A, Rehm B, Sotoude M, Razavi A, Abhari RS, Borzooy Z: Therapeutic approach by a novel designed anti-inflammatory drug, M2000, in experimental immune complex glomerulonephritis. Immunopharmacol Immunotoxicol; 2007;29(1):49-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic approach by a novel designed anti-inflammatory drug, M2000, in experimental immune complex glomerulonephritis.
  • The therapeutic efficacy of novel designed nonsteroidal anti-inflammatory drug, M2000 (beta- D- mannuronic acid) on experimental immune complex glomerulonephritis was evaluated.
  • Onset of treatment was day 56.
  • Serum (creatinine, blood urea nitrogen, cholesterol, and triglyceride) and urine (protein, urea, and creatinine) determinants were measured at the time of sacrifice.
  • The fibrosarcoma cell line was used for assaying tolerability and matrix metalloproteinase type 2 (MMP-2) activity.
  • Our data showed that M2000 therapy could significantly reduce the urinary protein excretion in treated rats versus non-treated controls.
  • Cytotoxicity analysis of M2000 showed a much higher tolerability compared with other tested drugs (diclofenac, piroxicam and dexamethasone).
  • Moreover, the toxicological study revealed that M2000 had no influence on serum (BUN, creatinine, triglyceride and cholesterol) determinants, urinary protein excretion and glomerular histology in healthy group receiving drug.
  • CONCLUSIONS: These findings suggest that treatment with M2000 can reduce proteinuria, diminish antibody production, and suppress the progression of disease in a rat model of immune complex glomerulonephritis.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Glomerulonephritis / drug therapy. Hexuronic Acids / pharmacology
  • [MeSH-minor] Animals. Antigen-Antibody Complex / metabolism. Drug Design. Drug Evaluation, Preclinical. Female. Matrix Metalloproteinase 2 / metabolism. Proteinuria / blood. Proteinuria / chemically induced. Proteinuria / drug therapy. Proteinuria / pathology. Proteinuria / urine. Rats. Rats, Sprague-Dawley. Serum Albumin, Bovine / toxicity

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  • (PMID = 17464766.001).
  • [ISSN] 0892-3973
  • [Journal-full-title] Immunopharmacology and immunotoxicology
  • [ISO-abbreviation] Immunopharmacol Immunotoxicol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antigen-Antibody Complex; 0 / Hexuronic Acids; 0 / Serum Albumin, Bovine; 980IT47Y34 / mannuronic acid; EC 3.4.24.24 / Matrix Metalloproteinase 2
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18. Gonzalez-Nicolini V, Sanchez-Bustamante CD, Hartenbach S, Fussenegger M: Adenoviral vector platform for transduction of constitutive and regulated tricistronic or triple-transcript transgene expression in mammalian cells and microtissues. J Gene Med; 2006 Oct;8(10):1208-22
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  • BACKGROUND: Adenoviral particles can efficiently transduce a broad spectrum of cell types, so they are widely used in basic research and clinical trials.
  • METHODS: We have developed a novel adenoviral vector platform for delivery of constitutive or streptogramin-inducible expression of up to three therapeutic transgenes into a variety of murine and human cell lines, primary cells and microtissues.
  • The constitutive multigene expression design enabled coordinated high-level expression of the Bacillus stearothermophilus-derived secreted alpha-amylase (SAMY), the human vascular endothelial growth factor 121 (VEGF(121)) and the human placental secreted alkaline phosphatase (SEAP) in monolayer populations and microtissues of Chinese hamster ovary cells (CHO-K1), human fibrosarcoma cells (HT-1080), primary neonatal rat cardiomyocytes (NRCs) and primary human aortic fibroblasts (HAFs).
  • Streptogramin-inducible tricistronic SAMY-VEGF(121)-SEAP expression provided excellent regulation performance-high-level induction in the presence of the streptogramin antibiotic pristinamycin I (PI), near-undetectable basal expression in the absence of PI, optimal adjustability and perfect reversibility-in all cell types, in particular in NRCs and NRC-derived myocardial microtissues.
  • CONCLUSIONS: Triple-transcript and tricistronic expression configurations conserve the DNA packaging capacity of the size-constrained viral transduction systems and enable coordinated and regulated expression of up to three therapeutic transgenes for concerted clinical interventions in future gene therapy scenarios.
  • [MeSH-minor] Animals. CHO Cells. Cells, Cultured. Cricetinae. Gene Expression Regulation / drug effects. Genes. Genetic Engineering / methods. Humans. Rats. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Regulon. Streptogramins / pharmacology

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  • [Copyright] Copyright (c) 2006 John Wiley & Sons, Ltd.
  • (PMID = 16960915.001).
  • [ISSN] 1099-498X
  • [Journal-full-title] The journal of gene medicine
  • [ISO-abbreviation] J Gene Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; 0 / Streptogramins
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19. Mirshafiey A, Cuzzocrea S, Rehm BH, Matsuo H: M2000: a revolution in pharmacology. Med Sci Monit; 2005 Aug;11(8):PI53-63
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  • BACKGROUND: The tolerability and the anti-inflammatory and immunosuppressive properties of a novel designed non-steroidal anti-inflammatory drug, M2000 (beta-D-mannuronic acid), were investigated in various experimental models.
  • Its therapeutic potency on kidney diseases was studied using experimental models of nephrosis and immune complex glomerulonephritis (ICG).
  • Biocompatibility and pharmacotoxicology assessment of M2000 was carried out using a fibrosarcoma cell line, zymography, and serum and urine determinants.
  • Lymph node cell proliferation assay in EAE confirmed the immunosuppressive efficacy of the tested drug.
  • Moreover, this drug inhibited MMP-2 activity.
  • The pharmacotoxicology study showed that M2000 is the safest anti-inflammatory and immunosuppressive drug in comparison with dexamethasone and conventional NSAIDs tested.
  • Additionally, M2000 had no ulcerogenic effect on the rat stomach.
  • CONCLUSIONS: M2000 is the first novel designed NSAID with the lowest molecular weight, no gastro-nephrotoxicity, and therapeutic effects in glomerulonephritis and nephrosis and could be strongly recommended on an extensive scale as the safest drug for decreasing anti-inflammatory reactions.
  • [MeSH-major] Arthritis, Rheumatoid / drug therapy. Glomerulonephritis / drug therapy. Hydrocarbons / pharmacology. Hydrocarbons / therapeutic use. Multiple Sclerosis / drug therapy
  • [MeSH-minor] Animals. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antibodies / immunology. Arthritis, Experimental / drug therapy. Arthritis, Experimental / pathology. Cattle. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Hindlimb / drug effects. Hindlimb / pathology. Immunosuppression. Interleukin-6 / biosynthesis. Interleukin-6 / metabolism. Lipids / blood. Male. Matrix Metalloproteinase 2 / metabolism. Mice. Neurons / drug effects. Neurons / pathology. Rats. Rats, Inbred Lew. Serum Albumin, Bovine / immunology

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  • (PMID = 16049391.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antibodies; 0 / Hydrocarbons; 0 / Interleukin-6; 0 / Lipids; 0 / Serum Albumin, Bovine; EC 3.4.24.24 / Matrix Metalloproteinase 2
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20. Wiewrodt R, Amin K, Kiefer M, Jovanovic VP, Kapoor V, Force S, Chang M, Lanuti M, Black ME, Kaiser LR, Albelda SM: Adenovirus-mediated gene transfer of enhanced Herpes simplex virus thymidine kinase mutants improves prodrug-mediated tumor cell killing. Cancer Gene Ther; 2003 May;10(5):353-64
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Herpes simplex virus 1 (HSV) thymidine kinase (tk) suicide gene together with ganciclovir (GCV) have been successfully used for the in vivo treatment of various solid tumors and for the ablation of unwanted transfused stem cells in recent clinical trials.
  • With the aim of improving this therapeutic system, we compared the potential efficacy of adenoviral (Ad) vectors expressing enhanced tk mutants in vitro and in vivo.
  • Cells expressing the two TK mutants were two-to-five-fold more sensitive to GCV when compared with Ad.HSV-tk transduced cells in all cell lines tested (five human mesotheliomas, one human lung cancer, a human cervical carcinoma, a mouse fibrosarcoma, and a rat glioma line) at equal TK expression levels.
  • The use of adenovirus-mediated gene transfer of both tk mutants dm30-tk and sr39-tk for cancer suicide gene therapy should provide a more effective and safer alternative to wild-type HSV-tk.
  • [MeSH-major] Adenoviridae / genetics. Herpesvirus 1, Human / enzymology. Neoplasms / pathology. Prodrugs / therapeutic use. Thymidine Kinase / genetics
  • [MeSH-minor] Animals. Antiviral Agents / pharmacology. Apoptosis / drug effects. Binding Sites. Female. Ganciclovir / pharmacology. Gene Transfer Techniques. Genes, Transgenic, Suicide. Genetic Vectors. Humans. Mice. Mice, Inbred BALB C. Mice, SCID. Mutagenesis. Rats. Transfection. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12719705.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA85939; United States / PHS HHS / / P01 66726; United States / NCI NIH HHS / CA / P50-CA-83638
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Prodrugs; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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21. Harhaji-Trajkovic L, Vilimanovich U, Kravic-Stevovic T, Bumbasirevic V, Trajkovic V: AMPK-mediated autophagy inhibits apoptosis in cisplatin-treated tumour cells. J Cell Mol Med; 2009 Sep;13(9B):3644-54
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The role of autophagy in cisplatin anticancer action was investigated using human U251 glioma, rat C6 glioma and mouse L929 fibrosarcoma cell lines.
  • A dose- and time-dependent induction of autophagy was observed in tumour cells following cisplatin treatment, as demonstrated by up-regulation of autophagy-inducing protein beclin-1 and subsequent appearance of acridine orange-stained acidic autophagic vesicles.
  • [MeSH-major] AMP-Activated Protein Kinases / metabolism. Apoptosis. Cisplatin / pharmacology. Neoplasms / drug therapy. Neoplasms / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Autophagy. Cell Line, Tumor. Dose-Response Relationship, Drug. Gene Silencing. Humans. Mice. Microscopy, Electron, Transmission / methods. Rats. TOR Serine-Threonine Kinases / metabolism

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  • (PMID = 20196784.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / AMP-Activated Protein Kinases; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC4516513
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