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1. Ramalho RT, Aydos RD, Cereda MP: Evaluation of acetone cyanohydrin effect in 'in vitro' inativation of the Ehrlich ascites tumor cells. Acta Cir Bras; 2010 Feb;25(1):111-6
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  • [Title] Evaluation of acetone cyanohydrin effect in 'in vitro' inativation of the Ehrlich ascites tumor cells.
  • PURPOSE: To evaluate the antitumor effect of acetone cyanohydrin in Ehrlich ascites tumor cells in vitro.
  • METHODS: The Ehrlich ascites tumor cells and lymphocytes were incubated with different concentrations of acetone cyanohydrin (0, 0.5, 1.0, 2.0, 10.0, 20.0 and 30.0 microg x mL(-1)), After 1, 2, 3, 4, 18 and 24 hours cell viability tests were performed by the trypan blue method.
  • RESULTS: The results demonstrated a dose-dependent cytotoxic effect against the cells of Ehrlich ascites tumor.
  • CONCLUSIONS: At low concentrations of 0.5, 1.0 and 2.0 microg x mL(-1), more than 90% of cell death was observed only after 24 hours of incubation which is the evidence that the tumor cell has the ability to poison cumulatively and irreversibly itself with the acetone cyanohydrin when compared with the results presented by human lymphocytes that the same doses and at the same time of incubation reached a maximum of 30% of cell death, suggesting an activity of rhodanese differentiated between the two cells.

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  • (PMID = 20126898.001).
  • [ISSN] 1678-2674
  • [Journal-full-title] Acta cirurgica brasileira
  • [ISO-abbreviation] Acta Cir Bras
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitriles; CO1YOV1KFI / acetone cyanohydrin
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2. Hoffmann EK, Pedersen SF: Shrinkage insensitivity of NKCC1 in myosin II-depleted cytoplasts from Ehrlich ascites tumor cells. Am J Physiol Cell Physiol; 2007 May;292(5):C1854-66
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  • [Title] Shrinkage insensitivity of NKCC1 in myosin II-depleted cytoplasts from Ehrlich ascites tumor cells.
  • We show that in cytoplasts, plasma membrane vesicles detached from Ehrlich ascites tumor cells (EATC) by cytochalasin treatment, NKCC1 activity evaluated as bumetanide-sensitive (86)Rb influx was increased compared with the basal level in intact cells yet could not be further increased by osmotic shrinkage.
  • [MeSH-major] Actins / metabolism. Carcinoma, Ehrlich Tumor / metabolism. Cell Membrane / metabolism. Cell Size. Myosin Type II / metabolism. Myosin-Light-Chain Kinase / metabolism. Sodium-Potassium-Chloride Symporters / metabolism

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  • (PMID = 17229812.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Hypertonic Solutions; 0 / Isoquinolines; 0 / Oxazoles; 0 / Protein Kinase Inhibitors; 0 / Rubidium Radioisotopes; 0 / Slc12a2 protein, mouse; 0 / Sodium Potassium Chloride Symporter Inhibitors; 0 / Sodium-Potassium-Chloride Symporters; 0 / Solute Carrier Family 12, Member 2; 0 / Sulfonamides; 0Y2S3XUQ5H / Bumetanide; 101932-71-2 / calyculin A; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinase Type II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.18 / Myosin-Light-Chain Kinase; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.6.1.- / Myosin Type II; H88EPA0A3N / Staurosporine
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3. Kametani S, Kojima-Yuasa A, Kikuzaki H, Kennedy DO, Honzawa M, Matsui-Yuasa I: Chemical constituents of cape aloe and their synergistic growth-inhibiting effect on Ehrlich ascites tumor cells. Biosci Biotechnol Biochem; 2007 May;71(5):1220-9
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  • [Title] Chemical constituents of cape aloe and their synergistic growth-inhibiting effect on Ehrlich ascites tumor cells.
  • The constituents of cape aloe were investigated after a preliminary screening of the growth-inhibiting effect on Ehrlich ascites tumor cells (EATC) of several extracts of this plant.
  • [MeSH-major] Aloe / chemistry. Antineoplastic Agents / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Phytotherapy

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  • (PMID = 17485848.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Acetophenones; 0 / Anthraquinones; 0 / Antineoplastic Agents; 0 / Benzaldehydes; 0 / Catechols; 0 / Chromones; 0 / Plant Extracts; 0 / Powders; 588X2YUY0A / Methylene Chloride; C8IYT9CR7C / aloe emodin; G1L3HT4CMH / 4-hydroxyacetophenone; KA46RNI6HN / Emodin; LF3AJ089DQ / catechol; O1738X3Y38 / 4-hydroxybenzaldehyde
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4. Liu JZ, Chen SG, Bin Z, Wang CB, Li GY, Wang LX: Antitumor effect of the seashell protein Haishengsu on Ehrlich ascites tumor: an experimental study. J Nat Med; 2009 Oct;63(4):459-62
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  • [Title] Antitumor effect of the seashell protein Haishengsu on Ehrlich ascites tumor: an experimental study.
  • The aim of the study was to investigate the in vivo effect of the seashell protein Haishengsu (HSS) on Ehrlich ascites tumor.
  • Mice were inoculated with Ehrlich ascites tumor cells and randomly divided into three HSS groups and a control group.
  • In comparison with control group, the mice receiving pretreatment of HSS had longer survival times and greater life spans following inoculation of the ascites tumor (P < 0.05).
  • HSS therefore prolongs survival times and increases the life spans of mice bearing Ehrlich ascites tumor.
  • Pretreatment with HSS also diminishes the detrimental effect of Ehrlich ascites tumor on the prognosis of these animals.
  • [MeSH-major] Albumins / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Drugs, Chinese Herbal / therapeutic use

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  • (PMID = 19536610.001).
  • [ISSN] 1861-0293
  • [Journal-full-title] Journal of natural medicines
  • [ISO-abbreviation] J Nat Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Albumins; 0 / Antineoplastic Agents; 0 / Drugs, Chinese Herbal; 0 / haishengsu
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5. Kwiecień I, Sokołowska M, Włodek L: Nephroprotective effect of cystathionine is due to its diverse action on the kidney and Ehrlich ascites tumor cells. Pharmacol Rep; 2007 Sep-Oct;59(5):553-64
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  • [Title] Nephroprotective effect of cystathionine is due to its diverse action on the kidney and Ehrlich ascites tumor cells.
  • Tumor cells, unlike normal cells, are characterized by trace cystathionase (CST) activity and sulfane sulfur levels.
  • The present studies aimed to established whether cystathionine (CT), a substrate of cystathionase, can selectively influence the thiol-dependent antioxidant power of the kidney and Ehrlich ascites tumor (EAT).
  • CT treatment reversed the changes in renal concentrations of non-protein thiols (NPSH), reactive oxygen species (ROS), sulfane sulfur and activities of rhodanese, cystathionase and glutathione S-transferase (GST) in tumor-bearing mice, which returned to the level observed in healthy animals.
  • It indicates that CT can selectively protect the kidney of tumor-bearing mice against nephrotoxicity of drugs as well as restore biological function of sulfane sulfur.
  • On the other hand, cisplatin (CP) did not affect any of the parameters under study in the kidney of tumor-bearing mice.
  • Interestingly, cisplatin markedly lowered glutathione S-transferase activity and increased sulfane sulfur level and rhodanese activity in tumor cells.
  • It is also worth noting that CP doses devoid of nephrotoxic effect in tumor-bearing mice could enhance cystathionine action on the kidney, causing an additional increase in NPSH and CST and rhodanese activity.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Carcinoma, Ehrlich Tumor / metabolism. Cisplatin / adverse effects. Cystathionine / pharmacology. Kidney / drug effects. Protective Agents / pharmacology
  • [MeSH-minor] Anaerobiosis. Animals. Antioxidants / metabolism. Cystathionine gamma-Lyase / metabolism. Cysteine / metabolism. Female. Glutathione Transferase / metabolism. Mice. Reactive Oxygen Species / metabolism. Sulfhydryl Compounds / metabolism. Thiosulfate Sulfurtransferase / metabolism. Tumor Cells, Cultured. gamma-Glutamyltransferase / metabolism

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  • (PMID = 18048956.001).
  • [ISSN] 1734-1140
  • [Journal-full-title] Pharmacological reports : PR
  • [ISO-abbreviation] Pharmacol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Protective Agents; 0 / Reactive Oxygen Species; 0 / Sulfhydryl Compounds; 375YFJ481O / Cystathionine; EC 2.3.2.2 / gamma-Glutamyltransferase; EC 2.5.1.18 / Glutathione Transferase; EC 2.8.1.1 / Thiosulfate Sulfurtransferase; EC 4.4.1.1 / Cystathionine gamma-Lyase; K848JZ4886 / Cysteine; Q20Q21Q62J / Cisplatin
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6. Salgado FL, Lopes Filho GJ, de Moura LA: Effect of experimental ehrlich ascites tumors on healing of abdominal wall wounds in mice. Wounds; 2009 Oct;21(10):262-6
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  • [Title] Effect of experimental ehrlich ascites tumors on healing of abdominal wall wounds in mice.
  • The present study aimed to analyze histological modifications induced by the presence of Ehrlich ascites tumors on laparotomic surgical scars in BALB/c mice.
  • Half of the mice were injected with Ehrlich tumor cells, and 7 days later (day 7) all mice underwent laparotomy.
  • On day 11, the scar was resected in 10 mice with the tumor and in the 10 control mice.
  • Mice injected with tumor cells gained weight due to ascites growth.
  • Histologic results showed that Ehrlich ascites tumor cells did not affect initial acute inflammation, re-epithelization, and formation of granulation tissue (P = ns).
  • Chronic inflammation and fibroblast proliferation were, however, significantly decreased in mice with tumors, whereas collagenization had increased (P = 0.001).
  • These results show that Ehrlich ascites tumors affect the healing process in mice.

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  • (PMID = 25902710.001).
  • [ISSN] 1044-7946
  • [Journal-full-title] Wounds : a compendium of clinical research and practice
  • [ISO-abbreviation] Wounds
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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7. Kametani S, Oikawa T, Kojima-Yuasa A, Kennedy DO, Norikura T, Honzawa M, Matsui-Yuasa I: Mechanism of growth inhibitory effect of cape aloe extract in ehrlich ascites tumor cells. J Nutr Sci Vitaminol (Tokyo); 2007 Dec;53(6):540-6
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  • [Title] Mechanism of growth inhibitory effect of cape aloe extract in ehrlich ascites tumor cells.
  • However, the investigations on an anti-tumor activity in cape aloe extract are very few and subsequent mechanisms have not been well elucidated.
  • In this study, we examined the effect of the selective growth inhibitory activity of cape aloe extract and found that the cape aloe extract, especially the dichloromethane (CH(2)Cl(2)) extract, caused a dose-dependent growth inhibitory effect in Ehrlich ascites tumor cells (EATC), but not in mouse embryo fibroblast (NIH3T3) cells, which was used as a normal cell model.
  • [MeSH-major] Aloe. Carcinoma, Ehrlich Tumor / pathology. Growth Inhibitors / pharmacology. Plant Extracts / pharmacology
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA / biosynthesis. Dose-Response Relationship, Drug. G1 Phase / drug effects. G2 Phase / drug effects. Mice. NIH 3T3 Cells. Phosphorylation / drug effects. Retinoblastoma Protein / metabolism. S Phase / drug effects

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  • (PMID = 18202544.001).
  • [ISSN] 0301-4800
  • [Journal-full-title] Journal of nutritional science and vitaminology
  • [ISO-abbreviation] J. Nutr. Sci. Vitaminol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Growth Inhibitors; 0 / Plant Extracts; 0 / Retinoblastoma Protein; 9007-49-2 / DNA
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8. Prabhakar BT, Khanum SA, Jayashree K, Salimath BP, Shashikanth S: Anti-tumor and proapoptotic effect of novel synthetic benzophenone analogues in Ehrlich ascites tumor cells. Bioorg Med Chem; 2006 Jan 15;14(2):435-46
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  • [Title] Anti-tumor and proapoptotic effect of novel synthetic benzophenone analogues in Ehrlich ascites tumor cells.
  • In the present report, we investigated the anti-tumor and proapoptotic effect of benzophenones in Ehrlich ascites tumor (EAT) cells.
  • Treatment of benzophenones in vivo resulted in inhibition of proliferation of EAT cells and ascites formation.
  • These results suggest a further possible clinical application of these synthetic compounds as potent anti-tumor and proapoptotic compounds.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Benzophenones / pharmacology. Carcinoma, Ehrlich Tumor / pathology
  • [MeSH-minor] Animals. Caspase 3. Caspase Inhibitors. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. DNA, Neoplasm / drug effects. Female. Magnetic Resonance Spectroscopy. Mice. Phosphatidylserines / metabolism. Spectrometry, Mass, Electrospray Ionization. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16214348.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzophenones; 0 / Caspase Inhibitors; 0 / DNA, Neoplasm; 0 / Phosphatidylserines; 0 / Tumor Suppressor Protein p53; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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9. Rana I, Shivanandappa T: Mechanism of potentiation of endosulfan cytotoxicity by thiram in Ehrlich ascites tumor cells. Toxicol In Vitro; 2010 Feb;24(1):40-4
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  • [Title] Mechanism of potentiation of endosulfan cytotoxicity by thiram in Ehrlich ascites tumor cells.
  • Cytotoxicity of the two pesticides, thiram and endosulfan, have been studied in Ehrlich ascites tumor cells.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / pathology. Endosulfan / toxicity. Fungicides, Industrial / toxicity. Insecticides / toxicity. Thiram / toxicity

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  • (PMID = 19781625.001).
  • [ISSN] 1879-3177
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fungicides, Industrial; 0 / Insecticides; 0 / Reactive Oxygen Species; 0D771IS0FH / Thiram; 11062-77-4 / Superoxides; EC 1.1.1.27 / L-Lactate Dehydrogenase; GAN16C9B8O / Glutathione; OKA6A6ZD4K / Endosulfan
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10. Mondal N, Halder KK, Kamila MM, Debnath MC, Pal TK, Ghosal SK, Sarkar BR, Ganguly S: Preparation, characterization, and biodistribution of letrozole loaded PLGA nanoparticles in Ehrlich Ascites tumor bearing mice. Int J Pharm; 2010 Sep 15;397(1-2):194-200
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  • [Title] Preparation, characterization, and biodistribution of letrozole loaded PLGA nanoparticles in Ehrlich Ascites tumor bearing mice.
  • Biodistribution studies of (99m)Tc-labeled complexes were performed after intravenous administration in normal mice and Ehrlich Ascites tumor bearing mice.
  • The tumor concentration of LTZ-loaded PLGA NPs was 4.65 times higher than that of free LTZ at 4 h post-injection.
  • This study indicates the capability of PLGA nanopartcles in enhancing the tumor uptake of letrozole.
  • [MeSH-major] Aromatase Inhibitors / administration & dosage. Carcinoma, Ehrlich Tumor / drug therapy. Lactic Acid. Nitriles / administration & dosage. Polyglycolic Acid. Triazoles / administration & dosage

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20609382.001).
  • [ISSN] 1873-3476
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aromatase Inhibitors; 0 / Drug Carriers; 0 / Nitriles; 0 / Triazoles; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; 7440-26-8 / Technetium; 7A314HQM0I / Pentetic Acid; 7LKK855W8I / letrozole
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11. Filipek A: S100A6 and CacyBP/SIP - two proteins discovered in ehrlich ascites tumor cells that are potentially involved in the degradation of beta-catenin. Chemotherapy; 2006;52(1):32-4
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  • [Title] S100A6 and CacyBP/SIP - two proteins discovered in ehrlich ascites tumor cells that are potentially involved in the degradation of beta-catenin.
  • Originally, S100A6 was purified from Ehrlich ascites tumor cells, but later, it was found in fibroblasts, epithelial cells and in tumor cells with high metastatic activity.
  • When Ca(2+)-dependent interaction of S100A6 with target proteins was studied in Ehrlich ascites tumor cells, a novel protein, now called CacyBP/SIP, was discovered.
  • [MeSH-major] Calcium-Binding Proteins / metabolism. Carcinoma, Ehrlich Tumor / metabolism. beta Catenin / metabolism

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16340196.001).
  • [ISSN] 0009-3157
  • [Journal-full-title] Chemotherapy
  • [ISO-abbreviation] Chemotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / beta Catenin
  • [Number-of-references] 5
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12. Arimura T, Kojima-Yuasa A, Tatsumi Y, Kennedy DO, Matsui-Yuasa I: Involvement of polyamines in evening primrose extract-induced apoptosis in Ehrlich ascites tumor cells. Amino Acids; 2005 Feb;28(1):21-7
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  • [Title] Involvement of polyamines in evening primrose extract-induced apoptosis in Ehrlich ascites tumor cells.
  • We previously demonstrated that evening primrose extract (EPE) induced apoptosis and inhibited the DNA synthesis in Ehrlich ascites tumor cells (EATC) and suggested that EPE-induced inhibition of the growth of EATC are via at least two pathway differentially modulated by reactive oxygen species, notably intracellular peroxides.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Ehrlich Tumor / pathology. Oenothera biennis / chemistry. Plant Extracts / pharmacology. Polyamines / pharmacology
  • [MeSH-minor] Animals. Cell Survival / drug effects. Chromatography, High Pressure Liquid / methods. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / drug effects. Dose-Response Relationship, Drug. Putrescine / pharmacology. Spermidine / pharmacology. Spermine / pharmacology. Tumor Cells, Cultured

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  • (PMID = 15700107.001).
  • [ISSN] 0939-4451
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Plant Extracts; 0 / Polyamines; 2FZ7Y3VOQX / Spermine; U87FK77H25 / Spermidine; V10TVZ52E4 / Putrescine
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13. Belakavadi M, Prabhakar BT, Salimath BP: Purification and characterization of butyrate-induced protein phosphatase involved in apoptosis of Ehrlich ascites tumor cells. Biochim Biophys Acta; 2007 Jan;1770(1):39-47
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  • [Title] Purification and characterization of butyrate-induced protein phosphatase involved in apoptosis of Ehrlich ascites tumor cells.
  • As a model system, we used Ehrlich Ascites Tumor (EAT) cells in which BuA-treatment induces expression of a protein phosphatase enzyme.
  • [MeSH-major] Apoptosis. Butyrates / pharmacology. Carcinoma, Ehrlich Tumor / pathology. Phosphoprotein Phosphatases / metabolism

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  • (PMID = 17029793.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Butyrates; 3WHH0066W5 / Vanadates; EC 3.1.3.16 / Phosphoprotein Phosphatases
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14. Benkovic V, Horvat Knezevic A, Brozovic G, Knezevic F, Dikic D, Bevanda M, Basic I, Orsolic N: Enhanced antitumor activity of irinotecan combined with propolis and its polyphenolic compounds on Ehrlich ascites tumor in mice. Biomed Pharmacother; 2007 Jun;61(5):292-7
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  • [Title] Enhanced antitumor activity of irinotecan combined with propolis and its polyphenolic compounds on Ehrlich ascites tumor in mice.
  • The effects of the anticancer drug irinotecan combined with ethanolic extract of propolis (EEP), a water-soluble derivate of propolis (WSDP), quercetin and naringin on the growth of Ehrlich ascites tumor (EAT) and the life span of tumor-bearing Swiss albino mice were studied.
  • Irinotecan was administered i.p. at dose of 50mg kg(-1) on days 1, 13, and 19 after tumor cell inoculation.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Camptothecin / analogs & derivatives. Carcinoma, Ehrlich Tumor / drug therapy. Flavonoids / therapeutic use. Phenols / therapeutic use. Propolis / therapeutic use

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  • (PMID = 17412551.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Flavanones; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 7673326042 / irinotecan; 9009-62-5 / Propolis; 9IKM0I5T1E / Quercetin; N7TD9J649B / naringin; XT3Z54Z28A / Camptothecin
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15. Tomšík P, Stoklasová A, Mičuda S, Niang M, Šuba P, Knížek J, Řezáčová M: Evaluation of the Antineoplastic Activity of L-rhamnose in vitro. A Comparison with 2-deoxyglucose. Acta Medica (Hradec Kralove); 2008;51(2):113-119

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The effect of unsubstituted deoxyhexoses, 2-deoxy-D-glucose (2-DG) and L-fucose, on tumor cells has been reported in several papers throughout the last decades.
  • In the present study, we examined the effect of L-rhamnose on DNA and protein synthesis, growth and the potential induction of apoptosis of tumor cells in vitro.
  • Using 2-DG for comparison, we studied the effect of L-rhamnose in concentrations up to 20 (32 resp.) mmol/l on the initial velocity of the incorporation of labeled precursors of DNA and proteins in short term cultures of both mouse Ehrlich ascites tumor (EAT) and human HL-60 cells in vitro, and further, on cell proliferation and apoptosis induction in HL-60 cells.

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  • (PMID = 28550840.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; 2-deoxyglucose / Apoptosis / DNA synthesis / L-rhamnose / Protein synthesis / Tumor
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16. Davies C, Garson K, LeBoeuf F, Bell J, Weberpals J: Susceptibility of ascites tumor cells to ex-vivo killing by the oncolytic virus JX-963 in epithelial ovarian cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e16537

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Susceptibility of ascites tumor cells to ex-vivo killing by the oncolytic virus JX-963 in epithelial ovarian cancer.
  • One-third of patients with EOC will develop clinical ascites, an adverse prognostic factor.
  • The ascitic fluid is rich in tumor cells which can be purified and used as a valuable source of patient material for in vitro analysis.
  • In this study, we describe a method to evaluate the efficacy of ascitic tumor cell killing by the oncolytic virus, JX-963 (vaccinia strain) currently approved for use in a NCIC-CTG phase I trial.
  • RESULTS: A standardized protocol was developed for the collection and purification of EOC cells from patient ascites for subsequent infection and quantification of viral killing.
  • Although variable between individual samples, there was a strong correlation between escalating MOI and enhanced cell death in all patient ascites samples, when quantified by Alamar Blue assay and confirmed by flow cytometry and IHC.
  • Similar cell killing profiles by JX-963 were observed for ascites tumor cells derived from both chemotherapy-naïve patients and chemotherapy-exposed (>1 prior line of chemotherapy) patients.
  • CONCLUSIONS: EOC cells from patient ascites show effective but differential susceptibility to viral oncolysis by the JX-963 virus that appears to be independent of prior exposure to chemotherapy.

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  • (PMID = 27960776.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Bromberg N, Dreyfuss JL, Regatieri CV, Palladino MV, Durán N, Nader HB, Haun M, Justo GZ: Growth inhibition and pro-apoptotic activity of violacein in Ehrlich ascites tumor. Chem Biol Interact; 2010 Jun 7;186(1):43-52
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  • [Title] Growth inhibition and pro-apoptotic activity of violacein in Ehrlich ascites tumor.
  • Herein, violacein, a natural indolic pigment extracted from Chromobacterium violaceum, was evaluated for its antitumoral potential against the Ehrlich ascites tumor (EAT) in vivo and in vitro.
  • Moreover, doses of 0.1 and 1.0 microg kg(-1) violacein, administered intraperitoneally (i.p.) to EAT-bearing mice throughout the lifespan of the animals significantly inhibited tumor growth and increased survival of mice.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Carcinoma, Ehrlich Tumor / drug therapy. Chromobacterium / chemistry. Indoles / therapeutic use

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  • [Copyright] Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20416285.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Reactive Oxygen Species; 548-54-9 / violacein; GAN16C9B8O / Glutathione
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18. Li GY, Liu JZ, Chen SG, Wang CB, Bin Z, Wang LX: Effect of a seashell protein Haishengsu on the immunological function of mice with Ehrlich ascites tumor. Immunopharmacol Immunotoxicol; 2009;31(4):669-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of a seashell protein Haishengsu on the immunological function of mice with Ehrlich ascites tumor.
  • This study was designed to investigate the effect of a seashell protein Haishengsu (HSS) on the immuno logical function in mice with Ehrlich ascites tumor.
  • Ehrlich ascites tumor-bearing mice were divided into three HSS groups (25, 50 and 100 mg/kg, i.v., respectively), cyclophosphamide (10 mg i.p.) and control group.
  • We conclude that HSS has significant immune-modulating effect in mice with Ehrlich ascites tumor.
  • [MeSH-major] Albumins / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Ehrlich Tumor / immunology. Drugs, Chinese Herbal / therapeutic use

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  • (PMID = 19874239.001).
  • [ISSN] 1532-2513
  • [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] England
  • [Chemical-registry-number] 0 / Albumins; 0 / Drugs, Chinese Herbal; 0 / haishengsu
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19. Iciek M, Marcinek J, Mleczko U, Włodek L: Selective effects of diallyl disulfide, a sulfane sulfur precursor, in the liver and Ehrlich ascites tumor cells. Eur J Pharmacol; 2007 Aug 13;569(1-2):1-7
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  • [Title] Selective effects of diallyl disulfide, a sulfane sulfur precursor, in the liver and Ehrlich ascites tumor cells.
  • DADS efficiently corrected the concentrations of glutathione and sulfane sulfur, and ameliorated gamma-cystathionase activity that had been lowered in the livers of Ehrlich ascites tumor-bearing mice.
  • In Ehrlich ascites tumor cells, diallyl disulfide did not alter bound sulfane sulfur level, sulfotransferases activity or glutathione level.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / metabolism. Carcinoma, Ehrlich Tumor / pathology. Cell Line, Tumor. Cyanides / metabolism. Cystathionine gamma-Lyase / metabolism. Dose-Response Relationship, Drug. Female. Glutathione / metabolism. Mice. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / pathology. Neoplasms, Experimental / prevention & control. Protective Agents / metabolism. Protective Agents / pharmacology. Sulfhydryl Compounds / metabolism. Sulfides / chemistry. Sulfides / metabolism. Sulfides / pharmacology. Sulfur Compounds / metabolism. Sulfurtransferases / metabolism. Thiosulfate Sulfurtransferase / metabolism

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  • (PMID = 17560567.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Allyl Compounds; 0 / Cyanides; 0 / Disulfides; 0 / Protective Agents; 0 / Sulfhydryl Compounds; 0 / Sulfides; 0 / Sulfur Compounds; 0ZO1U5A3XX / diallyl trisulfide; 2179-57-9 / diallyl disulfide; 60G7CF7CWZ / allyl sulfide; EC 2.8.1.- / Sulfurtransferases; EC 2.8.1.1 / Thiosulfate Sulfurtransferase; EC 2.8.1.2 / 3-mercaptopyruvate sulphurtransferase; EC 4.4.1.1 / Cystathionine gamma-Lyase; GAN16C9B8O / Glutathione; I7K169J70F / n-propyl disulfide
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20. Sheela ML, Ramakrishna MK, Salimath BP: Angiogenic and proliferative effects of the cytokine VEGF in Ehrlich ascites tumor cells is inhibited by Glycyrrhiza glabra. Int Immunopharmacol; 2006 Mar;6(3):494-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiogenic and proliferative effects of the cytokine VEGF in Ehrlich ascites tumor cells is inhibited by Glycyrrhiza glabra.
  • Blood vessel plays a crucial role in solid tumor development.
  • The aqueous extract inhibits the in vivo and in vitro proliferation of Ehrlich ascites tumor cells.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / blood supply. Carcinoma, Ehrlich Tumor / drug therapy. Cell Proliferation / drug effects. Glycyrrhiza. Neovascularization, Pathologic / drug therapy. Plant Extracts / pharmacology. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Animals. Chick Embryo. Kinetics. Mice. Plant Roots / chemistry. Solvents. Tumor Cells, Cultured

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  • (PMID = 16428085.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Solvents; 0 / Vascular Endothelial Growth Factor A
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21. Ozaslan M, Didem Karagöz I, Kalender ME, Kilic IH, Sari I, Karagöz A: In vivo antitumoral effect of Plantago major L. extract on Balb/C mouse with Ehrlich ascites tumor. Am J Chin Med; 2007;35(5):841-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo antitumoral effect of Plantago major L. extract on Balb/C mouse with Ehrlich ascites tumor.
  • The aim of this study is to investigate the antitumor activity of Plantago major L. extract in Ehrlich ascites tumor (EAT) bearing Balb/C mice in vivo.
  • Treatment groups and the negative control group were injected with EAT (1 x 10(6) cells) intraperitoneally to develop ascites tumor. P. major L. extract (1%, 2% and 3% concentration extracts, 0.1 ml/day/mouse) were given p.o. for 10 alternate days.
  • Body weights of in 3 treatment groups and the negative control group were elevated because of tumor burden.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Plant Extracts / therapeutic use. Plantago / chemistry

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  • (PMID = 17963323.001).
  • [ISSN] 0192-415X
  • [Journal-full-title] The American journal of Chinese medicine
  • [ISO-abbreviation] Am. J. Chin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts
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22. Taşkin EI, Akgün-Dar K, Kapucu A, Osanç E, Doğruman H, Eraltan H, Ulukaya E: Apoptosis-inducing effects of Morinda citrifolia L. and doxorubicin on the Ehrlich ascites tumor in Balb-c mice. Cell Biochem Funct; 2009 Dec;27(8):542-6
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  • [Title] Apoptosis-inducing effects of Morinda citrifolia L. and doxorubicin on the Ehrlich ascites tumor in Balb-c mice.
  • Therefore, we investigated the cytotoxic potential of noni on Ehrlich ascites tumor grown in female Balb-c mice and also combined it with a potent anti-cancer agent, doxorubicin.
  • We found that short and long diameters of the tumor tissues were about 40-50% smaller, compared to those in control group.
  • [MeSH-major] Apoptosis / drug effects. Breast Neoplasms / drug therapy. Carcinoma, Ehrlich Tumor / drug therapy. Doxorubicin / agonists. Morinda / chemistry. Plant Extracts / administration & dosage
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Disease Models, Animal. Drug Evaluation, Preclinical. Drug Therapy, Combination. Female. Humans. Mice. Mice, Inbred BALB C. Random Allocation

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  • (PMID = 19908222.001).
  • [ISSN] 1099-0844
  • [Journal-full-title] Cell biochemistry and function
  • [ISO-abbreviation] Cell Biochem. Funct.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Plant Extracts; 80168379AG / Doxorubicin; EC 3.4.22.- / Caspase 3
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23. Tanaka H, Kageyama K, Kimura M, Iwamoto SI, Ueno Y, Asagi K, Asada R, Miwa N: Promotive effects of hyperthermia on the inhibition of DNA synthesis in ehrlich ascites tumor cells by eicosapentaenoic and docosahexaenoic acids. Exp Oncol; 2006 Sep;28(3):203-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promotive effects of hyperthermia on the inhibition of DNA synthesis in ehrlich ascites tumor cells by eicosapentaenoic and docosahexaenoic acids.
  • METHODS: A suspension of Ehrlich ascites tumor cells (EAT) was mixed with DHA or EPA in a glass tube, heated at 37 degrees C, 40 degrees C, or 42 degrees C for 1 h in a water bath, and cultured at 37 degrees C for 19 or 96 h.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / genetics. DNA Replication / drug effects. Docosahexaenoic Acids / pharmacology. Eicosapentaenoic Acid / pharmacology. Hot Temperature
  • [MeSH-minor] Animals. Biological Transport. Tumor Cells, Cultured

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  • (PMID = 17080013.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 25167-62-8 / Docosahexaenoic Acids; AAN7QOV9EA / Eicosapentaenoic Acid
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24. Tanaka H, Kageyama K, Asada R, Yoshimura N, Miwa N: Promotive effects of hyperthermia on the cytostatic activity to Ehrlich ascites tumor cells by diverse delta-alkyllactones. Exp Oncol; 2008 Jun;30(2):143-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promotive effects of hyperthermia on the cytostatic activity to Ehrlich ascites tumor cells by diverse delta-alkyllactones.
  • METHODS: A suspension of Ehrlich ascites tumor (EAT) cells was mixed with a DAL in a glass tube, heated at 37 or 42 degrees C for 30 min in a water bath, and cultured at 37 degrees C for 20 or 72 h.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / therapy. Hyperthermia, Induced. Lactones / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cell Survival. Models, Chemical. Oxidation-Reduction. Temperature

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  • (PMID = 18566579.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lactones
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25. Kumar CS, Chandru H, Sharada AC, Thimmegowda NR, Prasad SB, Kumar MK, Rangappa KS: Synthesis and evaluation of 1-benzhydryl-sulfonyl-piperazine derivatives as inhibitors of tumor growth and tumor angiogenesis of mouse ehrlich ascites tumor in vivo. Med Chem; 2008 Sep;4(5):466-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synthesis and evaluation of 1-benzhydryl-sulfonyl-piperazine derivatives as inhibitors of tumor growth and tumor angiogenesis of mouse ehrlich ascites tumor in vivo.
  • In the present study, the compounds 3(a-e) exhibited in vivo inhibition of Ehrlich ascites tumor (EAT) cell growth and increased the Median Survival Time (MST) and %ILS of EAT bearing mice.
  • Further treatment of derivatives in vivo resulted in reduction of EAT cell number and ascites formation.
  • The efficacy of the derivatives to inhibit the angiogenesis in vivo was evaluated in tumor bearing mice peritoneum and chorio allantoic membrane (CAM) model.
  • Among the compounds studied, 3e demonstrated highest tumor inhibitory and anti-angiogenic effects against mouse tumor.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Benzhydryl Compounds / pharmacology. Carcinoma, Ehrlich Tumor / pathology. Cell Proliferation / drug effects. Piperazines / pharmacology
  • [MeSH-minor] Animals. Cell Survival / drug effects. Chorioallantoic Membrane / blood supply. Chorioallantoic Membrane / metabolism. Chromatography, Liquid. Dose-Response Relationship, Drug. Magnetic Resonance Spectroscopy. Mass Spectrometry. Mice. Peritoneum / blood supply. Peritoneum / metabolism. Spectroscopy, Fourier Transform Infrared. Tumor Cells, Cultured

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  • (PMID = 18782043.001).
  • [ISSN] 1573-4064
  • [Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))
  • [ISO-abbreviation] Med Chem
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Benzhydryl Compounds; 0 / Piperazines
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26. Srivastava A, Shivanandappa T: Causal relationship between hexachlorocyclohexane cytotoxicity, oxidative stress and Na+, K +-ATPase in Ehrlich Ascites tumor cells. Mol Cell Biochem; 2006 Jun;286(1-2):87-93
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  • [Title] Causal relationship between hexachlorocyclohexane cytotoxicity, oxidative stress and Na+, K +-ATPase in Ehrlich Ascites tumor cells.
  • Role of oxidative stress and Na+,K+-ATPase in the cytotoxicity of hexachlorocyclohexane (HCH) on Ehrlich Ascites tumor (EAT) cells has been studied.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / metabolism. Carcinoma, Ehrlich Tumor / pathology. Catalase / antagonists & inhibitors. Catalase / metabolism. Cell Death / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Glutathione / metabolism. Insecticides / toxicity. L-Lactate Dehydrogenase / secretion. Lipid Peroxidation / drug effects. Male. Mice. Reactive Oxygen Species / metabolism. Superoxide Dismutase / antagonists & inhibitors. Superoxide Dismutase / metabolism. Tumor Cells, Cultured

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  • (PMID = 16432761.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Insecticides; 0 / Reactive Oxygen Species; 59NEE7PCAB / Lindane; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase; GAN16C9B8O / Glutathione
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27. Xu S, Kojima-Yuasa A, Azuma H, Kennedy DO, Konishi Y, Matsui-Yuasa I: Comparison of glutathione reductase activity and the intracellular glutathione reducing effects of 13 derivatives of 1'-acetoxychavicol acetate in Ehrlich ascites tumor cells. Chem Biol Interact; 2010 May 14;185(3):235-40
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  • [Title] Comparison of glutathione reductase activity and the intracellular glutathione reducing effects of 13 derivatives of 1'-acetoxychavicol acetate in Ehrlich ascites tumor cells.
  • In the current study, we investigated the inhibitory activities of 13 derivatives of (S)-ACA on tumor cell viability, intracellular GSH level and GR activity.
  • Correlations were found among a decrease in cell viability, intracellular GSH levels and the activity of GR in Ehrlich ascites tumor cells treated with the various ACA analogues.
  • [MeSH-major] Benzyl Alcohols / chemistry. Benzyl Alcohols / pharmacology. Carcinoma, Ehrlich Tumor / metabolism. Glutathione / metabolism. Glutathione Reductase / metabolism

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20230805.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Benzyl Alcohols; 52946-22-2 / 1'-acetoxychavicol acetate; EC 1.8.1.7 / Glutathione Reductase; GAN16C9B8O / Glutathione
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28. Kumar CA, Jayarama S, Basappa, Salimath BP, Rangappa KS: Pro-apoptotic activity of imidazole derivatives mediated by up-regulation of Bax and activation of CAD in Ehrlich Ascites Tumor cells. Invest New Drugs; 2007 Aug;25(4):343-50
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  • [Title] Pro-apoptotic activity of imidazole derivatives mediated by up-regulation of Bax and activation of CAD in Ehrlich Ascites Tumor cells.
  • In this study we report that, imidazole derivatives can induce apoptosis in Ehrlich ascites tumor (EAT) cells, which is clearly evident from annexin-V staining, flow cytometric analysis of cell cycle phase distribution and DNA fragmentation.
  • Delineating further into molecular mechanisms leading to apoptosis of EAT cells, we observed that imidazole derivatives induce tumor cell death by the up-regulation of proto-oncoprotein Bax, release of cytochrome c from the mitochondria which activates caspase-3 and activated caspase-3 activates CAD (Caspase Activated DNase) causes DNA fragmentation.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor. Caspase 3 / metabolism. Cytochromes c / biosynthesis. DNA Fragmentation / drug effects. Enzyme Activation. Female. Flow Cytometry. Mice. Protein Transport. Tumor Cells, Cultured. Up-Regulation

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  • (PMID = 17372679.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Imidazoles; 0 / bcl-2-Associated X Protein; 9007-43-6 / Cytochromes c; EC 3.1.- / Deoxyribonucleases; EC 3.1.- / caspase-activated deoxyribonuclease; EC 3.4.22.- / Caspase 3
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29. Zinchenko VP, Kasymov VA, Li VV, Kaĭmachnikov NP: [The calmodulin inhibitor R24571 induces a short-term Ca2+ entry and a pulse-like secretion of ATP in Ehrlich ascites tumor cells]. Biofizika; 2005 Nov-Dec;50(6):1055-69
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  • [Title] [The calmodulin inhibitor R24571 induces a short-term Ca2+ entry and a pulse-like secretion of ATP in Ehrlich ascites tumor cells].
  • The properties of the Ca2+ channel induced by a calmodulin inhibitor in Ehrlich ascites tumor cells were investigated using fluorescent indicators Indo-1 and chlortetracycline.
  • [MeSH-major] Adenosine Triphosphate / secretion. Calcium / metabolism. Calcium Channels / metabolism. Calmodulin / antagonists & inhibitors. Carcinoma, Ehrlich Tumor / metabolism. Enzyme Inhibitors / pharmacology. Imidazoles / pharmacology

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  • (PMID = 16358785.001).
  • [ISSN] 0006-3029
  • [Journal-full-title] Biofizika
  • [ISO-abbreviation] Biofizika
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Calmodulin; 0 / Enzyme Inhibitors; 0 / Imidazoles; 57265-65-3 / calmidazolium; 8L70Q75FXE / Adenosine Triphosphate; SY7Q814VUP / Calcium
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30. Thiry M, Ploton D: Isolation of nucleoli from Ehrlich ascites tumor cells and dynamics of nascent RNA within isolated nucleoli. Methods Mol Biol; 2008;463:111-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolation of nucleoli from Ehrlich ascites tumor cells and dynamics of nascent RNA within isolated nucleoli.
  • Here we describe a new, rapid method for isolating nucleoli from Ehrlich tumor cells that preserves their morphological integrity and high transcriptional activity.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / metabolism. Cell Nucleolus / metabolism. Cell Nucleus / metabolism. RNA / metabolism

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  • (PMID = 18951164.001).
  • [ISSN] 1940-6029
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA Precursors; 0 / RNA, Ribosomal; 63231-63-0 / RNA; UT0S826Z60 / Uridine Triphosphate
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31. Haeffner EW, Wittmann U, Kiesewetter L, Zimmermann HP, Stöhr M, Spiess E: Effect of reduced levels of the LDL receptor of Ehrlich ascites tumor cells on cholesterol uptake and cell proliferation: a coculture study with baby hamster kidney cells. Cell Biol Int; 2007 Aug;31(8):790-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of reduced levels of the LDL receptor of Ehrlich ascites tumor cells on cholesterol uptake and cell proliferation: a coculture study with baby hamster kidney cells.
  • We have introduced a heterologous coculture model between Ehrlich ascites tumor (EAT) and baby hamster kidney cells (PtK2), and we have studied the influence of PtK2 cells and their newly synthesized cholesterol on uptake and tumor cell proliferation.
  • PtK2 cells produce about five times more cholesterol as compared to EAT cells, and they support tumor cell growth in coculture experiments.
  • These data demonstrate a metabolic interaction between normal and tumor cells mediated via the exchange of cholesterol, an important membrane constituent.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / metabolism. Cell Proliferation. Cholesterol / metabolism. Receptors, LDL / metabolism

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  • (PMID = 17349806.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acyl Coenzyme A; 0 / Antibodies, Monoclonal; 0 / Receptors, LDL; 1553-55-5 / 3-hydroxy-3-methylglutaryl-coenzyme A; 97C5T2UQ7J / Cholesterol; 9LHU78OQFD / Lovastatin
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32. Gupta S, Mathur R, Dwarakanath BS: The glycolytic inhibitor 2-deoxy-D-glucose enhances the efficacy of etoposide in ehrlich ascites tumor-bearing mice. Cancer Biol Ther; 2005 Jan;4(1):87-94
Hazardous Substances Data Bank. ETOPOSIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The glycolytic inhibitor 2-deoxy-D-glucose enhances the efficacy of etoposide in ehrlich ascites tumor-bearing mice.
  • Earlier studies have shown that 2-deoxy-D-glucose (2-DG), a glucose analogue and inhibitor of glycolytic ATP production significantly enhances the cytotoxic effects of anticancer agents like topoisomerase inhibitors (etoposide and camptothecin) and a radiomimetic drug (bleomycin) in established human tumor cell lines.
  • Therefore, combination of 2-DG and DNA damage causing cytotoxic agents could be very useful in enhancing local tumor control.
  • The purpose of the present studies was to investigate the therapeutic effects of etoposide and 2-DG in Ehrlich ascites tumor (EAT) bearing mice, grown as solid tumor as well as in the ascites form.
  • Cell growth, cell cycle perturbations (flow cytometry), cytogenetic damage (micronuclei assay) and apoptosis (DNA content, morphological changes) were studied as parameters of cellular response, while delay in tumor growth and cure rate (tumor free survival) were evaluated as parameters of systemic response.
  • Intraperitoneal administration of etoposide (30 mg/Kg b. wt.) resulted in significant tumor growth delay and cure (approximately 11%) only in subcutaneous tumors leading to local tumor control.
  • ; 4 h after etoposide injection), these effects were further enhanced resulting in a cure rate of approximately 22% in case of subcutaneous tumors and 20% in ascites bearing mice.
  • Analysis of cells obtained from ascitic fluid as well as solid tumors during follow up clearly showed that etoposide induced cell death was mainly due to apoptosis, which was enhanced further by 2-DG.
  • These results indicate that the administration of 2-DG can improve the local control of tumors without increasing normal tissue toxicity, thereby enhancing the therapeutic efficacy of topoisomerase inhibitor based anticancer drugs like etoposide.
  • [MeSH-major] Antimetabolites / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Ehrlich Tumor / pathology. Deoxyglucose / pharmacology. Etoposide / pharmacology

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  • (PMID = 15711125.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 9G2MP84A8W / Deoxyglucose
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33. Lialiaris TS, Papachristou F, Mourelatos C, Simopoulou M: Antineoplastic and cytogenetic effects of chlorpromazine on human lymphocytes in vitro and on Ehrlich ascites tumor cells in vivo. Anticancer Drugs; 2009 Sep;20(8):746-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antineoplastic and cytogenetic effects of chlorpromazine on human lymphocytes in vitro and on Ehrlich ascites tumor cells in vivo.
  • The inhibitory effect of phenothiazines in tumor growth and cancer cell proliferation in vitro and in vivo has been established.
  • In-vitro studies were performed on human lymphocyte cultures and in-vivo studies involved Ehrilch ascites tumor (EAT) cells.
  • The combination of chlorpromazine plus mitomycin C exerted cytostatic and cytotoxic actions in EAT cells, significantly increased the survival span of the mice inoculated with EAT cells, and suppressed the expected tumor growth increase.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / drug therapy. Chlorpromazine / pharmacology. Chlorpromazine / therapeutic use. Lymphocytes / drug effects. Sister Chromatid Exchange / drug effects

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  • (PMID = 19584706.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 3G6A5W338E / Caffeine; 50SG953SK6 / Mitomycin; U42B7VYA4P / Chlorpromazine
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34. Ozcan Arican G, Ozalpan A: Evaluation of the effect of paclitaxel, epirubicin and tamoxifen by cell kinetics parameters in estrogen-receptor-positive ehrlich ascites tumor (eat) cells growing in vitro. Acta Biol Hung; 2007 Mar;58(1):49-59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the effect of paclitaxel, epirubicin and tamoxifen by cell kinetics parameters in estrogen-receptor-positive ehrlich ascites tumor (eat) cells growing in vitro.
  • In this study the antiproliferative effects of Paclitaxel (PAC), Epirubicin (EPI) and Tamoxifen (TAM) on growth kinetics of Ehrlich Ascites Tumor (EAT) cells were examined in culture.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / pathology. Cell Division / drug effects. Cell Survival / drug effects. Kinetics. Male. Mice. Mice, Inbred BALB C. Mitotic Index. Polyploidy. Tumor Cells, Cultured

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  • (PMID = 17385543.001).
  • [ISSN] 0236-5383
  • [Journal-full-title] Acta biologica Hungarica
  • [ISO-abbreviation] Acta. Biol. Hung.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 094ZI81Y45 / Tamoxifen; 3Z8479ZZ5X / Epirubicin; P88XT4IS4D / Paclitaxel
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35. Ramachandra S, D'Souza SS, Gururaj AE, Shaila MS, Salimath BP: Paracrine action of sFLT-1 secreted by stably-transfected Ehrlich ascites tumor cells and therapy using sFLT-1 inhibits ascites tumor growth in vivo. J Gene Med; 2009 May;11(5):422-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paracrine action of sFLT-1 secreted by stably-transfected Ehrlich ascites tumor cells and therapy using sFLT-1 inhibits ascites tumor growth in vivo.
  • A soluble form of Flt-1, a VEGF receptor, is potentially useful as an antagonist of VEGF, and accumulating evidence suggests the applicability of sFlt-1 in tumor suppression.
  • In the present study, we have developed and tested strategies targeted specifically to VEGF for the treatment of ascites formation.
  • METHODS: As an initial strategy, we produced recombinant sFLT-1 in the baculovirus expression system and used it as a trap to sequester VEGF in the murine ascites carcinoma model.
  • The effect of the treatment on the weight of the animal, cell number, ascites volume and proliferating endothelial cells was studied.
  • The second strategy involved, producing Ehrlich ascites tumor (EAT) cells stably transfected with vectors carrying cDNA encoding truncated form of Flt-1 and using these cells to inhibit ascites tumors in a nude mouse model.
  • RESULTS: The sFLT-1 produced by the baculovirus system showed potent anti-angiogenic activity as assessed by rat cornea and tube formation assay. sFLT-1 treatment resulted in reduced peritoneal angiogenesis with a concomitant decrease in tumor cell number, volume of ascites, amount of free VEGF and the number of invasive tumor cells as assayed by CD31 staining.
  • EAT cells stably transfected with truncated form of Flt-1 also effectively reduced the tumor burden in nude mice transplanted with these cells, and demonstrated a reduction in ascites formation and peritoneal angiogenesis.
  • CONCLUSIONS: The inhibition of peritoneal angiogenesis and tumor growth by sequestering VEGF with either sFlt-1 gene expression by recombinant EAT cells or by direct sFLT-1 protein therapy is shown to comprise a potential therapy.
  • [MeSH-major] Ascites / pathology. Ascites / therapy. Paracrine Communication. Transfection. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-1 / therapeutic use

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  • [Copyright] (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19266483.001).
  • [ISSN] 1521-2254
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
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36. Kumar A, D'Souza SS, Tickoo S, Salimath BP, Singh HB: Antiangiogenic and proapoptotic activities of allyl isothiocyanate inhibit ascites tumor growth in vivo. Integr Cancer Ther; 2009 Mar;8(1):75-87
Hazardous Substances Data Bank. ALLYL ISOTHIOCYANATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiangiogenic and proapoptotic activities of allyl isothiocyanate inhibit ascites tumor growth in vivo.
  • The authors investigate the antiangiogenic and proapoptotic effects of mustard essential oil containing allyl isothiocyanate (AITC) and explore its mechanism of action on Ehrlich ascites tumor (EAT) cells.
  • It significantly reduced ascites secretion and tumor cell proliferation by about 80% and inhibited vascular endothelial growth factor expression in tumor-bearing mice in vivo.
  • The results clearly suggest that AITC inhibits tumor growth by both antiangiogenic and proapoptotic mechanisms.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Isothiocyanates / pharmacology. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line. Cell Line, Tumor. Cell Proliferation / drug effects. G1 Phase / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mustard Plant / chemistry. Neoplasm Transplantation. Plant Oils / chemistry. Rabbits. Rats. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 19223371.001).
  • [ISSN] 1534-7354
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Isothiocyanates; 0 / Plant Oils; 0 / Vascular Endothelial Growth Factor A; BN34FX42G3 / allyl isothiocyanate
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37. Lambert IH, Klausen TK, Bergdahl A, Hougaard C, Hoffmann EK: ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl- channels in adherent Ehrlich Lettré and NIH3T3 cells. Am J Physiol Cell Physiol; 2009 Jul;297(1):C198-206
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl- channels in adherent Ehrlich Lettré and NIH3T3 cells.
  • Addition of H(2)O(2) (0.5 mM) to Ehrlich ascites tumor cells under isotonic conditions results in a substantial (22 +/- 1%) reduction in cell volume within 25 min.
  • It is suggested that H(2)O(2) activates electroneutral KCl cotransport in Ehrlich ascites tumor cells and not K(+) and Cl(-) channels.
  • The effect of H(2)O(2) on cell volume was blocked by the serine-threonine phosphatase inhibitor calyculin A, indicating an important role of serine-threonine phosphorylation in the H(2)O(2)-mediated activation of KCl cotransport in Ehrlich cells.
  • In contrast, addition of H(2)O(2) to adherent cells, e.g., Ehrlich Lettré ascites cells, a subtype of the Ehrlich ascites tumor cells, and NIH3T3 mouse fibroblasts increased the K(+) and Cl(-) conductances after hypotonic cell swelling.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / metabolism. Cell Adhesion. Chloride Channels / metabolism. Fibroblasts / metabolism. Oxidative Stress. Potassium Channels / metabolism. Reactive Oxygen Species / metabolism. Symporters / metabolism
  • [MeSH-minor] Animals. Carboxylic Acids / pharmacology. Cell Line, Tumor. Cell Size. Enzyme Inhibitors / pharmacology. Female. Hydrogen Peroxide / metabolism. Hypotonic Solutions. Indenes / pharmacology. Ion Transport. Mice. NIH 3T3 Cells. Nitrates / metabolism. Osmotic Pressure. Oxazoles / pharmacology. Phosphoprotein Phosphatases / metabolism. Phosphorylation. Time Factors

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  • (PMID = 19419998.001).
  • [ISSN] 1522-1563
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ((dihydroindenyl)oxy)alkanoic acid; 0 / Carboxylic Acids; 0 / Chloride Channels; 0 / Enzyme Inhibitors; 0 / Hypotonic Solutions; 0 / Indenes; 0 / Nitrates; 0 / Oxazoles; 0 / Potassium Channels; 0 / Reactive Oxygen Species; 0 / Symporters; 0 / potassium-chloride symporters; 101932-71-2 / calyculin A; BBX060AN9V / Hydrogen Peroxide; EC 3.1.3.16 / Phosphoprotein Phosphatases
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38. Teixeira AS, Araújo FA, Ferreira MA, Barcelos LS, Teixeira MM, Andrade SP: Angiogenesis and inflammation in skeletal muscle in response to ascites tumor in mice. Life Sci; 2006 Feb 28;78(14):1637-45
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  • [Title] Angiogenesis and inflammation in skeletal muscle in response to ascites tumor in mice.
  • This study addresses the interaction between Ehrlich ascites tumor and skeletal abdominal muscle, presenting quantitative analysis of ascites-induced angiogenesis and inflammation in this tissue of mice bearing-tumor.
  • Time-dependent changes in the muscle (cellular activity, angiogenesis, inflammation and cytokines production) were assessed by morphometric, functional, and biochemical parameters at days 1, 4 and 8 after i.p. inoculation of Ehrlich tumor cells (2.5 x 10(7)).
  • Likewise, the inflammatory process in the muscle, as assessed by myeloperoxidase (MPO) and n-acethylglucosaminidase (NAG) activities and the levels of the chemokines, keratinocyte-derived chemokine (CXC1-3/KC) and macrophage-chemoattractant protein (CCL2/MCP-1) increased with tumor development.
  • The combination of techniques used to describe angiogenesis and inflammation in a muscle model system has proved to be suited for quantitative measurements of microvascular changes and cellular infiltration occurring in the abdominal muscle wall of ascites-bearing mice.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / complications. Muscle, Skeletal / blood supply. Myositis / etiology. Neovascularization, Pathologic / etiology

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  • (PMID = 16313924.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Hemoglobins
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39. Belakavadi M, Salimath BP: Mechanism of inhibition of ascites tumor growth in mice by curcumin is mediated by NF-kB and caspase activated DNase. Mol Cell Biochem; 2005 May;273(1-2):57-67
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  • [Title] Mechanism of inhibition of ascites tumor growth in mice by curcumin is mediated by NF-kB and caspase activated DNase.
  • In the present report, we investigated the effect of curcumin on the activation of apoptotic and anti-angiogenic pathways in Ehrlich Ascites Tumor (EAT) cells.
  • Treatment with curcumin in vivo resulted in inhibition of proliferation of EAT cells and ascites formation.
  • On the other hand, the decreased secretion of ascites by EAT cells is corroborated by reduction in VEGF secretion upon curcumin treatment.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Carcinoma, Ehrlich Tumor / blood supply. Caspases / metabolism. Curcumin / pharmacology. Deoxyribonucleases / metabolism. NF-kappa B / metabolism. Neovascularization, Pathologic / prevention & control
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 3. Cell Nucleus / metabolism. Cell Proliferation / drug effects. Endothelium, Vascular / drug effects. Enzyme Activation / drug effects. Enzyme-Linked Immunosorbent Assay. Fluorescent Antibody Technique. Mice. Protein Transport. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16013440.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / NF-kappa B; 0 / Vascular Endothelial Growth Factor A; EC 3.1.- / Deoxyribonucleases; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; IT942ZTH98 / Curcumin
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40. Hu J, Qin G, Zhang Y, An R, Lan X: (99m)Tc-YIGSR as a receptor tracer in imaging the Ehrlich ascites tumor-bearing mice as compared with (99m)Tc-MIBI. J Huazhong Univ Sci Technolog Med Sci; 2007 Aug;27(4):471-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] (99m)Tc-YIGSR as a receptor tracer in imaging the Ehrlich ascites tumor-bearing mice as compared with (99m)Tc-MIBI.
  • The validity of (99m)Tc-YIGSR, a novel receptor radio-tracer, in imaging the Ehrlich ascites tumor was evaluated.
  • The mice of tumor group were intravenously injected 1-2 mCi of (99m)Tc-YIGSR or (99m)Tc-MIBI via caudal vein, immobilized and imaged under a Gamma camera.
  • The imagological study revealed obvious tumor accumulation of (99m)Tc-YIGSR 15 min after the injection, and the uptake peaked after 3 h with a tumor-to-muscle ratio (T/M) of 11.36.
  • As for blocked group, the tumor uptake of radiotracer was significantly lower, with the highest T/M being 4.61 after 3 h and 0.89 after 8 h.
  • The T/M was significantly higher in tumor group than in inflammatory group or control group (P<0.001).
  • It is concluded that YIGSR can be successfully radiolabelled by using S-Acetly-NH(3)-MAG(3). (99m)Tc-YIGSR has many advantages in tumor imaging, such as quick and clear visualization, high sensitivity and specificity, and satisfactory target/non-target ratio (N/NT).
  • It promises to be tumor radio-tracer.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / radionuclide imaging. Radiopharmaceuticals. Receptors, Laminin / metabolism. Technetium Tc 99m Mertiatide. Technetium Tc 99m Sestamibi

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  • (PMID = 17828515.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Radioactive Tracers; 0 / Radiopharmaceuticals; 0 / Receptors, Laminin; 36ITO9SKQJ / Technetium Tc 99m Mertiatide; 971Z4W1S09 / Technetium Tc 99m Sestamibi
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41. Attia WY, Gabry MS, El-Shaikh KA, Othman GA: The anti-tumor effect of bee honey in Ehrlich ascite tumor model of mice is coincided with stimulation of the immune cells. Egypt J Immunol; 2008;15(2):169-83

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The anti-tumor effect of bee honey in Ehrlich ascite tumor model of mice is coincided with stimulation of the immune cells.
  • The present study investigated the antitumor effect of bee honey against Ehrlich ascites tumor in mice and the possible mode of antitumor action.
  • Peroral administration of mice with honey (10, 100 or 1000 mg/ 100 g BW) every other day for 4 weeks before intraperitoneal inoculation with Ehrlich ascites tumor (EAT, 1 x 10(6) cells) increased the number bone marrow cells as well as peritoneal macrophages, but not peripheral blood leukocytes nor splenocytes.
  • In vitro studies on EAT cells demonstrated inhibitory effect of honey on tumor cell proliferation, viability % of tumor cells as well as the size of solid tumor.

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  • (PMID = 20306700.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Blood Proteins; 0 / Lipids; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
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42. Chandru H, Sharada AC, Bettadaiah BK, Kumar CS, Rangappa KS, Sunila, Jayashree K: In vivo growth inhibitory and anti-angiogenic effects of synthetic novel dienone cyclopropoxy curcumin analogs on mouse Ehrlich ascites tumor. Bioorg Med Chem; 2007 Dec 15;15(24):7696-703
Hazardous Substances Data Bank. CURCUMIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo growth inhibitory and anti-angiogenic effects of synthetic novel dienone cyclopropoxy curcumin analogs on mouse Ehrlich ascites tumor.
  • The tumor inhibitory and anti-angiogenic effects of the synthetic compounds were studied on mouse Ehrlich ascites tumor (EAT) in vivo.
  • The compounds 1a-4a increased the life span (% ILS) of EAT bearing mice with corresponding significant reduction in ascites volume and cell number and induced apoptotic bodies in EAT cells.
  • Our findings demonstrate that the tumor growth inhibitory effects of synthetic dienone cyclopropoxy curcumin analogs 1a-4a could be mediated by promoting apoptosis and inhibiting tumor angiogenesis.
  • [MeSH-major] Angiogenesis Inhibitors / chemistry. Angiogenesis Inhibitors / therapeutic use. Apoptosis / drug effects. Carcinoma, Ehrlich Tumor / drug therapy. Curcumin / analogs & derivatives. Curcumin / chemistry

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  • (PMID = 17869527.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; IT942ZTH98 / Curcumin
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43. Akev N, Turkay G, Can A, Gurel A, Yildiz F, Yardibi H, Ekiz EE, Uzun H: Effect of Aloe vera leaf pulp extract on Ehrlich ascites tumours in mice. Eur J Cancer Prev; 2007 Apr;16(2):151-7
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  • [Title] Effect of Aloe vera leaf pulp extract on Ehrlich ascites tumours in mice.
  • ) Burm. fil., a few recent studies have shown that preparations of the plant leaves can prevent or regress the growth of certain tumours.
  • In this study, undertaken with A. vera leaf pulp extract against Ehrlich ascites tumours in mice, the animals were separated into five groups: I - healthy control, II - tumour control, III - experiment 1 (extract given before tumour inoculation), IV - experiment 2 (extract given with tumour inoculation) and V - experiment 3 (extract given after tumour inoculation).
  • Ehrlich ascites tumours (0.33 ml) were injected subcutaneously into groups II-V.
  • Tumour size, thymus and spleen weights were measured, as well as leucocyte count, tumour necrosis factor-alpha and sialic acid as tumour markers.
  • The best inhibitory effect on tumour growth was obtained with the extract given prophylactically before tumour implantation (experiment 1), although Aloe extract also regressed tumour sizes when given simultaneously with (experiment 2), or therapeutically after (experiment 3), tumour implantation.
  • Accordingly, serum sialic acid and tumour necrosis factor-alpha levels, chosen as tumour markers, which were raised in the tumour control group, were significantly decreased by the prophylactic administration of the extract.
  • The increase in leucocyte count seen in experiment 1 and 2 groups, along with lymphoid hyperplasia observed in spleen and thymus necroscopy, lead us to think that the tumour preventive effect of Aloe could be due to its immunomodulatory activity.
  • [MeSH-major] Aloe. Carcinoma, Ehrlich Tumor / drug therapy. Phytotherapy. Plant Extracts / therapeutic use. Plant Leaves

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  • (PMID = 17297391.001).
  • [ISSN] 0959-8278
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Plant Extracts
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44. Suntres ZE, Lui EM: Prooxidative effect of copper--metallothionein in the acute cytotoxicity of hydrogen peroxide in Ehrlich ascites tumour cells. Toxicology; 2006 Jan 16;217(2-3):155-68
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  • [Title] Prooxidative effect of copper--metallothionein in the acute cytotoxicity of hydrogen peroxide in Ehrlich ascites tumour cells.
  • Hydrogen peroxide (H(2)O(2))-induced oxidative injury was examined in Ehrlich ascites tumour cells isolated from host mice pretreated with 0, 1 or 2mg of CuSO(4) (ip) 24h earlier.
  • Control Ehrlich cells contained low levels of Cu and Cu treatment produced dose-related increases in cellular Cu and Cu-MT levels and corresponding increases in sensitivity to oxidative toxicity of H(2)O(2) (LC(50), cell blebbing, lipid peroxidation, GSH depletion, and increase in intracellular free [Ca(2+)](i)).
  • [MeSH-minor] Animals. Calcium / metabolism. Carcinoma, Ehrlich Tumor / metabolism. Carcinoma, Ehrlich Tumor / pathology. Cell Survival / drug effects. Copper Sulfate / pharmacology. Deferoxamine / pharmacology. Dose-Response Relationship, Drug. Glutathione Disulfide / metabolism. Injections, Intraperitoneal. Iron / chemistry. Iron / metabolism. Lipid Peroxidation / drug effects. Male. Mannitol / pharmacology. Mice. Oxidative Stress / drug effects. Penicillamine / pharmacology. Pinocytosis / drug effects. Time Factors. Tumor Cells, Cultured. Zinc / chemistry. Zinc / metabolism

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  • (PMID = 16221516.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 3OWL53L36A / Mannitol; 789U1901C5 / Copper; 9038-94-2 / Metallothionein; BBX060AN9V / Hydrogen Peroxide; E1UOL152H7 / Iron; GNN1DV99GX / Penicillamine; J06Y7MXW4D / Deferoxamine; J41CSQ7QDS / Zinc; LRX7AJ16DT / Copper Sulfate; SY7Q814VUP / Calcium; ULW86O013H / Glutathione Disulfide
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45. Kumar A, D'Souza SS, Nagaraj SR, Gaonkar SL, Salimath BP, Rai KM: Antiangiogenic and antiproliferative effects of substituted-1,3,4-oxadiazole derivatives is mediated by down regulation of VEGF and inhibition of translocation of HIF-1alpha in Ehrlich ascites tumor cells. Cancer Chemother Pharmacol; 2009 Nov;64(6):1221-33
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  • [Title] Antiangiogenic and antiproliferative effects of substituted-1,3,4-oxadiazole derivatives is mediated by down regulation of VEGF and inhibition of translocation of HIF-1alpha in Ehrlich ascites tumor cells.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / drug therapy. Gene Expression Regulation, Neoplastic / drug effects. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Neovascularization, Pathologic / drug therapy. Oxadiazoles / pharmacology. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19370348.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Oxadiazoles; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 3.1.3.1 / Alkaline Phosphatase
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46. Hu J, Zhang YX, Lan XL, Qin GM, Zhang J, Hu ZH: An imaging study using laminin peptide 99mTc-YIGSR in mice bearing Ehrlich ascites tumour. Chin Med J (Engl); 2005 May 5;118(9):753-8
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  • [Title] An imaging study using laminin peptide 99mTc-YIGSR in mice bearing Ehrlich ascites tumour.
  • The purpose is to evaluate the usefulness of (99m)Tc-YIGSR, a novel tumour radiotracer, in the receptor imaging of Ehrlich ascites tumour.
  • METHODS: Using S-acetly-NH3-MAG3 as chelate, YIGSR, a pentapeptide from laminin, was tagged with (99m)Tc. (99m)Tc-YIGSR was detected in the tumour group bearing Ehrlich ascites tumour and blocked group.
  • Tumour, normal, inflammatory and blocked groups were imaged.
  • The imaging findings showed tumour tissue accumulated initial radioactivity at fifteen minutes after injection in the tumour group, and the uptake increased to peak at three hours with a tumour/muscle ratio (T/M) of 11.36, then cleared slowly to a T/M of 7.50 at eight hours.
  • The tumour uptake of radiotracer in blocked group was significantly lower with T/M of 4.61 at three hours and 0.89 at eight hours.
  • Compared with inflammatory group and control obstructive group, the ratio of T/M in tumour group was significantly different (P < 0.001).
  • CONCLUSIONS: Using S-acetly-NH3-MAG3, we radiolabelled YIGSR with (99m)Tc. (99m)Tc-YIGSR possesses many merits of tumour imaging: rapid visualization, high sensitivity and specificity, and satisfactory target/nontarget ratio.
  • Our data suggest (99m)Tc-YIGSR is a promising tumour radiotracer.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / radionuclide imaging. Laminin. Oligopeptides. Radiopharmaceuticals. Technetium

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  • (PMID = 15899138.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Laminin; 0 / Oligopeptides; 0 / Radiopharmaceuticals; 0 / laminin 1; 110590-64-2 / tyrosyl-isoleucyl-glycyl-seryl-arginine; 36ITO9SKQJ / Technetium Tc 99m Mertiatide; 7440-26-8 / Technetium
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47. Bincoletto C, Eberlin S, Figueiredo CA, Luengo MB, Queiroz ML: Effects produced by Royal Jelly on haematopoiesis: relation with host resistance against Ehrlich ascites tumour challenge. Int Immunopharmacol; 2005 Apr;5(4):679-88
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  • [Title] Effects produced by Royal Jelly on haematopoiesis: relation with host resistance against Ehrlich ascites tumour challenge.
  • In order to elucidate the mechanism whereby RJ activates the immunological system, we examined the role of this substance on the haematopoietic response of Ehrlich ascites tumour (EAT)-bearing mice.
  • Our results demonstrated that RJ prevented the myelosupression induced by the temporal evolution of the tumour and abrogated the splenic haematopoiesis observed in EAT-bearing mice.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Carcinoma, Ehrlich Tumor / immunology. Fatty Acids / pharmacology. Hematopoiesis / drug effects

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  • (PMID = 15710337.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Fatty Acids; 8031-67-2 / royal jelly; K7Q1JQR04M / Dinoprostone
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48. Moiseenko VM, Chudenko VA, Stukov AN, Anikin IV, Pozharisskiĭ KM, Maksimova NA: [Kinetic features of ascites and solid Ehrlich tumors]. Vopr Onkol; 2009;55(5):598-602
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  • [Title] [Kinetic features of ascites and solid Ehrlich tumors].
  • Such biological parameters as tumor volume, Ki-67 and p53, which characterize the development of ascites and solid tumor of Ehrlich were evaluated.
  • The kinetic curve of growth of ascites tumor was S-shaped (Gomperts) while that of the solid one--cubic (Speer-Retsky).
  • Moreover, no increase in cell death was observed when tumor growth slowed down.
  • [MeSH-major] Ascites / pathology. Biomarkers, Tumor / analysis. Carcinoma, Ehrlich Tumor / pathology
  • [MeSH-minor] Animals. Female. Ki-67 Antigen / analysis. Kinetics. Mice. Time Factors. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 20020656.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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49. Suntres ZE, Lui EMK: Antioxidant effect of zinc and zinc-metallothionein in the acute cytotoxicity of hydrogen peroxide in Ehrlich ascites tumour cells. Chem Biol Interact; 2006 Jul 25;162(1):11-23
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  • [Title] Antioxidant effect of zinc and zinc-metallothionein in the acute cytotoxicity of hydrogen peroxide in Ehrlich ascites tumour cells.
  • Hydrogen peroxide-induced oxidative injury was examined in Ehrlich ascites tumour cells isolated from control host mice, mice pretreated with 10 mg/kg ZnSO4 (i.p.) to increase cellular Zn/Zn-MT levels, and mice exposed to Zn-deficient diet to reduce the cellular Zn/Zn-MT levels.
  • The results of the present study showed that Ehrlich cells with seven-fold differences in Zn-MT concentrations could be obtained by manipulating the Zn status of host mice and that high Zn and Zn-MT levels can make Ehrlich cells more resistant to H2O2-induced oxidative injury (cell viability, lipid peroxidation, [Ca2+]i) while cells with reduced Zn/Zn-MT levels were more susceptible to this treatment.
  • Preincubation of Ehrlich cells with ZnSO4 in vitro also conferred some degree of resistance to H2O2 toxicity, suggesting the inherent antioxidative property of Zn ions.
  • [MeSH-major] Antioxidants / pharmacology. Carcinoma, Ehrlich Tumor / metabolism. Hydrogen Peroxide / toxicity. Metallothionein / pharmacology. Zinc / pharmacology
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Copper / pharmacology. Cytosol / metabolism. Glutathione / metabolism. Lipid Peroxidation / drug effects. Male. Mice. Neoplasm Transplantation. Protein Binding. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16730687.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antioxidants; 0 / zinc thionein; 789U1901C5 / Copper; 9038-94-2 / Metallothionein; BBX060AN9V / Hydrogen Peroxide; GAN16C9B8O / Glutathione; J41CSQ7QDS / Zinc; SY7Q814VUP / Calcium
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50. Orsolić N, Kosalec I, Basić I: Synergistic antitumor effect of polyphenolic components of water soluble derivative of propolis against Ehrlich ascites tumour. Biol Pharm Bull; 2005 Apr;28(4):694-700
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  • [Title] Synergistic antitumor effect of polyphenolic components of water soluble derivative of propolis against Ehrlich ascites tumour.
  • Effect of two preparation (Croatian and Brazilian) of water-soluble derivative of propolis (WSDP), caffeic acid, quercetin, chrysin, naringenin (components present in WSDP) on the development of Ehrlich ascites tumour (EAT) was evaluated.
  • It was observed that all test compounds effectively inhibited tumour growth and the proliferation of EAT.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Flavonoids / pharmacology. Phenols / pharmacology. Propolis / pharmacology

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  • (PMID = 15802812.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Caffeic Acids; 0 / Flavanones; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 3CN01F5ZJ5 / chrysin; 9009-62-5 / Propolis; 9IKM0I5T1E / Quercetin; HN5425SBF2 / naringenin; U2S3A33KVM / caffeic acid
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51. Akev N, Turkay G, Can A, Gurel A, Yildiz F, Yardibi H, Ekiz EE, Uzun H: Tumour preventive effect of Aloe vera leaf pulp lectin (Aloctin I) on Ehrlich ascites tumours in mice. Phytother Res; 2007 Nov;21(11):1070-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumour preventive effect of Aloe vera leaf pulp lectin (Aloctin I) on Ehrlich ascites tumours in mice.
  • In this study, the prophylactic effect of the main lectin present in Aloe vera leaf pulp extract (Aloctin I) was assayed against Ehrlich ascites tumours in mice.
  • The lectin administered prophylactically before tumour implantation regressed tumour size, however, this activity was less potent than that of the A. vera leaf pulp extract previously shown in our laboratory.
  • Accordingly, serum sialic acid and tumour necrosis factor alpha (TNFalpha) levels, chosen as tumour markers, were decreased significantly by the prophylactic administration of the lectin.
  • These findings, along with lymphoid hyperplasia observed in spleen and thymus, suggest that the tumour preventive effect of Aloctin I could be due to its immunomodulatory activity.
  • [MeSH-major] Aloe / chemistry. Carcinoma, Ehrlich Tumor / prevention & control. Plant Leaves / chemistry. Plant Lectins / therapeutic use
  • [MeSH-minor] Animals. Leukocyte Count. Male. Mice. N-Acetylneuraminic Acid / blood. Organ Size / drug effects. Spleen / drug effects. Spleen / pathology. Thymus Gland / drug effects. Thymus Gland / pathology. Tumor Necrosis Factor-alpha / blood

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  • [Copyright] Copyright (c) 2007 John Wiley & Sons, Ltd.
  • (PMID = 17685385.001).
  • [ISSN] 0951-418X
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Plant Lectins; 0 / Tumor Necrosis Factor-alpha; 0 / aloctin I, Aloe vera; GZP2782OP0 / N-Acetylneuraminic Acid
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52. Choudhury SM, Gupta M, Majumder UK: Antineoplastic activities of MT81 and its structural analogue in Ehrlich ascites carcinoma-bearing Swiss Albino mice. Oxid Med Cell Longev; 2010 Jan-Feb;3(1):61-70
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  • [Title] Antineoplastic activities of MT81 and its structural analogue in Ehrlich ascites carcinoma-bearing Swiss Albino mice.
  • Luteoskyrin,a hydroxyanthraquinone has been proved to be a potent inhibitor against Ehrlich ascites tumor cells.
  • The comparative antitumor activity and antioxidant status of MT81 and its structural analogue [Acetic acid-MT81 (Aa-MT81)] having polyhydroxyanthraquinone structure were assessed against Ehrlich ascites carcinoma (EAC) tumor in mice.
  • In in vivo study, MT81 and its structural analogue were administered (i.p.) at the two different doses (5, 7 mg MT81; 8.93, 11.48 mg Aa-MT81/kg body weight) for 7 days after 24 hrs. of tumor inoculation.
  • The activities were assessed using mean survival time (MST), increased life span (ILS), tumor volume, viable tumor cell count, peritoneal cell count, protein percentage and hematological parameters.
  • They decreased the tumor volume, viable tumor cell count, hemoglobin percentage and packed cell volume.
  • [MeSH-major] Anthraquinones / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy

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  • [Cites] Neoplasma. 1997;44(5):329-33 [9473795.001]
  • [Cites] Chem Phys Lipids. 1987 Nov-Dec;45(2-4):337-51 [3319232.001]
  • [Cites] Anal Biochem. 1979 Jun;95(2):351-8 [36810.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Int J Oncol. 2007 Sep;31(3):663-9 [17671695.001]
  • [Cites] Phytother Res. 2008 Aug;22(8):1097-103 [18570233.001]
  • [Cites] Mol Pharmacol. 2008 Oct;74(4):1132-40 [18635669.001]
  • [Cites] Phytomedicine. 2009 Mar;16(2-3):188-97 [19150236.001]
  • [Cites] Chem Biol Interact. 2009 May 15;179(2-3):145-53 [19161993.001]
  • [Cites] Clin Biochem. 1999 Nov;32(8):595-603 [10638941.001]
  • [Cites] J Ethnopharmacol. 2000 Jul;71(1-2):349-52 [10904185.001]
  • [Cites] Indian J Exp Biol. 1988 Apr;26(4):315-22 [3169853.001]
  • [Cites] J Biol Chem. 1988 Nov 25;263(33):17205-8 [3053703.001]
  • [Cites] Cancer Chemother Pharmacol. 1989;24(4):264-7 [2752509.001]
  • [Cites] Int J Cancer. 1989 Dec 15;44(6):1028-33 [2558077.001]
  • [Cites] Cancer Res. 1990 Mar 1;50(5):1431-9 [2302708.001]
  • [Cites] Free Radic Biol Med. 1990;8(6):583-99 [2193855.001]
  • [Cites] Br J Hosp Med. 1990 May;43(5):334-44 [2194616.001]
  • [Cites] Pharmazie. 1992 Apr;47(4):288-91 [1518888.001]
  • [Cites] Indian J Exp Biol. 1992 Feb;30(2):140-1 [1521863.001]
  • [Cites] Indian J Exp Biol. 1993 Nov;31(11):888-90 [8112762.001]
  • [Cites] Planta Med. 1994 Apr;60(2):106-9 [8202557.001]
  • [Cites] J Antibiot (Tokyo). 1997 Feb;50(2):111-8 [9099219.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] Indian J Exp Biol. 1997 May;35(5):473-7 [9378516.001]
  • [Cites] Adv Cancer Res. 1954;2:229-53 [13180440.001]
  • [Cites] Adv Cancer Res. 1958;5:199-290 [13533058.001]
  • [Cites] Prog Clin Cancer. 1965;10:625-63 [14283934.001]
  • [Cites] Cancer Lett. 2004 Dec 28;216(2):165-73 [15533592.001]
  • [Cites] J Antibiot (Tokyo). 2004 Nov;57(11):748-54 [15712670.001]
  • [Cites] J Ethnopharmacol. 2000 Sep;72(1-2):151-6 [10967466.001]
  • [Cites] Nature. 2001 May 17;411(6835):390-5 [11357148.001]
  • [Cites] Cancer Lett. 2001 Nov 28;173(2):115-25 [11597785.001]
  • [Cites] J Nat Prod. 2002 May;65(5):742-4 [12027756.001]
  • [Cites] Teratog Carcinog Mutagen. 2002;22(4):309-14 [12111715.001]
  • [Cites] Pharmazie. 2004 Jan;59(1):42-9 [14964421.001]
  • [Cites] Med Oncol. 2004;21(1):21-30 [15034210.001]
  • [Cites] Experientia. 1967 Dec 15;23(12):1001-2 [6077857.001]
  • [Cites] J Antibiot (Tokyo). 1968 Jul;21(7):463-4 [4303502.001]
  • [Cites] Jpn J Exp Med. 1971 Jun;41(3):177-88 [5314585.001]
  • [Cites] Eur J Biochem. 1974 Sep 16;47(3):469-74 [4215654.001]
  • [Cites] Cancer Chemother Pharmacol. 1979;2(3):181-2 [455572.001]
  • [Cites] Biochem Pharmacol. 1980 Jan 1;29(1):19-26 [6244827.001]
  • [Cites] Anal Biochem. 1980 Jul 15;106(1):207-12 [7416462.001]
  • [Cites] Cancer Res. 1982 May;42(5):1955-61 [7066906.001]
  • [Cites] Semin Oncol. 1982 Mar;9(1):95-102 [7071611.001]
  • [Cites] J Med Chem. 1982 May;25(5):579-89 [7086845.001]
  • [Cites] Science. 1985 Jan 25;227(4685):375-81 [2981433.001]
  • [Cites] J Med Chem. 1976 Nov;19(11):1339-42 [1003414.001]
  • (PMID = 20716929.001).
  • [ISSN] 1942-0994
  • [Journal-full-title] Oxidative medicine and cellular longevity
  • [ISO-abbreviation] Oxid Med Cell Longev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthraquinones; 0 / Antineoplastic Agents; 4Y8F71G49Q / Malondialdehyde; 82197-56-6 / MT81 mycotoxin; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione
  • [Other-IDs] NLM/ PMC2835890
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53. Kumar CA, Swamy SN, Gaonkar SL, Basappa, Salimath BP, Rangappa KS: N-Substituted-2-butyl-5-chloro-3H-imidazole-4-carbaldehyde derivatives as anti-tumor agents against Ehrlich ascites tumor cells in vivo. Med Chem; 2007 May;3(3):269-76
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  • [Title] N-Substituted-2-butyl-5-chloro-3H-imidazole-4-carbaldehyde derivatives as anti-tumor agents against Ehrlich ascites tumor cells in vivo.
  • Our results show that treatment of imidazole derivatives inhibit proliferation EAT cells, decreases the ascites volume and increases the survivability of the animals in vivo.
  • We have identified that pyrrolidine substituted imidazole derivative as potent anti-tumor compound.
  • These inhibitors could represent as promising candidates for anticancer therapies, where the formation of peritoneal malignant ascites is a major cause of morbidity and mortality.
  • [MeSH-major] Aldehydes / pharmacology. Antineoplastic Agents / chemistry. Carcinoma, Ehrlich Tumor / drug therapy. Imidazoles / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Screening Assays, Antitumor. Humans. Structure-Activity Relationship

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  • (PMID = 17504198.001).
  • [ISSN] 1573-4064
  • [Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))
  • [ISO-abbreviation] Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antineoplastic Agents; 0 / Imidazoles
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54. Xu S, Kojima-Yuasa A, Azuma H, Huang X, Norikura T, Kennedy DO, Matsui-Yuasa I: (1'S)-Acetoxychavicol acetate and its enantiomer inhibit tumor cells proliferation via different mechanisms. Chem Biol Interact; 2008 Apr 15;172(3):216-23
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  • [Title] (1'S)-Acetoxychavicol acetate and its enantiomer inhibit tumor cells proliferation via different mechanisms.
  • In this study, we prepared (S)-ACA and its enantiomer (R)-ACA by a lipase-catalyzed esterification method and sought to determine the mechanisms of action of (S)-ACA and (R)-ACA in the growth inhibitory effect in Ehrlich ascites tumor cells (EATC). (S)-ACA caused an accumulation of tumor cells in the G1 phase of the cell cycle, which was accompanied by a decrease in phosphorylated retinoblastoma protein (Rb), an increase in Rb and a decrease in the phosphorylation of p27kip1.
  • However, (R)-ACA caused an accumulation of tumor cells in the G2 phase of the cell cycle, an increase in hyperphosphorylated Rb and an increase in the phosphorylation of p27kip1.
  • The results obtained in the present study demonstrate for the first time, to the best of our knowledge, that both (S)-ACA and (R)-ACA caused the inhibition of tumor cells growth but the inhibition was caused via different mechanisms.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Cell Proliferation / drug effects. Retinoblastoma Protein / metabolism. Terpenes / pharmacology
  • [MeSH-minor] Animals. Benzyl Alcohols. Blotting, Western. Phosphorylation. Stereoisomerism. Time Factors. Tumor Cells, Cultured

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  • (PMID = 18281026.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzyl Alcohols; 0 / Retinoblastoma Protein; 0 / Terpenes; 52946-22-2 / 1'-acetoxychavicol acetate
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55. Jaganjac M, Poljak-Blazi M, Kirac I, Borovic S, Joerg Schaur R, Zarkovic N: Granulocytes as effective anticancer agent in experimental solid tumor models. Immunobiology; 2010 Dec;215(12):1015-20
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  • [Title] Granulocytes as effective anticancer agent in experimental solid tumor models.
  • The aim of the study was to elucidate the effects of murine granulocytes on the growth of solid murine tumors when administrated in the vicinity of W256 carcinoma growing in Sprague Dawley rats, and in the vicinity of Ehrlich ascites tumor (EAT) growing in BALBc mice.
  • The administration of granulocytes significantly improved the survival of W256-bearing rats, and increased the tumor regression incidence from 17% up to 75%.
  • Rats with regressing tumors had 2.5 times increased levels of granulocytes in peripheral blood, which were also cytotoxic in vitro for W256 carcinoma cells.
  • However, blood levels of cytokine-induced neutrophil chemoattractant-2, tumor necrosis factor α and interleukin 6 were similar between rats with regressing tumors and control healthy rats, suggesting that the observed regression of W256 carcinoma was caused by specific anticancer effects of the applied granulocytes.
  • Therefore, the administration of granulocytes, isolated from healthy animals and applied at the site of solid tumors in rats and in mice, reduced experimental tumor growth, and extended the survival of tumor-bearing animals, while in some rats it even caused a W256 regression.
  • [MeSH-major] Carcinoma 256, Walker / immunology. Carcinoma, Ehrlich Tumor / immunology. Granulocytes / immunology. Tumor Microenvironment / immunology
  • [MeSH-minor] Animals. Chemokines, CXC / blood. Immunotherapy, Adoptive / methods. Interleukin-6 / blood. Kaplan-Meier Estimate. Male. Mice. Mice, Inbred BALB C. Neoplasms, Experimental / immunology. Neoplasms, Experimental / pathology. Neoplasms, Experimental / therapy. Neutrophils / immunology. Rats. Rats, Sprague-Dawley. Tumor Burden / immunology. Tumor Necrosis Factor-alpha / blood

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  • [Copyright] Copyright © 2010 Elsevier GmbH. All rights reserved.
  • (PMID = 20122752.001).
  • [ISSN] 1878-3279
  • [Journal-full-title] Immunobiology
  • [ISO-abbreviation] Immunobiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chemokines, CXC; 0 / Gm1960 protein, rat; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
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56. Harish Prashanth KV, Tharanathan RN: Depolymerized products of chitosan as potent inhibitors of tumor-induced angiogenesis. Biochim Biophys Acta; 2005 Feb 11;1722(1):22-9
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  • [Title] Depolymerized products of chitosan as potent inhibitors of tumor-induced angiogenesis.
  • The effect of LMWC and COs on the growth of Ehrlich ascites tumor (EAT) cells and tumor-induced neovascularization was studied.

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  • (PMID = 15716061.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Oligosaccharides; 9012-76-4 / Chitosan
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57. Pathak A, Kumar P, Chuttani K, Jain S, Mishra AK, Vyas SP, Gupta KC: Gene expression, biodistribution, and pharmacoscintigraphic evaluation of chondroitin sulfate-PEI nanoconstructs mediated tumor gene therapy. ACS Nano; 2009 Jun 23;3(6):1493-505
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  • [Title] Gene expression, biodistribution, and pharmacoscintigraphic evaluation of chondroitin sulfate-PEI nanoconstructs mediated tumor gene therapy.
  • Tumor-specific gene delivery constitutes a primary challenge in nonviral mediated gene therapy.
  • In vivo studies were carried out with pDNA loaded CP-3 nanoconstruct after intravenous (iv) injection in Ehrlich ascites tumor (EAT)-bearing mice.
  • The outcome revealed higher concentration of CP-3 nanoconstruct in tumor mass.
  • These findings demonstrate that CP nanoconstructs could be exploited as carriers for nanomedicine for efficient management of solid tumor.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / metabolism. Cell Line. DNA / metabolism. Humans. Mice. Proteins / metabolism. Tissue Distribution

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  • (PMID = 19449835.001).
  • [ISSN] 1936-086X
  • [Journal-full-title] ACS nano
  • [ISO-abbreviation] ACS Nano
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins; 9002-98-6 / Polyethyleneimine; 9007-28-7 / Chondroitin Sulfates; 9007-49-2 / DNA
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58. D'Souza SS, Gururaj AE, Raj HM, Rössler J, Salimath BP: Inhibition of ascites tumor growth in vivo by sTie-2 is potentiated by a combinatorial therapy with sFLT-1. J Gene Med; 2010 Dec;12(12):968-80
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  • [Title] Inhibition of ascites tumor growth in vivo by sTie-2 is potentiated by a combinatorial therapy with sFLT-1.
  • BACKGROUND: Inhibition of tumor angiogenesis is a promising approach for cancer therapy and the Tie-2/angiopoietin pathway appears to play an important role.
  • METHODS: Ehrlich ascites tumor (EAT) cells were stably transfected to overexpress a truncated form of sTie-2.
  • Furthermore, recombinant sTie-2 produced by the baculovirus expression system was used to sequester angiopoietins in the murine ascites carcinoma model.
  • The effect of sTie-2 treatment alone or in combination with sFLT-1 on the weight of the animal, ascites cell number and volume was studied.
  • However, sTie-2 transfected EAT cells transplanted into nude mice reduced tumor burden and demonstrated a reduction in ascites formation and peritoneal angiogenesis.
  • Recombinant sTie-2 showed angiogenic activity in the tube formation and wound healing assay in vitro. sTie-2 treatment alone or in combination with sFLT-1 in an ascites tumor mouse model resulted in reduced peritoneal angiogenesis, with a concomitant decrease in tumor cell number, volume of ascites and the number of invasive tumor cells, as assayed by CD31 staining.
  • CONCLUSIONS: The findings of the present study demonstrate an important role for the Tie-2/angiopoietin pathway in the formation of tumor vasculature and suggest that sTie-2 might yield useful anticancer therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Ehrlich Tumor / pathology. Carcinoma, Ehrlich Tumor / therapy. Neovascularization, Pathologic / prevention & control. Receptor, TIE-2 / therapeutic use. Vascular Endothelial Growth Factor Receptor-1 / therapeutic use

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  • [Copyright] Copyright © 2010 John Wiley & Sons, Ltd.
  • (PMID = 21104971.001).
  • [ISSN] 1521-2254
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiopoietin-2; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
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59. Ramos AL, Torello CO, Queiroz ML: Chlorella vulgaris modulates immunomyelopoietic activity and enhances the resistance of tumor-bearing mice. Nutr Cancer; 2010;62(8):1170-80
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  • [Title] Chlorella vulgaris modulates immunomyelopoietic activity and enhances the resistance of tumor-bearing mice.
  • We studied the effects of Chlorella vulgaris (CV) on the interaction between stromal and hematopoietic stem cells in normal and Ehrlich ascites tumor (EAT)-bearing mice.
  • In tumor bearers, reduced capacity of stromal cell layer to support the growth and differentiation of granulocyte-macrophage progenitor cells (CFU-GM), concomitantly to decreased numbers of total nonadherent cells in LTBMC and reduced local production of IL-6 and IL-1α, were observed.
  • Presence of the tumor has not altered the number of stromal adherent cells.
  • Treatment of tumor-bearing mice with CV augmented CSA, SMC proliferation, NK cell activity, and the production of IL-2, IFN-γ, and TNF-α, whereas IL-10 levels where reduced.
  • Our results suggest that CV modulates immunehematopoietic cell activity and disengages tumor-induced suppression of these responses.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Ehrlich Tumor / immunology. Chlorella vulgaris. Immunologic Factors / therapeutic use. Myelopoiesis

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  • (PMID = 21058206.001).
  • [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] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Colony-Stimulating Factors; 0 / Cytokines; 0 / Immunologic Factors
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60. Hirai M, Minematsu H, Kondo N, Oie K, Igarashi K, Yamazaki N: Accumulation of liposome with Sialyl Lewis X to inflammation and tumor region: application to in vivo bio-imaging. Biochem Biophys Res Commun; 2007 Feb 16;353(3):553-8
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  • [Title] Accumulation of liposome with Sialyl Lewis X to inflammation and tumor region: application to in vivo bio-imaging.
  • We prepared the liposome binding Sialyl Lewis X (SLX) on the surface in order to specifically and efficiently deliver substances (fluorescent materials, chemical substances, proteins, genes, etc.) to inflammation or tumor regions.
  • The liposome with SLX (SLX-Lipo-Cy5.5), in which fluorescent substance Cy5.5 was included, was administered intravenously to arthritis or Ehrlich Ascites Tumor (EAT) bearing mouse, and the accumulation of liposome was observed using two types of in vivo fluorescent imaging equipment.
  • The result was that the accumulation of SLX-Lipo-Cy5.5 to inflammation or tumor regions was significantly higher than the control liposome without sugar chain (Lipo-Cy5.5) at 24 and 48 h after administration.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / metabolism. Inflammation / metabolism. Lewis Blood-Group System. Liposomes / pharmacokinetics. Oligosaccharides / administration & dosage

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  • (PMID = 17189617.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine; 0 / CY5.5 cyanine dye; 0 / Carbocyanines; 0 / Fluorescent Dyes; 0 / Lewis Blood-Group System; 0 / Liposomes; 0 / Oligosaccharides
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61. Kwiecień I, Michalska M, Włodek L: The selective effect of cystathionine on doxorubicin hepatotoxicity in tumor-bearing mice. Eur J Pharmacol; 2006 Nov 21;550(1-3):39-46
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  • [Title] The selective effect of cystathionine on doxorubicin hepatotoxicity in tumor-bearing mice.
  • The aim of the present study was to examine the protective effect of cystathionine as a cysteine precursor on doxorubicin toxicity in the liver of Ehrlich ascites tumor (EAT)-bearing mice and in the EAT cells.
  • All these data indicate that cystathionine action is selectively beneficial for normal cells because it corrects harmful effects induced by EAT development and protects the organism against doxorubicin cytotoxicity without impairing cytotoxicity of this drug to tumor cells.
  • [MeSH-major] Antibiotics, Antineoplastic / antagonists & inhibitors. Antibiotics, Antineoplastic / toxicity. Carcinoma, Ehrlich Tumor / pathology. Cystathionine / pharmacology. Doxorubicin / antagonists & inhibitors. Doxorubicin / toxicity. Drug-Induced Liver Injury / prevention & control

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  • (PMID = 17034787.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Indicators and Reagents; 0 / Reactive Oxygen Species; 375YFJ481O / Cystathionine; 4Y8F71G49Q / Malondialdehyde; 80168379AG / Doxorubicin; EC 2.3.2.2 / gamma-Glutamyltransferase; EC 2.5.1.18 / Glutathione Transferase; EC 3.1.3.1 / Alkaline Phosphatase; EC 4.4.1.1 / Cystathionine gamma-Lyase; GAN16C9B8O / Glutathione
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62. Wei HM, Qin SK, Yin XJ, Chen YL: [Therapeutic features of endostar, a modified endostatin, on ascites tumor in mice]. Nan Fang Yi Ke Da Xue Xue Bao; 2010 Jul;30(7):1509-13

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Therapeutic features of endostar, a modified endostatin, on ascites tumor in mice].
  • OBJECTIVE: To investigate the effect of endostar in controlling ascites tumor formation in mice.
  • METHODS: Mouse models bearing ascites tumors were established via intraperitoneal injection of H22 and S180 cell lines.
  • The body weight curve of mice was drawn, and the cumulative ascites volume and number of red cells and tumor cells in the malignant ascites were determined.
  • RESULTS: Compared with the control group, the mice receiving daily endostar injection showed obviously lower ascites accumulation and peritoneal capillary permeability (P<0.05) with reduced count of ascites tumor cells and red cells and tumor burden of the abdominal cavity.
  • CONCLUSIONS: Continuous intraperitoneal injection can be the optimal means for endostar administration for treatment of malignant ascites.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / blood supply. Endostatins / administration & dosage. Endostatins / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Humans. Mice. Mice, Inbred ICR. Neovascularization, Pathologic. Recombinant Proteins / administration & dosage. Recombinant Proteins / pharmacology. Recombinant Proteins / therapeutic use

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  • (PMID = 20650753.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Endostatins; 0 / Recombinant Proteins; 0 / endostar protein
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63. Kumar S, Kumar Mishra A, Chhikara BS, Chuttani K, Kumar Sharma R: Preparation and pharmacological evaluation of a new radiopharmaceutical, technetium-99m-5-fluorouracil, for tumor scintigraphy. Hell J Nucl Med; 2008 May-Aug;11(2):91-5
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  • [Title] Preparation and pharmacological evaluation of a new radiopharmaceutical, technetium-99m-5-fluorouracil, for tumor scintigraphy.
  • There are reports of use of (18)F and (19)F analogues of 5-FU for tumor studies using PET and NMR respectively.
  • Blood kinetics were studied in rabbits and biodistribution was carried out in normal as well as tumor bearing mice.
  • In vivo and in vitro tumor uptake of the radiocomplex was evaluated in Ehrlich Ascites Tumor (EAT) bearing mice and human breast cancer cell line (MDA-MB-468).
  • High extraction of (99m)Tc-5-FU by the liver (36.41+/-2.79% of injected dose/g tissue) has been observed in mice, along with time dependent increase in the solid tumor to muscle ratio (2:1) measured at 4 h.
  • CONCLUSION: It can be concluded that the (99m)Tc-5-FU possesses selectivity towards solid tumor tissue.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / metabolism. Carcinoma, Ehrlich Tumor / radionuclide imaging. Fluorouracil / analogs & derivatives. Organotechnetium Compounds / pharmacokinetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Isotope Labeling / methods. Metabolic Clearance Rate. Mice. Mice, Inbred BALB C. Organ Specificity. Radiopharmaceuticals / chemical synthesis. Radiopharmaceuticals / pharmacokinetics. Tissue Distribution

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  • (PMID = 18815662.001).
  • [ISSN] 1790-5427
  • [Journal-full-title] Hellenic journal of nuclear medicine
  • [ISO-abbreviation] Hell J Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Organotechnetium Compounds; 0 / Radiopharmaceuticals; 0 / technetium 99m 5-fluorouracil; U3P01618RT / Fluorouracil
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64. de Souza AR, Coelho EP, Zyngier SB: Comparison of the anti-neoplastic effects of dirhodium(II) tetrapropionate and its adducts with nicotinate and isonicotinate anions in mice bearing Ehrlich tumors. Eur J Med Chem; 2006 Oct;41(10):1214-6
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  • [Title] Comparison of the anti-neoplastic effects of dirhodium(II) tetrapropionate and its adducts with nicotinate and isonicotinate anions in mice bearing Ehrlich tumors.
  • The compound effects on the survival rate of mice bearing Ehrlich ascites tumors were tested and presented in the form of a survival table, and analyzed by the Mantel-Haenszel chi-square test for N animals in each group.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Isonicotinic Acids / chemistry. Niacin / chemistry. Organometallic Compounds / pharmacology. Propionates / chemistry. Rhodium / chemistry

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  • (PMID = 16822594.001).
  • [ISSN] 0223-5234
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anions; 0 / Antineoplastic Agents; 0 / Isonicotinic Acids; 0 / Organometallic Compounds; 0 / Propionates; 2679MF687A / Niacin; DMK383DSAC / Rhodium
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65. Unahara Y, Kojima-Yuasa A, Higashida M, Kennedy DO, Murakami A, Ohigashi H, Matsui-Yuasa I: Cellular thiol status-dependent inhibition of tumor cell growth via modulation of p27(kip1) translocation and retinoblastoma protein phosphorylation by 1'-acetoxychavicol acetate. Amino Acids; 2007 Sep;33(3):469-76
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  • [Title] Cellular thiol status-dependent inhibition of tumor cell growth via modulation of p27(kip1) translocation and retinoblastoma protein phosphorylation by 1'-acetoxychavicol acetate.
  • 1'-Acetoxychavicol acetate (ACA) has been shown to inhibit tumor cell growth, but there is limited information on its effects on cell signaling and the cell cycle control pathway.
  • In this study, we sought to determine how ACA alters cell cycle and its related control factors in its growth inhibitory effect in Ehrlich ascites tumor cells (EATC).
  • [MeSH-minor] Acetylcysteine / metabolism. Animals. Benzyl Alcohols. Carcinoma, Ehrlich Tumor. Cell Line, Tumor. DNA / biosynthesis. Glutathione / analogs & derivatives. Glutathione / metabolism. Humans. Phosphorylation. Plant Extracts / chemistry. Plant Extracts / metabolism

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  • (PMID = 17031475.001).
  • [ISSN] 1438-2199
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Benzyl Alcohols; 0 / Plant Extracts; 0 / Retinoblastoma Protein; 0 / Sulfhydryl Compounds; 0 / Terpenes; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 24425-52-3 / S-ethyl glutathione; 52946-22-2 / 1'-acetoxychavicol acetate; 9007-49-2 / DNA; GAN16C9B8O / Glutathione; WYQ7N0BPYC / Acetylcysteine
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66. Tanaka H, Kageyama K, Yoshimura N, Asada R, Kusumoto K, Miwa N: Anti-tumor and anti-invasive effects of diverse delta-alkyllactones: dependence on molecular side-chain length, action period and intracellular uptake. Life Sci; 2007 Apr 24;80(20):1851-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-tumor and anti-invasive effects of diverse delta-alkyllactones: dependence on molecular side-chain length, action period and intracellular uptake.
  • Of the DALs with 11, 12, 13, 14, or 16 carbon atoms, delta-hexadecalactone (DH16:0) was the most carcinostatic when administered to Ehrlich ascites tumor (EAT) cells at 37 degrees C for 20 h, and measured by the mitochondrial dehydrogenase-based WST-1 assay.
  • The lifespan of EAT-cell-transplanted mice was markedly prolonged with DH16:0, presumably due to excellent distribution throughout the body and tumor cells.
  • [MeSH-minor] Camptothecin / chemistry. Camptothecin / pharmacokinetics. Camptothecin / pharmacology. Humans. Tumor Cells, Cultured

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  • (PMID = 17382354.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lactones; 131774-59-9 / sultriecin; XT3Z54Z28A / Camptothecin
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67. da Silva SL, Figueiredo PM, Yano T: Chemotherapeutic potential of the volatile oils from Zanthoxylum rhoifolium Lam leaves. Eur J Pharmacol; 2007 Dec 8;576(1-3):180-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this work, the anti-tumor properties of the volatile oil from Zanthoxylum rhoifolium Lam leaves and some terpenes (alpha-humulene, beta-caryophyllene, alpha-pinene and beta-pinene) were investigated in vitro and in vivo using the Ehrlich ascites tumor model.
  • Treatment of Ehrlich ascites tumor-bearing mice with 20 mg/kg of the volatile oil and beta-caryophyllene for 4 days has significantly increased survival, whereas administration of alpha-humulene, alpha-pinene and beta-pinene were ineffective in affording protection.
  • Volatile oil and beta-caryophyllene exhibited little direct activity against Ehrlich tumor cells in vitro, while alpha-humulene, alpha-pinene and beta-pinene did not such activity.
  • Investigation of the effects of the volatile oil (and terpenes) treatment on total natural killer cells (NK cell) activity from tumor-bearing mice as a possible mechanism of these compounds in vivo revealed that volatile oil and beta-caryophyllene significantly improved NK cell cytotoxicity against YAC-1, a Moloney virus-induced mouse T-cell lymphoma of A/SN origin and Ehrlich ascites cells.
  • As expected, tumor growth in non-treated mice markedly suppressed NK cell cytolysis while the volatile oil and beta-caryophyllene reversed this effect when mice were treated with 20-mg/kg dosages of these compounds for 4 days.
  • Summing up, volatile oil exhibits anti-tumor efficacy and significative immunomodulatory action in vivo, which may be related to beta-caryophyllene associated to the synergism of other natural compounds presented in volatile oil from Z. rhoifolium Lam leaves.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Oils, Volatile / therapeutic use. Zanthoxylum / chemistry
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Male. Mice. Mice, Inbred BALB C. Plant Leaves / chemistry. Rats. Rats, Sprague-Dawley. Terpenes / blood. Terpenes / pharmacology. Terpenes / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 17716654.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oils, Volatile; 0 / Terpenes
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68. Xie QJ, Zhang X, Wang X, Bai L, Li HY: [The inhibitory effects of Realgar bioleaching solution on S180 ascites-tumor and its toxicity]. Zhong Yao Cai; 2009 Jun;32(6):933-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The inhibitory effects of Realgar bioleaching solution on S180 ascites-tumor and its toxicity].
  • OBJECTIVE: To investigate the inhibitory effect of Realgar bioleaching solution (RBS) on tumor S180 cells line and estimate its toxicity, to provide experimental evidence for the further exploit of Realgar.
  • METHODS: 24 hours after the models of ascites-tumor bearing mice were established, the mice were injected RBS once a day.
  • The survival rates of S180 ascites-tumor bearing mice injected in RBS was studied, and the RBS acute toxicity of mice produced by oral, intraperitoneal or intravenous was evaluated by Drug Median Lethal Dose (LD50).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Carcinoma, Ehrlich Tumor / pathology. Sarcoma 180 / pathology. Sulfides / pharmacology

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  • (PMID = 19764334.001).
  • [ISSN] 1001-4454
  • [Journal-full-title] Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials
  • [ISO-abbreviation] Zhong Yao Cai
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Sulfides; 56320-22-0 / arsenic disulfide
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69. Orsolić N, Basić I: Water-soluble derivative of propolis and its polyphenolic compounds enhance tumoricidal activity of macrophages. J Ethnopharmacol; 2005 Oct 31;102(1):37-45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The effect of two water-soluble propolis derivatives (WSDP) from Croatia and Brazil, caffeic acid, quercetin, chrysin and naringenin which are present in WSDP was assessed on the development of Ehrlich ascites tumor (EAT).
  • It was observed that WSDP and its compounds effectively inhibited tumor growth and proliferation of EAT.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / drug therapy. Macrophage Activation / drug effects. Male. Mice. Peritoneal Cavity / cytology. Phytotherapy. Polyphenols

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  • (PMID = 16054317.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 9009-62-5 / Propolis
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70. Higashida M, Xu S, Kojima-Yuasa A, Kennedy DO, Murakami A, Ohigashi H, Matsui-Yuasa I: 1'-Acetoxychavicol acetate-induced cytotoxicity is accompanied by a rapid and drastic modulation of glutathione metabolism. Amino Acids; 2009 Jan;36(1):107-13

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The effect of 1'-acetoxychavicol acetate (ACA), an anticarcinogenic compound naturally obtained from rhizomes and seeds of South East Asia plants, on the intracellular concentration of glutathione and the activities of enzymes related to glutathione metabolism was studied in Ehrlich ascites tumor cells.
  • We showed in a previous study that ACA induced apoptosis in tumor cells and the cell death was reversed by the addition of N-acetlycysteine or glutathione ethylester.
  • These results show that ACA caused the decrease in the intracellular GSH levels in Ehrlich ascites tumor cells, suggesting that ACA-induced decrease of the cellular GSH levels can lead to growth arrest of cancer and enhancement of the efficacy other anticancer drugs.

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  • (PMID = 18266054.001).
  • [ISSN] 1438-2199
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Benzyl Alcohols; 52946-22-2 / 1'-acetoxychavicol acetate; EC 1.11.1.9 / Glutathione Peroxidase; GAN16C9B8O / Glutathione
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71. Belakavadi M, Prabhakar BT, Salimath BP: Butyrate-induced proapoptotic and antiangiogenic pathways in EAT cells require activation of CAD and downregulation of VEGF. Biochem Biophys Res Commun; 2005 Oct 7;335(4):993-1001
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this report, we study the effects of butyrate (BuA) on the growth of Ehrlich ascites tumor (EAT) cells in vivo.
  • [MeSH-major] Apoptosis / drug effects. Butyric Acid / administration & dosage. Carcinoma, Ehrlich Tumor / blood supply. Carcinoma, Ehrlich Tumor / metabolism. Deoxyribonucleases / metabolism. Neovascularization, Pathologic / metabolism. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Down-Regulation / drug effects. Enzyme Activation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Mice. Signal Transduction / drug effects

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  • Hazardous Substances Data Bank. n-BUTYRIC ACID .
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  • (PMID = 16105646.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 107-92-6 / Butyric Acid; EC 3.1.- / Deoxyribonucleases; EC 3.1.- / caspase-activated deoxyribonuclease
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72. Thippeswamy G, Sheela ML, Salimath BP: Octacosanol isolated from Tinospora cordifolia downregulates VEGF gene expression by inhibiting nuclear translocation of NF-&lt;kappa&gt;B and its DNA binding activity. Eur J Pharmacol; 2008 Jul 7;588(2-3):141-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is known that angiogenesis is involved in tumor growth and metastasis.
  • Our results showed that octacosanol (i) inhibits proliferation of endothelial cells and Ehrlich ascites tumor cells, (ii) inhibits neovascularization induced by angiogenic factors in chick chorioallantoic membrane and rat cornea in vivo angiogenesis assays, (iii) inhibits secretion of ascites fluid in the growing tumor cells in vivo.
  • Concerning the mechanism of action, octacosanol inhibited secretion of vascular endothelial growth factor into ascites fluid by the tumor cells.
  • The mechanism of inhibition of angiogenesis by octacosanol reflects on its effect on tumor angiogenesis and metastasis.
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Animals. Carcinoma, Ehrlich Tumor / drug therapy. Cell Proliferation / drug effects. Cells, Cultured. Chickens. Down-Regulation. Humans. Matrix Metalloproteinase Inhibitors. Mice. Rats

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  • (PMID = 18513715.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Fatty Alcohols; 0 / Matrix Metalloproteinase Inhibitors; 0 / NF-kappa B; 0 / Vascular Endothelial Growth Factor A; 81I2215OVK / 1-octacosanol; 9007-49-2 / DNA
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73. Dongre SH, Badami S, Natesan S, H RC: Antitumor Activity of the Methanol Extract of Hypericum hookerianum Stem Against Ehrlich Ascites Carcinoma in Swiss Albino Mice. J Pharmacol Sci; 2007 Apr;103(4):354-9
Hazardous Substances Data Bank. METHANOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor Activity of the Methanol Extract of Hypericum hookerianum Stem Against Ehrlich Ascites Carcinoma in Swiss Albino Mice.
  • In the present study, the high performance liquid chromatography (HPLC) standardized MEHH was tested for in vivo antitumor properties against Ehrlich ascites carcinoma (EAC) tumor bearing mice at 100, 200, and 400 mg/kg body weight doses given orally once daily for 14 days.
  • The results indicate that administration of the extract not only increased the survival of animals with ascites tumor, decreased the body weight induced by the tumor burden, and reduced packed cell volume and viable tissue cell count, but also altered many hematological parameters changed during tumor progression, indicating the potent antitumor nature of the extract.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Ehrlich Tumor / prevention & control. Hypericum / chemistry. Plant Extracts / pharmacology. Plant Stems / chemistry
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Female. Male. Methanol. Mice. Neoplasm Transplantation. Phytotherapy / methods. Survival Analysis. Time Factors

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  • (PMID = 17443057.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts; Y4S76JWI15 / Methanol
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74. Alonso FJ, Segura JA, Lora J, Lobo C, Fernández-Molina B, Márquez J, Matés JM: Sensitisation of Ehrlich ascitic tumour cells to methotrexate by inhibiting glutaminase. Anticancer Res; 2005 Sep-Oct;25(5):3315-20
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sensitisation of Ehrlich ascitic tumour cells to methotrexate by inhibiting glutaminase.
  • Ehrlich ascites tumour cells (EATC) and their derivative 0.28AS-2 cells, which express antisense glutaminase mRNA, show differences in both morphology and tumorigenic capacity.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Ehrlich Tumor / enzymology. Glutaminase / antagonists & inhibitors. Hydrogen Peroxide / pharmacology. Methotrexate / pharmacology

  • Hazardous Substances Data Bank. METHOTREXATE .
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  • (PMID = 16101144.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / RNA, Antisense; 0 / RNA, Messenger; BBX060AN9V / Hydrogen Peroxide; EC 3.5.1.2 / Glutaminase; YL5FZ2Y5U1 / Methotrexate
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75. Yadav AK, Mishra P, Jain S, Mishra P, Mishra AK, Agrawal GP: Preparation and characterization of HA-PEG-PCL intelligent core-corona nanoparticles for delivery of doxorubicin. J Drug Target; 2008 Jul;16(6):464-78
Hazardous Substances Data Bank. HYALURONIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The objective of the present study was to synthesize core-corona nanoparticles of doxorubicin (DOX) using hyaluronic acid-polyethyleneglycol-polycaprolactone (HA-PEG-PCL) copolymer for tumor targeting.
  • The tissue distribution study and tumor growth inhibition were performed after intravenous injection of nanoparticles in Ehrlich ascites tumor (EAT)-bearing mice.
  • The nanoparticles of HA-PEG-PCL copolymer accomplishes efficient delivery of DOX in EAT tumor when compared with the MPEG-PCL nanoparticles by the process of receptor-mediated endocytosis, as well as enhanced permeability and retention effect.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Ehrlich Tumor / metabolism. Carcinoma, Ehrlich Tumor / pathology. Delayed-Action Preparations. Drug Carriers. Female. In Vitro Techniques. Mice. Rabbits. Rats. Rats, Sprague-Dawley. Tissue Distribution

  • Hazardous Substances Data Bank. DOXORUBICIN .
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  • (PMID = 18604659.001).
  • [ISSN] 1029-2330
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Delayed-Action Preparations; 0 / Drug Carriers; 0 / Polyesters; 0 / hyaluronic acid-polyethyleneglycol-polycaprolactone copolymer; 80168379AG / Doxorubicin; 9004-61-9 / Hyaluronic Acid
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76. Guruvayoorappan C, Kuttan G: Effect of Biophytum sensitivum on cell-mediated immune response in mice. Immunopharmacol Immunotoxicol; 2007;29(3-4):337-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Effect of Biophytum sensitivum on cell-mediated immune response was studied in normal as well as Ehrlich ascites tumor bearing BALB/c mice.
  • Natural killer (NK) cell activity was enhanced significantly by Biophytum sensitivum in both the normal (43.6% cell lysis on day 5) and the tumor bearing group (48.2% cell lysis on day 5), and it was found to be earlier than tumor bearing control animals (maximum of 13.4% cell lysis on day 9).
  • Antibody dependent cellular cytotoxicity (ADCC) was also enhanced significantly in both Biophytum treated normal (35% cell lysis on day 7) as well as tumor bearing animals (40.2% cell lysis on day 7) compared to untreated control tumor bearing animals (maximum of 12.3% cell lysis on day 11).
  • An early antibody dependent complement mediated cytotoxicity (ACC) was also observed in the Biophytum treated normal (22.6% cell lysis, on day 15) and tumor bearing animals (26.4% cell lysis, on day 15).
  • [MeSH-minor] Animals. Antibody-Dependent Cell Cytotoxicity / drug effects. Bone Marrow Cells / drug effects. Carcinoma, Ehrlich Tumor / immunology. Cell Line, Tumor. Cell Proliferation / drug effects. Complement System Proteins / drug effects. Complement System Proteins / physiology. Humans. Indicators and Reagents. Killer Cells, Natural / drug effects. Lymphocyte Activation / drug effects. Male. Mice. Mice, Inbred BALB C. Mitogens / pharmacology. Plant Extracts / pharmacology. Spleen / cytology. Spleen / drug effects. T-Lymphocytes / drug effects

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  • (PMID = 18075848.001).
  • [ISSN] 0892-3973
  • [Journal-full-title] Immunopharmacology and immunotoxicology
  • [ISO-abbreviation] Immunopharmacol Immunotoxicol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indicators and Reagents; 0 / Mitogens; 0 / Plant Extracts; 9007-36-7 / Complement System Proteins
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77. Yadav AK, Agarwal A, Rai G, Mishra P, Jain S, Mishra AK, Agrawal H, Agrawal GP: Development and characterization of hyaluronic acid decorated PLGA nanoparticles for delivery of 5-fluorouracil. Drug Deliv; 2010 Nov;17(8):561-72
Hazardous Substances Data Bank. HYALURONIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cytotoxicity studies were performed on Ehrlich ascites tumor (EAT) cell lines using MTT cell proliferation assay.
  • The in vivo tumor inhibition study was also performed after i.v. administration of HA-PEG-PLGA-FU nanoparticles.
  • The tissue distribution studies displayed that HA-PEG-PLGA-FU were able to deliver a higher concentration of 5-FU in the tumor mass.
  • In addition, the HA-PEG-PLGA-FU nanoparticles reduced tumor volume significantly in comparison with 5-FU.
  • Thus, it was concluded that the conjugation of HA imparts targetability to the formulation, and enhanced permeation and retention effect ruled out its access to the non-tumor tissues, at the same time favored selective entry in tumors, thereby reducing the side-effects both in vitro and in vivo.
  • [MeSH-minor] Animals. Biocompatible Materials / administration & dosage. Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Ehrlich Tumor / metabolism. Cell Line, Tumor. Chemistry, Pharmaceutical. Drug Carriers / administration & dosage. Magnetic Resonance Imaging. Mice. Microscopy, Electron, Transmission. Particle Size. Spectroscopy, Fourier Transform Infrared. Toxicity Tests. X-Ray Diffraction

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  • (PMID = 20738221.001).
  • [ISSN] 1521-0464
  • [Journal-full-title] Drug delivery
  • [ISO-abbreviation] Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biocompatible Materials; 0 / Drug Carriers; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; 9004-61-9 / Hyaluronic Acid; U3P01618RT / Fluorouracil
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78. Nogueira IA, Leão AB, Vieira Mde S, Benfica PL, da Cunha LC, Valadares MC: Antitumoral and antiangiogenic activity of Synadenium umbellatum Pax. J Ethnopharmacol; 2008 Dec 8;120(3):474-8
MedlinePlus Health Information. consumer health - Herbal Medicine.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM OF THE STUDY: Synadenium umbellatum Pax (SU), a plant used in the Midwestern region of Brazil, was tested for its antitumor and antiangiogenic activities in vitro, using K-562 and Ehrlich ascites tumor (EAT) cells, and in vivo, using the EAT-bearing model.
  • MATERIALS AND METHODS: The viability of tumor cells was evaluated by MTT and trypan blue exclusion assays, after incubation with the ethanolic extract of SU (EESU) (0.15-20mg/mL) or equivalent concentrations of its partitioned fractions (chloroformic, hexanic, and methanolic).
  • [MeSH-minor] Animals. Brazil. Carcinoma, Ehrlich Tumor / drug therapy. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. K562 Cells. Leukemia / drug therapy. Male. Medicine, Traditional. Mice. Survival Analysis. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 18805473.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Plant Extracts; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse
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79. Srivastava A, Shivanandappa T: Stereospecificity in the cytotoxic action of hexachlorocyclohexane isomers. Chem Biol Interact; 2010 Jan 5;183(1):34-9
Hazardous Substances Data Bank. LINDANE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have investigated the toxicity of HCH isomers and its mechanism in Ehrlich Ascites tumor (EAT) cells.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / drug therapy. Caspase 3 / metabolism. Glutathione / metabolism. L-Lactate Dehydrogenase / metabolism. Lipid Peroxidation / drug effects. NADPH Oxidase / metabolism. Reactive Oxygen Species / metabolism. Sodium-Potassium-Exchanging ATPase / metabolism. Stereoisomerism

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  • (PMID = 19818741.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Insecticides; 0 / Reactive Oxygen Species; 59NEE7PCAB / Lindane; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 1.6.3.1 / NADPH Oxidase; EC 3.4.22.- / Caspase 3; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase; GAN16C9B8O / Glutathione
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80. Silva LA, Nascimento KA, Maciel MC, Pinheiro MT, Sousa PR, Ferreira SC, Azevedo AP, Guerra RN, Nascimento FR: Sunflower seed oil-enriched product can inhibit Ehrlich solid tumor growth in mice. Chemotherapy; 2006;52(2):91-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sunflower seed oil-enriched product can inhibit Ehrlich solid tumor growth in mice.
  • BACKGROUND: Sunflower seed oil (SSO) effect on solid and ascitic forms of Ehrlich tumor was evaluated.
  • METHODS: Solid or ascitic Ehrlich tumor-bearing Swiss mice were treated daily, by subcutaneous route, with 200 microl of SSO.
  • The solid tumor-bearing footpad was measured every 3 days and ascitic tumor-bearing mice had their ascites collected and quantified.
  • RESULTS: Subcutaneous treatment with SSO inhibits the solid tumor growth and increases lymph node cell number in animals with solid tumor, but has no effect on animals with ascitic tumor.
  • CONCLUSIONS: SSO can delay the solid tumor growth, possibly due to better absorption of this treatment by draining lymph nodes.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / drug therapy. Plant Oils / therapeutic use

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16462141.001).
  • [ISSN] 0009-3157
  • [Journal-full-title] Chemotherapy
  • [ISO-abbreviation] Chemotherapy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Plant Oils; 8001-21-6 / sunflower seed oil
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81. Roy S, Maity P: Effect of glutamine analogue-acivicin on tumor induced angiogenesis in Ehrlich ascites carcinoma. Indian J Exp Biol; 2005 May;43(5):407-13

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  • [Title] Effect of glutamine analogue-acivicin on tumor induced angiogenesis in Ehrlich ascites carcinoma.
  • The inhibition of tumor growth and tumor induced angiogenesis by the glutamine antimetabolite acivicin was evaluated in 6-7 weeks old male Swiss albino mice bearing Ehrlich ascites carcinoma (EAC) transplanted by intraperitoneal (ip) injections of EAC cells.
  • Treatment involving ip injections with two different doses of acivicin (0.05 and 0.41microg/g body weight/day) in saline revealed decrease in tumor volumes and reduced number of blood vessels on peritoneal wall after 10 and 15 days of treatment when compared to control (i.e. injected with saline only).
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Carcinoma, Ehrlich Tumor / blood supply. Isoxazoles / pharmacology. Neovascularization, Pathologic / prevention & control

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  • (PMID = 15900904.001).
  • [ISSN] 0019-5189
  • [Journal-full-title] Indian journal of experimental biology
  • [ISO-abbreviation] Indian J. Exp. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Isoxazoles; O0X60K76I6 / acivicin
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82. Tanaka H, Kageyama K, Kusumoto K, Asada R, Miwa N: Antitumor and anti-invasive effects of diverse new macrocyclic lactones, alkylolides and alkenylolides, and their enhancement by hyperthermia. Oncol Rep; 2007 Nov;18(5):1257-62

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  • Alkylolides and alkenylolides of 198-254 Da such as hexadecan-16-olide and 9-hexadecen-16-olide were chemically synthesized in the present study as new macrocyclic lactones that are structurally different from widespread natural macrocyclic lactones including bryostatin (887 Da) and rhizoxin (613 Da), and were investigated for antitumor activity to Ehrlich ascites tumor cells by mitochondrial dehydroganase-based WST-1 assay and dye-exclusion assay.
  • H16:0 also exhibited the most inhibitory activity to tumor invasion in addition to the highest carcinostatic activity.
  • Thus diverse alkyl-/alkenylolides, may be potent multi-applicable anticancer agents in terms of either dual inhibitory activities against both tumor progression and invasion or hyperthermia-combined therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Fibrosarcoma / drug therapy. Hyperthermia, Induced. Lactones / pharmacology
  • [MeSH-minor] Animals. Bryostatins / pharmacology. Cell Survival / drug effects. Combined Modality Therapy. Humans. Macrolides / pharmacology. Neoplasm Invasiveness. Tumor Cells, Cultured / drug effects

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  • (PMID = 17914582.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bryostatins; 0 / Lactones; 0 / Macrolides; 37O2X55Y9E / bryostatin 1; 90996-54-6 / rhizoxin
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83. Sacoman JL, Monteiro KM, Possenti A, Figueira GM, Foglio MA, Carvalho JE: Cytotoxicity and antitumoral activity of dichloromethane extract and its fractions from Pothomorphe umbellata. Braz J Med Biol Res; 2008 May;41(5):411-5
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  • DCE (100, 200, 300 and 400 mg/kg, ip) was also evaluated in the Ehrlich ascites tumor model.

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  • (PMID = 18545814.001).
  • [ISSN] 1414-431X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts; 588X2YUY0A / Methylene Chloride
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84. Martín-Rufián M, Segura JA, Lobo C, Matés JM, Márquez J, Alonso FJ: Identification of genes downregulated in tumor cells expressing antisense glutaminase mRNA by differential display. Cancer Biol Ther; 2006 Jan;5(1):54-8
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  • [Title] Identification of genes downregulated in tumor cells expressing antisense glutaminase mRNA by differential display.
  • Ehrlich ascites tumor cells (EATC) is a highly proliferative malignant cell line derived from mouse mammary epithelia, whereas their derivative, 0.28AS-2 cells, expressing antisense glutaminase mRNA, show a less transformed phenotype and loss of their tumorigenic capacity in vivo correlated with an inhibition of glutaminase expression.
  • Our results show the validity of mRNA differential display technique to get insights into the molecular mechanisms underlying the acquisition of a more differentiated phenotype by tumor cells after inhibition of glutaminase expression.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / enzymology. Carcinoma, Ehrlich Tumor / genetics. Gene Expression Regulation, Neoplastic. Glutaminase / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. DNA, Complementary / genetics. Down-Regulation. Gene Expression Regulation, Enzymologic. Mice. RNA, Antisense / genetics. RNA, Antisense / metabolism. RNA, Messenger / analysis. Rats

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  • (PMID = 16294018.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / RNA, Antisense; 0 / RNA, Messenger; EC 3.5.1.2 / Glutaminase
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85. Upadhyay KK, Bhatt AN, Castro E, Mishra AK, Chuttani K, Dwarakanath BS, Schatz C, Le Meins JF, Misra A, Lecommandoux S: In vitro and in vivo evaluation of docetaxel loaded biodegradable polymersomes. Macromol Biosci; 2010 May 14;10(5):503-12
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  • In addition, PolyDOC uptake in Ehrlich Ascites Tumor (EAT) tumor bearing mice was larger at each time point compared to DS, making such a polymer vesicle formulation an efficient drug nanocarrier for improved DOC cancer therapy.
  • [MeSH-minor] Animals. Capsules. Cell Line, Tumor. Female. Humans. Mice. Mice, Inbred BALB C. Rabbits

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  • (PMID = 20232310.001).
  • [ISSN] 1616-5195
  • [Journal-full-title] Macromolecular bioscience
  • [ISO-abbreviation] Macromol Biosci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Capsules; 0 / Delayed-Action Preparations; 0 / Taxoids; 0 / poly(gamma-benzyl glutamate)-b-hyaluronan; 15H5577CQD / docetaxel; 25513-46-6 / Polyglutamic Acid; 9004-61-9 / Hyaluronic Acid
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86. Jaganathan SK, Mondhe D, Wani ZA, Pal HC, Mandal M: Effect of honey and eugenol on Ehrlich ascites and solid carcinoma. J Biomed Biotechnol; 2010;2010:989163
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  • [Title] Effect of honey and eugenol on Ehrlich ascites and solid carcinoma.
  • Ehrlich ascites carcinoma is a spontaneous murine mammary adenocarcinoma adapted to ascites form and carried in outbred mice by serial intraperitoneal (i/p) passages.
  • In this work, we extended our research to screen the antitumor activity of two selected honey samples and eugenol (one of the phenolic constituents of honey) against murine Ehrlich ascites and solid carcinoma models.
  • Honey containing higher phenolic content was found to significantly inhibit the growth of Ehrlich ascites carcinoma as compared to other samples.
  • When honey containing higher phenolic content was given at 25% (volume/volume) intraperitoneally (i/p), the maximum tumor growth inhibition was found to be 39.98%.
  • However, honey was found to be less potent in inhibiting the growth of Ehrlich solid carcinoma.
  • On the other hand, eugenol at a dose of 100 mg/kg i/p was able to inhibit the growth of Ehrlich ascites by 28.88%.
  • In case of solid carcinoma, eugenol (100 mg/kg; i/p) showed 24.35% tumor growth inhibition.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / drug therapy. Eugenol / pharmacology. Honey

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  • [Cites] Indian J Physiol Pharmacol. 1994 Oct;38(4):306-8 [7883300.001]
  • [Cites] Ann N Y Acad Sci. 1956 Mar 14;63(5):728-37 [13314431.001]
  • [Cites] J Biol Chem. 2005 Feb 18;280(7):5812-9 [15574415.001]
  • [Cites] Invest New Drugs. 2010 Oct;28(5):624-33 [19705065.001]
  • [Cites] Vopr Onkol. 1990;36(6):704-9 [2378090.001]
  • [Cites] Carcinogenesis. 2003 Jan;24(1):75-80 [12538351.001]
  • [Cites] Int J Urol. 2003 Apr;10(4):213-9 [12657101.001]
  • [Cites] Nature. 1970 Feb 21;225(5234):734-5 [5412777.001]
  • [Cites] Am J Clin Nutr. 1978 Mar;31(3):457-65 [629217.001]
  • [Cites] Nat Prod Res. 2010 Sep;24(14):1295-306 [20803373.001]
  • (PMID = 20369055.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3T8H1794QW / Eugenol
  • [Other-IDs] NLM/ PMC2846731
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87. Deepak AV, Salimath BP: Antiangiogenic and proapoptotic activity of a novel glycoprotein from U. indica is mediated by NF-kappaB and Caspase activated DNase in ascites tumor model. Biochimie; 2006 Mar-Apr;88(3-4):297-307

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiangiogenic and proapoptotic activity of a novel glycoprotein from U. indica is mediated by NF-kappaB and Caspase activated DNase in ascites tumor model.
  • We have identified a novel glycoprotein from Urginea indica bulbs with potent in vivo antitumor activity against growth of an ascites tumor, mouse mammary carcinoma.
  • The mechanism of antiangiogenesis involved inhibition of translocation of nuclear factor kappa B to the nucleus resulting in decreased expression of vascular endothelial growth factor gene as is demonstrated by our results on quantification of vascular endothelial growth factor levels in the glycoprotein treated tumor bearing mice.
  • Our results on activation of Caspase-3 with concomitant translocation of caspase activated DNase to the tumor cell nuclei resulting in DNA fragmentation induced by the glycoprotein in vivo clearly demonstrated a parallel proapoptotic activity of the glycoprotein.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis. Carcinoma, Ehrlich Tumor / drug therapy. Deoxyribonucleases / metabolism. Glycoproteins / pharmacology. NF-kappa B / antagonists & inhibitors
  • [MeSH-minor] Animals. Antigens, CD31 / immunology. Antigens, CD31 / metabolism. Caspase 3. Caspases / metabolism. Cell Proliferation / drug effects. Cells, Cultured. DNA Fragmentation. Disease Models, Animal. Endothelial Cells / metabolism. Female. Humans. Mice. Plant Roots / cytology. Plant Roots / metabolism. Plants, Medicinal / cytology. Plants, Medicinal / metabolism. Protein Transport. Sequence Homology. Umbilical Veins / cytology. Urginea / chemistry. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / pharmacology

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  • (PMID = 16216405.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Antineoplastic Agents, Phytogenic; 0 / Glycoproteins; 0 / NF-kappa B; 0 / Vascular Endothelial Growth Factor A; EC 3.1.- / Deoxyribonucleases; EC 3.1.- / Dffb protein, mouse; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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88. Ghoneum M, Badr El-Din NK, Noaman E, Tolentino L: Saccharomyces cerevisiae, the Baker's Yeast, suppresses the growth of Ehrlich carcinoma-bearing mice. Cancer Immunol Immunother; 2008 Apr;57(4):581-92
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  • [Title] Saccharomyces cerevisiae, the Baker's Yeast, suppresses the growth of Ehrlich carcinoma-bearing mice.
  • This study was undertaken to evaluate the effectiveness and mechanisms of anti-tumor activity of Baker's yeast, Saccharomyces cerevisiae, in immunocompetent mice.
  • Swiss albino mice were inoculated intramuscularly in the right thigh with Ehrlich Ascites Carcinoma (EAC) cells.
  • At day 8, mice bearing Solid Ehrlich Carcinoma tumor (SEC) were intratumorally (IT) injected with killed S. cerevisiae (10 x 10(6) and 20 x 10(6) cells) for 35 days.
  • Histopathology of yeast-treated mice showed extensive tumor degeneration, apoptosis, and ischemic (coagulative) and liquefactive necrosis.
  • These changes are associated with a tumor growth curve that demonstrates a significant antitumor response that peaked at 35 days.
  • Yeast treatment (20 x 10(6) cells) three times a week resulted in a significant decrease in tumor volume (TV) (67.1%, P < 0.01) as compared to PBS-treated mice.
  • Administration of yeast significantly enhanced the recruitment of leukocytes, including macrophages, into the tumors and triggered apoptosis in SEC cells as determined by flow cytometry (78.6%, P < 0.01) at 20 x 10(6) cells, as compared to PBS-treated mice (42.6%).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Ehrlich Tumor / pathology. Carcinoma, Ehrlich Tumor / therapy. Saccharomyces cerevisiae

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  • (PMID = 17891396.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines
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89. Pathak A, Swami A, Patnaik S, Jain S, Chuttani K, Mishra AK, Vyas SP, Kumar P, Gupta KC: Efficient tumor targeting by polysaccharide decked polyethylenimine based nanocomposites. J Biomed Nanotechnol; 2009 Jun;5(3):264-77
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  • [Title] Efficient tumor targeting by polysaccharide decked polyethylenimine based nanocomposites.
  • Hyaluronic acid (HA)-polyethylenimine (PEI, 25 kDa) (HP) nanocomposites were fabricated for efficient targeting to solid tumors.
  • The specificity of HP nanocomposites to target tumor was investigated in vivo by injecting pDNA-loaded HP-4 nanocomposite or PEI intravenously into mice bearing Ehrlich ascites tumor (EAT).
  • The gamma scintigraphic studies showed a higher accumulation of HP-4 nanocomposite in the solid tumor compared to PEI.

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  • (PMID = 20055008.001).
  • [ISSN] 1550-7033
  • [Journal-full-title] Journal of biomedical nanotechnology
  • [ISO-abbreviation] J Biomed Nanotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Polysaccharides; 9002-98-6 / Polyethyleneimine; 9007-49-2 / DNA; 91D9GV0Z28 / Durapatite
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90. Ustun F, Durmus-Altun G, Cukur Z, Altaner S, Berkarda S: Glucose-induced alteration of accumulation of organotechnetium complexes accumulation in Pgp-negative tumor-bearing mice. Cancer Biother Radiopharm; 2009 Jun;24(3):333-8
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  • [Title] Glucose-induced alteration of accumulation of organotechnetium complexes accumulation in Pgp-negative tumor-bearing mice.
  • The biologic and microenvironmental factors determining (99m)Tc sestamibi (MIBI) and (99m)Tc tetrofosmin (TF) uptake in breast tumors are incompletely understood, especially in P-glycoprotein (Pgp)-negative tumors.
  • We analyzed the influence of glucose administration on the uptake and retention of MIBI and TF in Pgp-negative tumor-bearing mice in vivo.
  • Twenty (20) mice bearing Ehrlich ascites tumor cell (EATC) xenografts were divided into four groups:.
  • Increased blood glucose level affected the MIBI uptake of tumor tissue, particularly for E-UPR.
  • [MeSH-minor] Animals. Blood Glucose / drug effects. Blood Glucose / metabolism. Carcinoma, Ehrlich Tumor / genetics. Carcinoma, Ehrlich Tumor / metabolism. Carcinoma, Ehrlich Tumor / pathology. Data Interpretation, Statistical. Female. Metabolism / drug effects. Mice. Mice, Inbred BALB C. Organophosphorus Compounds / metabolism. Radiopharmaceuticals / metabolism. Technetium Tc 99m Sestamibi / metabolism

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  • (PMID = 19538056.001).
  • [ISSN] 1557-8852
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Organophosphorus Compounds; 0 / Organotechnetium Compounds; 0 / P-Glycoprotein; 0 / Radiopharmaceuticals; 0 / technetium Tc 99m 1,2-bis(bis(2-ethoxyethyl)phosphino)ethane; 971Z4W1S09 / Technetium Tc 99m Sestamibi; IY9XDZ35W2 / Glucose
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91. Sinha D, Shukla G, Tiwari AK, Chaturvedi S, Chuttani K, Chandra H, Mishra AK: 99mTc-DTPA-amino acids conjugate as specific SPECT pharmaceuticals for tumor imaging. Chem Biol Drug Des; 2009 Aug;74(2):159-64
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  • [Title] 99mTc-DTPA-amino acids conjugate as specific SPECT pharmaceuticals for tumor imaging.
  • (99m)Tc-Diethylene triamine pentaacetic acid-bis (amide) conjugates have been synthesized and evaluated as a potential radiopharmaceutical for tumor imaging.
  • Imaging and biodistribution studies were performed in mice bearing Ehrlich ascites tumor (EAT) tumors in right thigh.
  • Radioconjugate derived from l-5-hydroxytryptophan exhibited remarkable localization at tumor site; whereas radiotracer derived from l-methyl tryptophan shows relatively less accumulation at the tumor site.
  • Tumor-to-muscles ratios were 5.07 +/- 0.001, and 4.2 +/- 0.001 at 1 and 4 h for (99m)Tc-DTPA-(Me trp)(2) and 4.97 +/- 0.001 and 5.8 +/- 0.001 at 1 and 4 h after postinjection for (99m)Tc-DTPA-(5HT)(2), respectively.
  • The preliminary results with these amino acid based ligands are encouraging to carrying out further in vivo experiments for targeted tumor imaging.
  • [MeSH-major] 5-Hydroxytryptophan / analogs & derivatives. Carcinoma, Ehrlich Tumor / radionuclide imaging. Pentetic Acid / analogs & derivatives. Radiopharmaceuticals / pharmacokinetics. Tryptophan / pharmacokinetics
  • [MeSH-minor] Amino Acids / chemistry. Animals. Cell Line, Tumor. Humans. Mice. Mice, Inbred BALB C. Rabbits. Technetium Tc 99m Pentetate / chemistry. Tissue Distribution. Tomography, Emission-Computed, Single-Photon

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  • (PMID = 19614681.001).
  • [ISSN] 1747-0285
  • [Journal-full-title] Chemical biology & drug design
  • [ISO-abbreviation] Chem Biol Drug Des
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Radiopharmaceuticals; 7303-49-3 / tryptophan methyl ester; 7A314HQM0I / Pentetic Acid; 8DUH1N11BX / Tryptophan; C1LJO185Q9 / 5-Hydroxytryptophan; VW78417PU1 / Technetium Tc 99m Pentetate
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92. Ponnappa KC, Saviour P, Ramachandra NB, Kini RM, Gowda TV: INN-toxin, a highly lethal peptide from the venom of Indian cobra (Naja naja) venom-Isolation, characterization and pharmacological actions. Peptides; 2008 Nov;29(11):1893-900
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  • It is toxic to Ehrlich ascites tumor (EAT) cells, but it is not toxic to leukocyte culture.

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  • (PMID = 18760317.001).
  • [ISSN] 0196-9781
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cobra Neurotoxin Proteins; 0 / Cobra Venoms; 0 / INN-toxin, Naja naja
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93. Inzhevatkin EV, Fomenko EIu, Slepov EV, Savchenko AA: [Metabolic changes of lymphocytes and neoplastic cells in mice with Ehrlich ascites carcinoma during tumor growth]. Izv Akad Nauk Ser Biol; 2007 May-Jun;(3):376-80
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  • [Title] [Metabolic changes of lymphocytes and neoplastic cells in mice with Ehrlich ascites carcinoma during tumor growth].
  • Changes in the activities of NAD+- and NADP-dependent dehydrogenases of lymphocytes and tumor cells were studied in mice with Ehrlich ascites carcinoma, as well as changes in the concentrations of oxaloacetate, lactate, and NAD+ in the course of tumor growth.
  • During the major period of tumor growth, conditions are produced in the lymphocytes for increased intensity of aerobic reactions directed at energy reproduction combined with a somewhat decreased intensity of synthetic processes.
  • In the tumor cells, conditions predominantly arise for intensification of plastic metabolic reactions and reactions related to anaerobic energy reproduction.

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  • (PMID = 17853702.001).
  • [ISSN] 1026-3470
  • [Journal-full-title] Izvestiia Akademii nauk. Seriia biologicheskaia
  • [ISO-abbreviation] Izv. Akad. Nauk. Ser. Biol.
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0U46U6E8UK / NAD; 2F399MM81J / Oxaloacetic Acid; 33X04XA5AT / Lactic Acid; 53-59-8 / NADP; EC 1.- / Oxidoreductases
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94. Novikov GV, Novikov VV, Fesenko EE: [Effect of weak combined static and low-frequency alternating magnetic fields on the Ehrlich ascites carcinoma in mice]. Biofizika; 2009 Nov-Dec;54(6):1120-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of weak combined static and low-frequency alternating magnetic fields on the Ehrlich ascites carcinoma in mice].
  • The exposure to these magnetic fields inhibits the tumor growth in mice with the intraperitoneally transplanted Ehrlich ascites carcinoma.
  • The effect manifests itself in an increase in the life of tumor-bearing animals and in the content of damaged tumor cells.
  • It was found that the death of tumor cells by the action of weak fields occurs predominantly by the mechanism of necrosis.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / therapy. Magnetic Field Therapy

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  • (PMID = 20067194.001).
  • [ISSN] 0006-3029
  • [Journal-full-title] Biofizika
  • [ISO-abbreviation] Biofizika
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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95. Lingaraju SM, Keshavaiah K, Salimath BP: Inhibition of in vivo angiogenesis by Anacardium occidentale L. involves repression of the cytokine VEGF gene expression. Drug Discov Ther; 2008 Aug;2(4):234-44

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Lethal tumor growth and progression cannot occur without angiogenesis, which facilitates cancer cell proliferation, survival, and dissemination.
  • In this study, we have tested the crude ethanolic extract of the leaves of Anacardium occidentale Linn, on Ehrlich ascites tumor cells (EAT) in vivo and in vitro.
  • The extract inhibited cell proliferation of different tumor cells such as EAT, BeWo, and MCF-7 in vitro in a dose-dependent manner and it reduced the VEGF level in the ascites of treated mice.

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  • (PMID = 22504635.001).
  • [ISSN] 1881-7831
  • [Journal-full-title] Drug discoveries & therapeutics
  • [ISO-abbreviation] Drug Discov Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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96. Asada R, Kageyama K, Tanaka H, Matsui H, Kimura M, Saitoh Y, Miwa N: Antitumor effects of nano-bubble hydrogen-dissolved water are enhanced by coexistent platinum colloid and the combined hyperthermia with apoptosis-like cell death. Oncol Rep; 2010 Dec;24(6):1463-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In order to erase reactive oxygen species (ROS) related with the proliferation of tumor cells by reducing activity of hydrogen, we developed functional water containing nano-bubbles (diameters: <900 nm for 71%/population) hydrogen of 1.1-1.5 ppm (the theoretical maximum: 1.6 ppm) with a reducing ability (an oxidation-reduction potential -650 mV, normal water: +100-200 mV) using a microporous-filter hydrogen-jetting device.
  • We showed that hydrogen water erased ROS indispensable for tumor cell growth by ESR/spin trap, the redox indicator CDCFH-DA assay, and was cytotoxic to Ehrlich ascites tumor cells as assessed by WST-8 assay, crystal violet dye stain and scanning electron microscopy, after 24-h or 48-h incubation sequent to warming at 37°C or 42°C.
  • Thus, the nano-bubble hydrogen water with platinum colloid is potent as an anti-tumor agent.

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  • (PMID = 21042740.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Colloids; 0 / Gases; 059QF0KO0R / Water; 49DFR088MY / Platinum; 7YNJ3PO35Z / Hydrogen
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97. Chandrashekar NS, Hiremath SR: Transdermal delivery of 5-fluorouracil for induced ehrlich ascites carcinoma tumor in BALB/c mice and pharmacokinetic study. Recent Pat Anticancer Drug Discov; 2007 Nov;2(3):235-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transdermal delivery of 5-fluorouracil for induced ehrlich ascites carcinoma tumor in BALB/c mice and pharmacokinetic study.
  • The purpose of this study was to determine the permeation of the hydrophilic compound 5-fluorouracil through human epidermal membranes, Ehrlich Ascites Carcinoma (EAC) cells were used as a model cell line to evaluate the cytotoxic concentration and anti-tumor activity of 5-fluorouracil (5-FU) through transdermal drug delivery for tumors.
  • For 5-fluorouracil monolithic matrix transdermal patch, the results were statistically significant (p<0.05) compared to untreated control, anti-tumor activity was very effective compared to intravenous therapy.
  • Recent patents has been reported for suitable treatment of tumors and cancer, by topical and transdermal applications.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Ehrlich Tumor / drug therapy. Fluorouracil / administration & dosage. Fluorouracil / therapeutic use
  • [MeSH-minor] Adhesiveness. Administration, Cutaneous. Animals. Cell Line, Tumor. Chemistry, Physical. Drug Delivery Systems. Humans. Irritants / toxicity. Mice. Mice, Inbred BALB C. Physicochemical Phenomena. Rabbits. Survival Analysis

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  • (PMID = 18221066.001).
  • [ISSN] 1574-8928
  • [Journal-full-title] Recent patents on anti-cancer drug discovery
  • [ISO-abbreviation] Recent Pat Anticancer Drug Discov
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Irritants; U3P01618RT / Fluorouracil
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98. Nikolin VP, Popova NA, Sebeleva TE, Strunkin DN, Rogachev VA, Semënov DV, Bogachev SS, Iakubov LA, Shurdov MA: [Effect of exogenous DNA on the growth of transplantable tumors]. Vopr Onkol; 2006;52(1):66-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of exogenous DNA on the growth of transplantable tumors].
  • Using transplantable Ehrlich ascites tumor, hepatoma HA-1 and Lewis carcinoma it was shown, that preparations of fragmented genomic DNA can more or less effectively inhibit such tumors as well as the growth of their metastases.
  • Such effects were produced by DNA preparations derived from tissues of mice, both syngeneic or allogeneic to tumor-bearer, as well as from human tissues.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / drug therapy. Carcinoma, Lewis Lung / drug therapy. DNA / pharmacology. DNA Fragmentation. Liver Neoplasms, Experimental / drug therapy

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  • (PMID = 16715707.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 9007-49-2 / DNA
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99. Jagetia GC, Venkatesh P, Baliga MS: Aegle marmelos (L.) Correa inhibits the proliferation of transplanted Ehrlich ascites carcinoma in mice. Biol Pharm Bull; 2005 Jan;28(1):58-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aegle marmelos (L.) Correa inhibits the proliferation of transplanted Ehrlich ascites carcinoma in mice.
  • The anticancer effect of hydroalcoholic extract of Aegle marmelos (AME) was studied in the Ehrlich ascites carcinoma bearing Swiss albino mice.
  • The spatial effect of various AME administration schedules showed that six-day administration increased the survival of tumor bearing mice.
  • Administration of AME once daily for six consecutive days to the tumor bearing mice caused a dose dependent remission of the tumor at 400 mg/kg body weight, where the greatest antitumor effect was observed and the higher doses showed toxic manifestations.
  • This dose of 400 mg/kg was considered as the best dose, where the animals survived up to 43 d post-tumor-cell inoculation as against no survivors in the saline treated control group.
  • Stage specific evaluation of AME inhibited the increase in body weight gain in animals due to tumor development during early stages only.
  • [MeSH-major] Aegle. Carcinoma, Ehrlich Tumor / drug therapy. Cell Proliferation / drug effects

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  • (PMID = 15635164.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Plant Extracts
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100. Zamay TN, Zamay AS: Influence of ATP on Ehrlich ascites carcinoma cell free cytoplasmic calcium concentration in the course of tumor growth. Biochemistry (Mosc); 2006 Oct;71(10):1090-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of ATP on Ehrlich ascites carcinoma cell free cytoplasmic calcium concentration in the course of tumor growth.
  • The changes in free cytoplasmic calcium concentration ([Ca2+](in)) and the effects of extracellular ATP on [Ca2+](in) have been studied in Ehrlich ascites carcinoma cells in the dynamics of their growth.
  • The basal level of [Ca2+](in) and the effects of ATP on the ascites cells were determined by the stage of tumor growth and depended on the content of reactive oxygen species (ROS).
  • The sharp increase in basal and ATP-induced elevation of [Ca2+](in) levels were observed at the 12th day of ascites cell growth.
  • We suggest that the increased sensitivity of the ascites cells to ATP observed on the 12th day may be also attributed to a decrease in ecto-ATPase activity.
  • [MeSH-minor] Acetylcysteine / pharmacology. Adenosine Triphosphatases / metabolism. Animals. Carcinoma, Ehrlich Tumor / metabolism. Carcinoma, Ehrlich Tumor / pathology. Egtazic Acid / pharmacology. Mice. Mice, Inbred ICR. Reactive Oxygen Species / metabolism. Time Factors. Tumor Cells, Cultured

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  • (PMID = 17125456.001).
  • [ISSN] 0006-2979
  • [Journal-full-title] Biochemistry. Biokhimii︠a︡
  • [ISO-abbreviation] Biochemistry Mosc.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 526U7A2651 / Egtazic Acid; 8L70Q75FXE / Adenosine Triphosphate; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / ectoATPase; SY7Q814VUP / Calcium; WYQ7N0BPYC / Acetylcysteine
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