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1. Kagawa Y, Noge I, Higashigawa M, Komada Y: Combined antitumor effect of cyclophosphamide and bromodeoxyuridine in BDF1 mice bearing L1210 ascites tumors. Biol Pharm Bull; 2008 Jan;31(1):57-61
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  • [Title] Combined antitumor effect of cyclophosphamide and bromodeoxyuridine in BDF1 mice bearing L1210 ascites tumors.
  • We investigated the combined effect of cyclophosphamide (CPA) and 5-bromo-2'-deoxyuridine (BrdUrd) both in mice bearing L1210 ascites tumors and in L1210 leukemic cells in vitro.

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  • (PMID = 18175942.001).
  • [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] 1XBF4E50HS / 4-hydroxycyclophosphamide; 8N3DW7272P / Cyclophosphamide; G34N38R2N1 / Bromodeoxyuridine
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2. 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

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  • [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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3. Shafren DR, Sylvester D, Johansson ES, Campbell IG, Barry RD: Oncolysis of human ovarian cancers by echovirus type 1. Int J Cancer; 2005 Jun 10;115(2):320-8
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  • The therapeutic efficacy of EV1 was demonstrated by rapid reduction of tumor burden by a single viral intratumoral injection in SCID mice bearing multiple preformed s.c. xenografts.
  • Using an in vivo i.p. human ovarian cancer xenograft model, administration of EV1 was further shown to significantly inhibit the formation and burden of ascites tumors.
  • [MeSH-minor] Animals. Epithelial Cells / metabolism. Epithelial Cells / pathology. Epithelial Cells / virology. Female. Humans. Integrin alpha2beta1 / metabolism. Mice. Mice, SCID. Spheroids, Cellular / metabolism. Spheroids, Cellular / pathology. Spheroids, Cellular / virology. Transplantation, Heterologous. Tumor Cells, Cultured. Viremia. Virus Replication

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 15688406.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alpha2beta1
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4. 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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5. Potter M: Brief historical sketch of chromosomal translocations and tumors. J Natl Cancer Inst Monogr; 2008;(39):2-7
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  • [Title] Brief historical sketch of chromosomal translocations and tumors.
  • Many of his predictions would have to wait for confirmation until the 1950--1960s, when mammalian cytogenetics became feasible with the use of ascites tumors as sources of metaphases.
  • This advance coupled with the discovery of G banding by Caspersson and his associates led to finding characteristic recurring chromosomal abnormalities in certain kinds of tumors.

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  • (PMID = 18647993.001).
  • [ISSN] 1052-6773
  • [Journal-full-title] Journal of the National Cancer Institute. Monographs
  • [ISO-abbreviation] J. Natl. Cancer Inst. Monographs
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article
  • [Publication-country] United States
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6. 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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  • Hazardous Substances Data Bank. CATECHOL .
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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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7. 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
Hazardous Substances Data Bank. ACETONE CYANOHYDRIN .

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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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8. 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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9. Liu A, Yang N, Song W, Cao D, Wang W: Cartilage polysaccharide induces apoptotic cell death of L1210 cells. Leuk Lymphoma; 2009 Jun;50(6):1017-29

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  • We investigated the antitumor effect of a short-chain polysaccharide (PS) extracted from porcine cartilage both in L1210 leukemic cells in vitro and in mice bearing L1210 ascites tumors.
  • [MeSH-minor] Animals. Blotting, Western. Caspase 3 / metabolism. Caspase 9 / metabolism. Cell Line, Tumor. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Female. Fluorescent Antibody Technique. Mice. Mice, Inbred DBA. Proteins. Proto-Oncogene Proteins c-bcl-2 / metabolism. Swine. Time Factors. bcl-2-Associated X Protein / metabolism

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  • (PMID = 19431040.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bax protein, mouse; 0 / Bcl2l2 protein, mouse; 0 / Polysaccharides; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
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10. 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
Hazardous Substances Data Bank. RHODIUM .

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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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11. Pain A, Samanta S, Dutta S, Saxena AK, Shanmugavel M, Sharma M, Qazi GN, Sanyal U: Synthesis and evaluation of ethylnitrosoureas of substituted naphthalimides as anticancer compounds. Acta Pol Pharm; 2007 Jan-Feb;64(1):27-33
Hazardous Substances Data Bank. LOMUSTINE .

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  • Their anti-tumor efficacies were assessed in vivo in two murine ascites tumors namely Sarcoma-180 (S-180) and Ehrlich ascites carcinoma (EAC) by measuring the increase in median survival times (MST) of drug treated (T) over untreated control (C) mice.
  • The representative compound 3a has displayed marginal anti-tumoral activity in these tumors.
  • Three compounds were further screened in vitro in 4 different human tumor cell lines but no significant activity was observed in those lines.
  • These compounds moderately inhibit the synthesis of DNA and RNA in S-180 tumor cells.
  • [MeSH-major] Antineoplastic Agents, Alkylating / chemical synthesis. Carcinoma, Ehrlich Tumor / drug therapy. Naphthalimides / chemical synthesis. Nitrosourea Compounds / chemical synthesis. Sarcoma 180 / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA / biosynthesis. DNA / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Imides / pharmacology. Isoquinolines / pharmacology. Lomustine / pharmacology. Mice. RNA / biosynthesis. RNA / drug effects. Structure-Activity Relationship

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  • (PMID = 17665847.001).
  • [ISSN] 0001-6837
  • [Journal-full-title] Acta poloniae pharmaceutica
  • [ISO-abbreviation] Acta Pol Pharm
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Imides; 0 / Isoquinolines; 0 / Naphthalimides; 0 / Nitrosourea Compounds; 06Q0V17SI9 / mitonafide; 63231-63-0 / RNA; 7BRF0Z81KG / Lomustine; 9007-49-2 / DNA
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12. Chen T, Li D, Fu YL, Hu W: Screening of QHF formula for effective ingredients from Chinese herbs and its anti-hepatic cell cancer effect in combination with chemotherapy. Chin Med J (Engl); 2008 Feb 20;121(4):363-8
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

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  • The QHF formula and the best ratio of ingredients were evaluated in H(22) mouse (KM) models with solid tumors and ascites tumors by uniform design and monitoring inhibition of tumor growth and survival.
  • We then observed the anti-hepatic cell cancer (HCC) effect of QHF when combined with cisplatin (DDP) in H(22) mouse (Balb/c) models with solid tumors and ascites tumors.
  • Evaluating of the therapeutic effect included the general condition of the mice, inhibition of tumor growth, survival, changes in body weight, thymus index, spleen index and WBC counts.
  • Treatment was more efficient in inhibiting the growth of transplanted tumors in H(22) mice when using the QHF formula (55.91%) than using Cinobufotalin (33.25%), Ginsenosides Rg3 (35.11%), PNS (27.12%) or Lentinan (4.97%) separately.
  • QHF also prolonged the life of H(22) ascites hepatic cancer mice more efficiently (38.13%) than Cinobufotalin (25.00%), Ginsenosides Rg3 (27.27%), PNS (23.30%) or Lentinan (24.43%).
  • Combining QHF with DDP the tumor growth inhibition reached 82.54% with a 66.83% increase in survival.
  • QHF combined with DDP can attenuate tumor growth and suppresses the DDP-induced toxic reactions.

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  • (PMID = 18304471.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; Q20Q21Q62J / Cisplatin
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13. Oršolić N, Benković V, Lisičić D, Dikić D, Erhardt J, Knežević AH: Protective effects of propolis and related polyphenolic/flavonoid compounds against toxicity induced by irinotecan. Med Oncol; 2010 Dec;27(4):1346-58

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  • This study was carried out to find whether propolis preparations and related flavonoids (quercetin, naringin) might enhance irinotecan-induced cytotoxicity to tumor cells in mice bearing Ehrlich ascites tumors (EAT) while protecting normal blood, liver, and kidney cells.
  • Irinotecan was administered ip at dose of 50 mg kg(-1) on days 3, 4, and 5 after tumor cell inoculation.
  • However, when mice were pre-treated with test components prior to irinotecan, the frequencies of irinotecan-induced micronuclei (MN) was decreased but in mice bearing tumor QU and EEP increased number of micronucleated cells.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / toxicity. Camptothecin / analogs & derivatives. Carcinoma, Ehrlich Tumor / drug therapy. Flavonoids / therapeutic use. Immunologic Factors / therapeutic use. Phenols / therapeutic use. Propolis / therapeutic use

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  • (PMID = 20013318.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Flavonoids; 0 / Immunologic Factors; 0 / Phenols; 0H43101T0J / irinotecan; 9009-62-5 / Propolis; XT3Z54Z28A / Camptothecin
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14. Samanta S, Pain A, Dutta S, Saxena AK, Shanmugavel M, Pandita RM, Qazi GN, Sanyal U: Antitumor activity of Nitronaphthal-NU, a novel mixed-function agent. J Exp Ther Oncol; 2005;5(1):15-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In vitro screening in four human tumor cell lines namely SNB-78 CNS, HOP-62 Lung, T47D Breast and SiHa - cervix revealed significant cytotoxicity in the former two cell lines much greater than CCNU and comparable to Mitonafide used as standards.
  • In vivo antitumoral potency assessed in the murine ascites tumors Sarcoma-180 (S-180) and Ehrlich ascites carcinoma (EAC) by measuring the increase in median survival times of drug treated (T) over untreated control (C) mice, revealed highly significant (p<0.001) tumor regression effects greater than standards.
  • Life span of mice bearing advanced tumor for 10 days before the drug challenge was also considerably increased.
  • The compound comparable to standards inhibited the synthesis of DNA and RNA in S-1 80 tumor cells.
  • [MeSH-minor] Alkylation. Animals. Cell Line, Tumor. DNA / drug effects. DNA / metabolism. DNA, Neoplasm / biosynthesis. Drug Screening Assays, Antitumor. Drug Synergism. Humans. Imides / therapeutic use. Isoquinolines / therapeutic use. Lomustine / therapeutic use. Mice. Naphthalimides. Neoplasm Transplantation. RNA, Neoplasm / biosynthesis. Sarcoma 180 / metabolism. Thymidine / metabolism. Uridine / metabolism

  • Hazardous Substances Data Bank. LOMUSTINE .
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  • (PMID = 16416597.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / Imides; 0 / Isoquinolines; 0 / Naphthalenes; 0 / Naphthalimides; 0 / RNA, Neoplasm; 0 / nitronaphthal-NU; 06Q0V17SI9 / mitonafide; 7BRF0Z81KG / Lomustine; 9007-49-2 / DNA; VC2W18DGKR / Thymidine; WHI7HQ7H85 / Uridine
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15. Chan SL, Mo FK, Koh J, Hui EP, Yu SC, Lai PB, Chan HL, Chan VT, Chan AT, Yeo W, Mok T: Predictors of treatment outcomes in early stage hepatocellular carcinoma (HCC) detected in a surveillance program. J Clin Oncol; 2009 May 20;27(15_suppl):4584

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictors of treatment outcomes in early stage hepatocellular carcinoma (HCC) detected in a surveillance program.
  • : 4584 Background: Surveillance for HCC in hepatitis B virus (HBV) carriers aims to improve survival by detection of early resectable tumor.
  • In 2005, our group reported low surgical resection rates despite detection of small sized tumors in a prospective surveillance cohort of 1018 HBV carriers (Mok TS et al.
  • We updated the database in Dec 2008 and performed univariate and multivariate analysis on clinical (age, sex, cirrhosis, ascites, anti-viral therapy, bilirubin, ALT, albumin, INR), tumorous (size, number, resection) and virologic factors (HBV DNA, Genotype) for prediction of outcome in HCC patients (pts).
  • Fifty seven pts (54.3%) had solitary tumor but only 34 (32.4%) are amenable to resection.
  • Absence of cirrhosis (p=0.0072) and normal albumin level (p=0.0379) are predictors of surgical resection while tumor size and number are not.
  • Liver function is more important than tumor characteristics in determining the outcome of HCC detected in the surveillance program.

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  • (PMID = 27963096.001).
  • [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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16. Lu L, Schafer P, Bartlett JB: Inhibition by lenalidomide of growth factor and hypoxia-induced signaling in endothelial and epithelial tumor cells, and effects within the tumor cell microenvironment. J Clin Oncol; 2009 May 20;27(15_suppl):e14620

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition by lenalidomide of growth factor and hypoxia-induced signaling in endothelial and epithelial tumor cells, and effects within the tumor cell microenvironment.
  • It has direct anti-proliferative activity in hematological cells but there is no evidence of direct activity in solid tumor cells.
  • In solid tumors, lenalidomide is being advanced in combination with other agents to take advantage of its immune-enhancing properties in combination with direct anti-tumor agents.
  • Lysophosphatidic acid (LPA) is a key pro-survival factor present at high levels within the ascites of ovarian cancer patients which confers increased tumor invasiveness and reduced survival.
  • Hypoxia-induced factor (HIF)-1α is the key initiator of angiogenesis and tumor invasiveness.
  • Treatment of ovarian tumor cells with LPA increased tumor cell invasiveness via enhanced p-Akt.
  • Hypoxic endothelial cells and epithelial tumor cells showed enhanced HIF-1α expression.
  • Lenalidomide inhibited hypoxia-induced HIF-1α expression by endothelial cells and by epithelial tumor cells, including prostate, breast, pancreatic, renal and ovarian tumor cells.
  • CONCLUSIONS: Lenalidomide may act within the tumor microenvironment to inhibit key signals of tumor cells survival, growth, and invasiveness.
  • These studies support the potential utility of lenalidomide in combination with other agents in the treatment of patients with solid tumors.

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  • (PMID = 27964203.001).
  • [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. Daniels JR, Katz MD, Hart M, Fong T, Donovan JA, El-Khoueiry AB, Wallman MA: Retrospective analysis of salvage percutaneous cryoablation of hepatocellular cancer (HCC) in liver. J Clin Oncol; 2009 May 20;27(15_suppl):e15649

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • ; C, 2 pts Candidate pts had residual disease after intra-arterial chemotherapy.
  • Median follow-up was 342 days (range 30-947) Results: Tumors ranged from 1.3 to 5.8 cm.
  • Three pts died within 30 days: 2 following intra-peritoneal hemorrhage despite control of bleeding and 1 from ischemic liver injury following a TIPSS for hydrothorax in a pt with refractory ascites.
  • Risk of bleeding was associated with ascites (P = 0.013).
  • One pt had cutaneous needle tract tumor seeding caused by needle repositioning prior to freezing.
  • Thirteen pts are alive without recurrence of whom 6 had liver transplant with no (4) or < 5% (2) residual disease.
  • Multiple tumors at baseline predicts for hepatic recurrence.
  • CONCLUSIONS: Percutaneous cryoablation effectively manages selected hepatic HCC tumors.
  • Cirrhotic pts with ascites have significant risk for hemorrhage.

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  • (PMID = 27962739.001).
  • [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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18. de Jong D, Dodge JE, Freedman O, Lo E, Rosen BP, Mackay H: Predictors for optimal cytoreduction following neoadjuvant chemotherapy in advanced epithelial ovarian carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):5512

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictors for optimal cytoreduction following neoadjuvant chemotherapy in advanced epithelial ovarian carcinoma.
  • DS following NAC offers a survival benefit to those pts in whom optimal cytoreduction (< 1 cm residual tumor) is achieved.
  • Pts with synchronous primary tumors or final pathology inconsistent with EOC were excluded.
  • Age, presence of ascites, Pre NAC hemoglobin (Hb), platelet count (Pls), and CA-125 were explored as possible predictors of attempting DS and of optimal cytoreduction using Kruskal-Wallis analysis and multivariate regression analysis with backward elimination.
  • Pre NAC Hb, CA125, and ascites were not predictors of DS.
  • Presence of ascites, pre-NAC Hb, pre-NAC Pls, and pre-NAC CA-125 were not predictors of optimal cytoreduction.

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  • (PMID = 27962464.001).
  • [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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19. 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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20. Parsons S, Hennig M, Linke R, Klein A, Lahr A, Lindhofer H, Heiss M: Clinical benefit of catumaxomab in malignant ascites in patient subpopulations in a pivotal phase II/III trial. J Clin Oncol; 2009 May 20;27(15_suppl):e14000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical benefit of catumaxomab in malignant ascites in patient subpopulations in a pivotal phase II/III trial.
  • : e14000 Background: Parsons et al. (ASCO 2008) reported the results of a pivotal phase II/III trial in patients with malignant ascites due to epithelial cancer.
  • Malignant ascites is a typical late-stage manifestation of cancer associated with a poor prognosis and survival.
  • METHODS: A post-hoc analysis was performed on the 258 patients with epithelial tumors treated with catumaxomab + paracentesis or paracentesis alone (control) in the pivotal trial to investigate any association between the primary endpoint (puncture-free survival) and the primary tumor, metastases, or other prognostic parameters.
  • RESULTS: Puncture-free survival was lower in patients with non-ovarian vs ovarian tumors and those with a poor prognosis (metastases vs no metastases, elderly vs younger, or low vs serum protein level).
  • CONCLUSION: Catumaxomab demonstrated a significant clinical benefit in patients with malignant ascites independent of the primary tumor or other prognostic factors.

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  • (PMID = 27961494.001).
  • [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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21. Lindhofer H, Schoberth A, Pelster D, Hess J, Herold J, Jäger M: Elimination of cancer stem cells (CD133+/EpCAM+) from malignant ascites by the trifunctional antibody catumaxomab: Results from a pivotal phase II/III study. J Clin Oncol; 2009 May 20;27(15_suppl):3014

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elimination of cancer stem cells (CD133+/EpCAM+) from malignant ascites by the trifunctional antibody catumaxomab: Results from a pivotal phase II/III study.
  • : 3014 Background: Putative cancer stems cells (CSCs) are defined as "tumor-initiating cells" that have the capacity to self-renew and to give rise to the variety of differentiated cells found in the malignancy.
  • The CD133 membrane glycoprotein represents a CSC marker that has been previously demonstrated to be capable of identifying a cancer-initiating subpopulation in brain tumors, melanoma, and EpCAM+ solid tumors.
  • The trifunctional anti-EpCAM x anti-CD3 antibody catumaxomab efficiently eliminates tumor cells from the peritoneal fluid of malignant ascites (MA) patients as demonstrated in a pivotal phase II/III trial (Parsons et al., ASCO 2008).
  • METHODS: 18 CTX-refractory patients with MA caused by a variety of primary carcinoma diseases (i.e., ovarian, pancreas, and gastric cancer) were analyzed for the presence CD133+/EpCAM+ cells in peritoneal fluids by means of CD133+/EpCAM+ double staining on cytospin preparations.
  • CONCLUSIONS: In a preliminary monitoring study, putative CSCs (CD133+/EpCAM+) were present in peritoneal fluids of 78 % of analyzed MA patients with different underlying primary tumor entities.

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  • (PMID = 27962058.001).
  • [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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22. Ishigami H, Kitayama J, Kaisaki S, Hidemura A, Kato M, Otani K, Kamei T, Soma D, Miyato H, Yamashita H, Nagawa H: Phase II study of weekly intravenous and intraperitoneal paclitaxel combined with S-1 for advanced gastric cancer with peritoneal metastasis. J Clin Oncol; 2009 May 20;27(15_suppl):4542

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Secondary endpoints were the response rate, efficacy against malignant ascites and safety.
  • RESULTS: Forty patients were enrolled, including 21 with primary tumors with peritoneal dissemination confirmed by staging laparoscopy, 13 with peritoneal recurrence, and 6 with positive peritoneal cytology only.
  • Malignant ascites disappeared or decreased in 13 of 21 (62%) patients.

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  • (PMID = 27963015.001).
  • [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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23. 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
COS Scholar Universe. author profiles.

  • [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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24. 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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25. Mukherjee A, Dutta S, Sanyal U: Evaluation of dimethoxydop-NU as a novel anti-tumor agent. J Exp Clin Cancer Res; 2007 Dec;26(4):489-97

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of dimethoxydop-NU as a novel anti-tumor agent.
  • Dimethoxydop-NU, 1-[2-{3-(2-Chloroethyl)-3-nitrosoureido}ethyl]-3,4-dimethoxy-benzene (Compound 1), was synthesized from 3,4-dimethoxy-phenethylamine as a novel anti-tumor agent based on the structures of the clinical drug CCNU and dopamine, an important endogenous biological amine having anti-angiogenesis property.
  • In vitro screening in two human tumor cell lines, namely promyelocytic leukemia HL-60 and histiocytic lymphoma U-937, revealed its cytotoxicity greater than that of hydroxyurea and comparable to BCNU used as standards.
  • Its in vivo anti-tumoral potency was assessed in the murine ascites tumors Sarcoma-180 (S-180) and Ehrlich ascites carcinoma (EAC) by measuring the increase in median survival times of drug treated (T) over untreated control (C) mice.
  • Results revealed significant tumor regression effects in these tumors.
  • Compound 1 comparable to standards inhibited the synthesis of DNA and RNA in S-180 tumor cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Evaluation, Preclinical. Drug Screening Assays, Antitumor. Humans. Mice. Thymidine / metabolism. Uridine / metabolism

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  • (PMID = 18365543.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 1-(2-(3-(2-chloroethyl)-3-nitrosoureido)ethyl)-3,4-dimethoxy-benzene; 0 / Antineoplastic Agents; 0 / Nitrosourea Compounds; VC2W18DGKR / Thymidine; WHI7HQ7H85 / Uridine
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26. Mukherjee A, Dutta S, Chashoo G, Bhagat M, Saxena AK, Sanyal U: Evaluation of fluoren-NU as a novel antitumor agent. Oncol Res; 2009;17(9):387-96

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In vitro screening in six human tumor cell lines, namely SK-N-SH CNS, IMR-32 neuroblastoma, A549 lung, DU-145 prostate, HL-60 leukemia, and U-937 lymphoma, revealed its significant cytotoxicity in SK-N-SH.
  • Its in vivo antitumoral potency was assessed in murine ascites tumors Ehrlich ascites carcinoma (EAC) and Sarcoma-180 (S-180) by measuring the increase in median survival times (MST) of drug-treated (T) over untreated control (C) mice.
  • Results revealed significant tumor regression effects in both of these tumors.
  • Life span of mice bearing advanced tumor for 5 days before the drug challenge was also considerably increased.
  • Compared to Mitonafide and CCNU used as standards it also significantly inhibited DNA and RNA synthesis in EAC tumor cells in vitro at 8 microM concentration.
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Evaluation. Humans. Liver / drug effects. Male. Mice. Neoplasms, Experimental / drug therapy. Thymidine / metabolism. Uridine / metabolism

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  • (PMID = 19718945.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-(2-(3-(2-chloroethyl)-3-nitrosouriedo)ethyl)spiro(5,9'-fluorenyl)imidazolidiine-2,4-dione; 0 / Antineoplastic Agents; 0 / Hydantoins; 0 / Nitrosourea Compounds; VC2W18DGKR / Thymidine; WHI7HQ7H85 / Uridine
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27. Sinkovics JG: A notable phenomenon recapitulated. A fusion product of a murine lymphoma cell and a leukemia virus-neutralizing antibody-producer host plasma cell formed spontaneously and secreting the specific antibody continuously. Acta Microbiol Immunol Hung; 2005;52(1):1-40
Genetic Alliance. consumer health - Plasma cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the mid-1960s the #620 cell passage line of a murine lymphoma-leukemia was developed at the Section of Clinical Tumor Virology and Immunology, Department of Medicine, The University of Texas M.D.
  • The #818 cells grew in suspension cultures and in the form of large, lethal ascitic tumors in YAS mice.
  • When passaged in YAS mice these cells induced lethal ascites tumors.
  • It should be investigated further if human lymphoma-leukemia cells could fuse with an immune plasma cell of the host and thus alter the clinical course of the disease.
  • [MeSH-major] Antibodies, Viral / biosynthesis. Cell Line, Tumor / immunology. Hybrid Cells / immunology. Leukemia Virus, Murine. Leukemia, Experimental / immunology. Plasma Cells / immunology. Retroviridae / immunology. Retroviridae Infections / immunology. Tumor Virus Infections / immunology

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  • (PMID = 15957233.001).
  • [ISSN] 1217-8950
  • [Journal-full-title] Acta microbiologica et immunologica Hungarica
  • [ISO-abbreviation] Acta Microbiol Immunol Hung
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-7923; United States / NCI NIH HHS / CA / K-3-CA-16747
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Antigens, Viral; 0 / Immune Sera
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28. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] J Pharmacol Sci. 2007 Apr;103(4):354-9 [17443057.001]
  • [Cites] Clin Invest Med. 2008;31(4):E218-21 [18682046.001]
  • [Cites] Complement Ther Med. 2009 Jan;17(1):51-5 [19114229.001]
  • (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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29. 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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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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32. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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33. 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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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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35. 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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36. 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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37. 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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38. 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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39. 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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40. 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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41. 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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42. 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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43. 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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44. 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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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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46. 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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  • [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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47. 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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48. 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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49. 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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50. 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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51. 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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  • [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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52. 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
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  • [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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53. 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

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  • [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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54. 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
Hazardous Substances Data Bank. CAFFEINE .

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  • [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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55. 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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56. Antos F, Dytrych P, Vítek P, Ryska O, Marvan J, Serclovlá Z: [Malignant ascites--optional management using hyperthermic peroperative chemotherapy (HIPEC)]. Rozhl Chir; 2010 Apr;89(4):237-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Malignant ascites--optional management using hyperthermic peroperative chemotherapy (HIPEC)].
  • [Transliterated title] Maligní ascites--moznost ovlivnĕní tvorby pomocí hypertermické peroperacní chemoterapie (HIPEC).
  • During these procedures, ascites was detected in 30 subjects (24.8%) and its volume was 250-11,000 ml.
  • The patients concerned could not undergo radical surgery for their GIT or gynecological tumors.
  • Subgroup A (22 subjects) included subjects, in whom at least palliative debulking of the tumors (usually total omentectomy) was feasible, and the procedure was followed by HIPEC.
  • Out of the total of 22 subjects in Subgroup A, ascites was not postoperatively recorded in 17 patients.
  • In 5 patients, ascites was gradually formed from month 6.3 onwards, however, it only reached subclinical levels.
  • In Subgroup B (8 patients), no ascites was detected in 3 subjects until their death (37.5%), further 5 subjects presented with ascites at the mean postoperative month 7.25.
  • There was a statistically significant difference between the two subgoups in the survival time parametres (p = 0.009), thereas, the difference in ascites relapse rates was statistically insignificant (p = 0.12).
  • CONCLUSIONS: HIPEC with/without debulking is an efficient method for controlling, managing or preventing the development of malignant ascites, it extends the mean survival time of the patients (especially when bulking is feasible) with low morbidity and lethality rates of the procedure.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Ascites / therapy. Hyperthermia, Induced. Intraoperative Care. Neoplasms / complications. Neoplasms / surgery

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  • (PMID = 20586160.001).
  • [ISSN] 0035-9351
  • [Journal-full-title] Rozhledy v chirurgii : měsíčník Československé chirurgické společnosti
  • [ISO-abbreviation] Rozhl Chir
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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57. 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
Hazardous Substances Data Bank. EPIRUBICIN .

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  • [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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58. 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 .

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  • [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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59. 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

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  • [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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60. 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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61. 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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62. 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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63. 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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64. 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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65. Hirai M, Hiramatsu Y, Iwashita S, Otani T, Chen L, Li YG, Okada M, Oie K, Igarashi K, Wakita H, Seno M: E-selectin targeting to visualize tumors in vivo. Contrast Media Mol Imaging; 2010 Mar-Apr;5(2):70-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] E-selectin targeting to visualize tumors in vivo.
  • Generally angiogenic factors induce the expression of E-selectin in vascular endothelial cells in the tumors.
  • In this study, we employed an anti-E-selectin monoclonal antibody to target tumors in vivo and evaluated an optical imaging reagent to visualize tumor regions.
  • Cy5.5 encapsulated into liposomes that were conjugated with an anti-E-selectin antibody successfully visualized Ehrlich ascites tumor cells when transplanted into mice.
  • Thus, E-selectin targeting with liposomes containing a near-infrared fluorescent dye was found effective in visualizing tumors in vivo.
  • This strategy should be extremely useful as a method to identify sentinel lymphatic nodes and angiogenic tumors as well as use for drug delivery to tumor cells.
  • [MeSH-minor] Animals. Carcinoma, Ehrlich Tumor / diagnosis. Endothelial Cells / cytology. Endothelium, Vascular. Humans. Liposomes. Mice. Neovascularization, Pathologic / diagnosis. Umbilical Veins

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  • [Copyright] 2010 John Wiley & Sons, Ltd.
  • (PMID = 20235150.001).
  • [ISSN] 1555-4317
  • [Journal-full-title] Contrast media & molecular imaging
  • [ISO-abbreviation] Contrast Media Mol Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / E-Selectin; 0 / Immunoconjugates; 0 / Liposomes
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66. 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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67. 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
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  • [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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68. 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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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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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. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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72. 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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73. 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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74. 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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75. Hofland KF, Thougaard AV, Dejligbjerg M, Jensen LH, Kristjansen PE, Rengtved P, Sehested M, Jensen PB: Combining etoposide and dexrazoxane synergizes with radiotherapy and improves survival in mice with central nervous system tumors. Clin Cancer Res; 2005 Sep 15;11(18):6722-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combining etoposide and dexrazoxane synergizes with radiotherapy and improves survival in mice with central nervous system tumors.
  • EXPERIMENTAL DESIGN: Mice with cerebrally inoculated Ehrlich ascites tumor (EHR2) cells were treated with combinations of etoposide + dexrazoxane + cerebral radiotherapy.
  • This indicates a direct dexrazoxane modulation of the combined effects of etoposide and radiation in brain tumors.
  • CONCLUSION: Combining etoposide (high or normal doses) and dexrazoxane synergizes with cerebral radiotherapy and significantly improves survival in mice with central nervous system tumors.
  • This regimen may thus improve radiation therapy of central nervous system tumors.
  • [MeSH-minor] Animals. Blood-Brain Barrier / drug effects. Blood-Brain Barrier / pathology. Blood-Brain Barrier / radiation effects. Combined Modality Therapy. DNA Damage. DNA, Neoplasm / drug effects. DNA, Neoplasm / genetics. DNA, Neoplasm / radiation effects. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Etoposide / administration & dosage. Female. Mice. Mice, Inbred Strains. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / pathology. Neoplasms, Experimental / radiotherapy. Razoxane / administration & dosage. Survival Analysis. Time Factors. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 16166453.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 5AR83PR647 / Razoxane; 6PLQ3CP4P3 / Etoposide
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76. Hu L, Hofmann J, Holash J, Yancopoulos GD, Sood AK, Jaffe RB: Vascular endothelial growth factor trap combined with paclitaxel strikingly inhibits tumor and ascites, prolonging survival in a human ovarian cancer model. Clin Cancer Res; 2005 Oct 1;11(19 Pt 1):6966-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular endothelial growth factor trap combined with paclitaxel strikingly inhibits tumor and ascites, prolonging survival in a human ovarian cancer model.
  • Ovarian cancer is characterized by i.p. carcinomatosis and massive ascites.
  • Vascular endothelial growth factor (VEGF) plays a pivotal role in tumor angiogenesis and vascular leakage leading to ascites.
  • Tumor burden after VEGF Trap plus paclitaxel was reduced by approximately 98% versus controls.
  • No measurable ascites developed in the treated group.
  • Morphologic studies showed that most residual tumor had degenerative changes.
  • Diaphragmatic and hepatic tumors were not found in the VEGF Trap plus paclitaxel group in contrast to controls, indicating lack of metastasis.
  • In vivo FITC-lectin tumor vessel imaging showed sparse, short, straight vessels in treated mice as compared to controls, in which vessels were numerous, irregular, tortuous, and leaky.
  • In a survival study, all controls underwent euthanasia between 29 and 58 days after tumor cell inoculation (cachexia, extensive ascites, and tumor masses).
  • In the VEGF Trap plus paclitaxel group, mice were ambulating and eating normally with no signs of disease for at least 81 days after tumor cell inoculation, and survival occurred for 129.9 +/- 38.88 days with no further treatment.
  • We conclude that combination therapy with VEGF Trap plus paclitaxel may provide a novel, long-lasting therapeutic strategy for treatment of patients with ovarian cancer associated with ascites.
  • [MeSH-minor] Analysis of Variance. Animals. Apoptosis. Ascites / metabolism. Cell Line, Tumor. Disease Models, Animal. Female. Humans. Mice. Mice, Nude. Necrosis. Neoplasm Metastasis. Neoplasm Transplantation. Time Factors. Treatment Outcome

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  • (PMID = 16203789.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50-CA 83609
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Vascular Endothelial Growth Factor A; P88XT4IS4D / Paclitaxel
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77. Hsieh JL, Lee CH, Teo ML, Lin YJ, Huang YS, Wu CL, Shiau AL: Transthyretin-driven oncolytic adenovirus suppresses tumor growth in orthotopic and ascites models of hepatocellular carcinoma. Cancer Sci; 2009 Mar;100(3):537-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transthyretin-driven oncolytic adenovirus suppresses tumor growth in orthotopic and ascites models of hepatocellular carcinoma.
  • We have previously shown that E1B-55 kDa-deleted adenovirus, designated Ad5WS1, has therapeutic potential for treating hepatocellular carcinoma (HCC).
  • Our results showed that Ad5WS2 could replicate within tumor cells where the transthyretin gene was expressed.
  • Peritoneal administration of Ad5WS2 into mice bearing liver tumors grown in ascites resulted in enhanced survival.
  • Furthermore, the antitumor effect of Ad5WS2 could be enhanced when combined with chemotherapeutic agent cisplatin in the ascites tumor model.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. Oncolytic Virotherapy / methods. Prealbumin / genetics
  • [MeSH-minor] Adenoviridae / genetics. Adenovirus E1A Proteins / genetics. Adenovirus E1B Proteins / deficiency. Adenovirus E1B Proteins / genetics. Animals. Antineoplastic Agents / pharmacology. Ascites / pathology. Ascites / virology. Cisplatin / pharmacology. Combined Modality Therapy. Female. Humans. Mice. Oncolytic Viruses / genetics. Promoter Regions, Genetic

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  • (PMID = 19134007.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / Adenovirus E1B Proteins; 0 / Antineoplastic Agents; 0 / Prealbumin; Q20Q21Q62J / Cisplatin
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78. 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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  • [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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79. 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
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  • 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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80. 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

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  • 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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81. 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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82. 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
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  • 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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  • (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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83. 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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84. 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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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. 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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87. 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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  • 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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88. 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

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  • 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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89. Beyrouti MI, Beyrouti R, Frikha F, Ben Amar M, Abid M, Ben Ameur H, Ben Salah K, Guirat A, Boujelben S: [Peritoneal gelatinous ascites]. Presse Med; 2007 Jul-Aug;36(7-8):1141-7
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  • [Title] [Peritoneal gelatinous ascites].
  • Pseudomyxoma peritonei or gelatinous ascites is a rare clinical entity, and its pathogenesis remains obscure.
  • It most often follows a mucinous tumor of the appendix.
  • Magnetic resonance imaging, by showing the gelatinous ascites, their septa and the scalloping of liver and spleen, can strengthen the probability of the diagnosis.
  • Recurrence is more frequent in the forms associated with malignant or bipolar tumors.

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  • (PMID = 17603922.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 50
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90. 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
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  • [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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91. 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
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  • [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

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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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92. Bamias A, Tsiatas ML, Kafantari E, Liakou C, Rodolakis A, Voulgaris Z, Vlahos G, Papageorgiou T, Tsitsilonis O, Bamia C, Papatheodoridis G, Politi E, Archimandritis A, Antsaklis A, Dimopoulos MA: Significant differences of lymphocytes isolated from ascites of patients with ovarian cancer compared to blood and tumor lymphocytes. Association of CD3+CD56+ cells with platinum resistance. Gynecol Oncol; 2007 Jul;106(1):75-81
MedlinePlus Health Information. consumer health - Ovarian Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significant differences of lymphocytes isolated from ascites of patients with ovarian cancer compared to blood and tumor lymphocytes. Association of CD3+CD56+ cells with platinum resistance.
  • OBJECTIVES: Tumor infiltrating lymphocytes (TILs) and T regulatory cells (Tregs) have been associated with prognosis in ovarian cancer, but their prognostic significance in ascites has not been studied.
  • We performed a prospective study of T lymphocytes isolated from ascites from patients with ovarian carcinoma and we compared them with the respective populations in blood and tumors.
  • METHODS: Mononuclear cells from ascites (n=71) and blood were isolated by Ficoll, while tumor lymphocytes (n=20) were obtained upon mechanical dissociation.
  • Ascites from 10 patients with cirrhosis was used as control.
  • RESULTS: Tregs containing CD4(+)CD25(+) cells, NK-T containing CD3(+)CD56(+) cells and CD69 and HLADR expression of CD4 and CD8 lymphocytes were significantly increased in tumor ascites compared to blood and control ascites.
  • A selective accumulation of these populations in the ascites of cancer patients, was suggested by the significantly higher ascites/blood (A/B) ratios in cancer patients but not controls.
  • Cancer cell content in ascites was correlated with CD4(+)CD25(+), CD4(+)CD69(+), CD4(+)HLADR(+) and CD8(+)CD69(+) cells.
  • There was no correlation of lymphocyte populations between ascites and samples from peritoneal metastases.
  • Higher tumor grade was associated with increased A/B CD4(+)CD25(+) ratio and reduced CD3(+)CD56(+) cells, while platinum resistance was associated with reduced A/B CD3(+)CD56(+) ratio.
  • CONCLUSIONS: There are significant differences of CD3(+)CD56(+) and CD25(+)CD4(+) lymphocytes and increase in lymphocyte activation between blood, ascites and peritoneal metastases from patients with ovarian cancer.
  • The selective accumulation of CD3(+)CD56(+) population in ascites may be a predictive factor for platinum resistance.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Ascites / immunology. Ascites / pathology. Drug Resistance, Neoplasm. Female. Flow Cytometry. Humans. Interleukin-2 Receptor alpha Subunit / biosynthesis. Interleukin-2 Receptor alpha Subunit / immunology. Middle Aged. Neoplasm Staging

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  • (PMID = 17433425.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, CD56; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Organoplatinum Compounds
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93. Turan T, Aykan B, Koc S, Boran N, Tulunay G, Karacay O, Erdogan Z, Kose F: Analysis of metastatic ovarian tumors from extragenital primary sites. Tumori; 2006 Nov-Dec;92(6):491-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of metastatic ovarian tumors from extragenital primary sites.
  • AIMS AND BACKGROUND: The aim of this study was to evaluate patients with metastatic ovarian tumors from extragenital primary sites.
  • METHODS: The medical records of 75 patients were reviewed retrospectively for age at diagnosis, presenting symptoms, preoperative tumor marker levels, preoperative diagnostic workup, operative technique, intraoperative evaluation, frozen-section and pathology results, laterality of metastasis, and primary tumor site.
  • The specific impact of metastasis from colorectal and gastric primary sites on laterality, gross features and dimensions of ovarian mass, volume of ascites and tumor marker levels was investigated.
  • It was not possible to identify the primary tumor site in 8 (10.7%) patients.
  • Bilateral metastasis was found in 86.4% patients; 42.7% of the metastatic ovarian tumors were Krukenberg tumors; 50.7% of the ovarian masses were solid.
  • The mean preoperative serum levels of tumor markers were 298.7 U/mL, 178 U/mL and 113.3 U/mL for CA 125, CA 19-9 and CA 15-3, respectively.
  • The presence of ascites was more frequent in ovarian tumors originating from colorectal and gastric primaries.
  • CONCLUSIONS: Surgery is essential for the diagnosis of the primary tumor and necessary for relief of symptoms.
  • [MeSH-major] Biomarkers, Tumor / blood. Breast Neoplasms / diagnosis. Digestive System Neoplasms / diagnosis. Lymphoma / diagnosis. Ovarian Neoplasms / secondary
  • [MeSH-minor] Adult. Aged. Ascites / etiology. CA-125 Antigen / blood. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Female. Frozen Sections. Humans. Middle Aged. Neoplasm Staging. Retrospective Studies. alpha-Fetoproteins / metabolism

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  • (PMID = 17260489.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 0 / alpha-Fetoproteins
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94. 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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95. 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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  • 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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96. 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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97. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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98. 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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99. 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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100. 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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