[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 21 of about 21
1. Nakamura K, Yashiro M, Matsuoka T, Tendo M, Shimizu T, Miwa A, Hirakawa K: A novel molecular targeting compound as K-samII/FGF-R2 phosphorylation inhibitor, Ki23057, for Scirrhous gastric cancer. Gastroenterology; 2006 Nov;131(5):1530-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel molecular targeting compound as K-samII/FGF-R2 phosphorylation inhibitor, Ki23057, for Scirrhous gastric cancer.
  • BACKGROUND & AIMS: Scirrhous gastric carcinoma carries the highest mortality of all gastric cancers.
  • The poor prognosis is reported to be associated with K-samII amplification, which encodes fibroblast growth factor receptor type 2 (FGF-R2).
  • Ki23057, a newly developed small molecule-acting K-samII/FGF-R2 autophosphorylation inhibitor, is a tyrosine kinase inhibitor that competes with adenosine triphosphate for the binding site.
  • The aim of the current study is to clarify the possibility of molecular target therapy with Ki23057 for treating scirrhous gastric cancer.
  • METHODS: Five human gastric cancer cell lines were used.
  • The influences of Ki23057 on the mitogen-activated protein kinase and phosphatidylinositol 3 kinase signaling pathways and the apoptosis pathway in the gastric cancer cells were also examined.
  • For in vivo experiments, the Ki23057 was administered orally to mouse models of peritoneal dissemination.
  • Ki23057 significantly inhibited the proliferation of scirrhous cancer cells but not nonscirrhous gastric carcinoma cells.
  • CONCLUSIONS: A novel K-samII/FGF-R2 phosphorylation inhibitor, Ki23057, appears therapeutically promising in scirrhous gastric carcinoma with K-samII amplification.
  • [MeSH-major] Adenocarcinoma, Scirrhous / drug therapy. Protein Kinase Inhibitors / pharmacology. Quinolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Peritoneal Neoplasms / pathology. Phosphorylation. Receptor, ErbB-2. Signal Transduction. Transplantation, Heterologous


2. Smith LM, Nesterova A, Ryan MC, Duniho S, Jonas M, Anderson M, Zabinski RF, Sutherland MK, Gerber HP, Van Orden KL, Moore PA, Ruben SM, Carter PJ: CD133/prominin-1 is a potential therapeutic target for antibody-drug conjugates in hepatocellular and gastric cancers. Br J Cancer; 2008 Jul 8;99(1):100-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD133/prominin-1 is a potential therapeutic target for antibody-drug conjugates in hepatocellular and gastric cancers.
  • CD133 was found here to be highly expressed in >or=50% of pancreatic, gastric and intrahepatic cholangiocarcinomas.
  • Quantitative flow cytometric analysis showed that a panel of established hepatocellular, pancreatic and gastric cancer cell lines expressed CD133 at levels higher than normal epithelial cells or bone marrow progenitor cells.
  • A murine anti-human CD133 antibody (AC133) conjugated to a potent cytotoxic drug, monomethyl auristatin F (MMAF), effectively inhibited the growth of Hep3B hepatocellular and KATO III gastric cancer cells in vitro with IC(50) values of 2-7 ng ml(-1).
  • The anti-CD133-drug conjugate (AC133-vcMMAF) was shown to internalise and colocalised with the lysosomal marker CD107a in the sensitive cell lines.
  • Anti-CD133-drug conjugate treatment resulted in significant delay of Hep3B tumour growth in SCID mice.
  • Anti-CD133 antibody-drug conjugates warrant further evaluation as a therapeutic strategy to eradicate CD133+ tumours.
  • [MeSH-minor] Antigens, CD / biosynthesis. Apoptosis / drug effects. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. Hepatocytes. Humans. Hybridomas. Immunohistochemistry. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism. Stomach Neoplasms / drug therapy. Stomach Neoplasms / metabolism

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Biochem Cell Biol. 2005 Apr;37(4):715-9 [15694831.001]
  • [Cites] J Biol Chem. 2006 Apr 14;281(15):10540-7 [16484228.001]
  • [Cites] Leukemia. 2000 Apr;14(4):770-2 [10764169.001]
  • [Cites] Cell Biol Toxicol. 2002;18(3):157-73 [12083422.001]
  • [Cites] Bioconjug Chem. 2002 Jul-Aug;13(4):855-69 [12121142.001]
  • [Cites] J Virol. 2002 Nov;76(22):11440-6 [12388705.001]
  • [Cites] Ann N Y Acad Sci. 2003 May;996:141-51 [12799292.001]
  • [Cites] Nat Biotechnol. 2003 Jul;21(7):778-84 [12778055.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1458-65 [12714494.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] J Natl Cancer Inst. 2004 Apr 21;96(8):583-5 [15100335.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Blood. 1997 Dec 15;90(12):5002-12 [9389720.001]
  • [Cites] Blood. 1997 Dec 15;90(12):5013-21 [9389721.001]
  • [Cites] Blood. 1999 Feb 15;93(4):1435-7 [10075457.001]
  • [Cites] Blood. 1999 Jul 15;94(2):832-3 [10438201.001]
  • [Cites] Leukemia. 1999 Sep;13(9):1466-7 [10483002.001]
  • [Cites] Mol Cancer Ther. 2004 Nov;3(11):1493-501 [15542788.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Clin Cancer Res. 2004 Dec 1;10(23):7842-51 [15585616.001]
  • [Cites] Cell Tissue Res. 2005 Jan;319(1):15-26 [15558321.001]
  • [Cites] J Cell Sci. 2005 Jul 1;118(Pt 13):2849-58 [15976444.001]
  • [Cites] J Immunol. 2005 Sep 1;175(5):2890-9 [16116175.001]
  • [Cites] Nat Clin Pract Oncol. 2005 May;2(5):224-5 [16264940.001]
  • [Cites] Cell Prolif. 2005 Dec;38(6):363-74 [16300650.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10946-51 [16322242.001]
  • [Cites] Blood. 2006 Jan 15;107(2):431-4 [16150939.001]
  • [Cites] Mol Cancer Ther. 2006 Jun;5(6):1474-82 [16818506.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9339-44 [16990346.001]
  • [Cites] Nat Med. 2006 Oct;12(10):1167-74 [16998484.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):111-5 [17122771.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):106-10 [17122772.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Apr 20;355(4):855-9 [17307142.001]
  • [Cites] Br J Haematol. 2007 Jul;138(2):186-95 [17593025.001]
  • [Cites] FASEB J. 2007 Dec;21(14):3777-85 [17625071.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Cell Stem Cell. 2007 Sep 13;1(3):313-23 [18371365.001]
  • [Cites] Mol Cancer Ther. 2005 May;4(5):704-14 [15897234.001]
  • [Cites] Bioconjug Chem. 2006 Jan-Feb;17(1):114-24 [16417259.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2328-37 [16489038.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3214-21 [16540673.001]
  • [CommentIn] Br J Cancer. 2009 Apr 21;100(8):1365-6; author reply 1367 [19367288.001]
  • (PMID = 18542072.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Glycoproteins; 0 / Peptides
  • [Other-IDs] NLM/ PMC2453027
  •  go-up   go-down


3. Ahn CM, Tak JA, Choi SJ: Synthesis and in vitro antitumor activity of 2-alkyl, 2-aryl, and 2-piperazinyl benzimidazole-4,7-dione derivatives. Arch Pharm Res; 2000 Aug;23(4):288-301
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A series of 2-alkyl, 2-aryl, and 2-piperazinyl benzimidazole-4,7-dione derivatives (7a-h) and 16m-o) were prepared, and their cytotoxicities were tested against three cancer cell lines (mouse lymphocytic leukemia cell line P388, and human gastric carcinoma cell lines SNU-1 and SNU-16).
  • [MeSH-minor] Animals. Humans. Leukemia P388 / drug therapy. Leukemia P388 / pathology. Mice. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology. Structure-Activity Relationship. Tumor Cells, Cultured

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10976573.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] KOREA (SOUTH)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzimidazoles
  •  go-up   go-down


Advertisement
4. [Tuberculosis in compromised hosts]. Kekkaku; 2003 Nov;78(11):717-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Many new findings and useful reports for practical medical treatment are submitted; why these compromised hosts are predisposed to tuberculosis, tuberculosis diagnostic and remedial notes of those compromised hosts etc.
  • In 1980, Saiki and co-workers reported that host defense and delayed-type hypersensitivity response to M. tuberculosis was hampered in a mouse DM model established by injecting streptozotocin (Infect Immun.
  • Patients who have undergone gastric resection are considered at increased risk of developing pulmonary tuberculosis.
  • Of 654 pulmonary tuberculosis patients admitted to National Chiba-Higashi Hospital from January 1999 to December 2001, 55 patients (31-84 years old, mean 63.5 +/- 12.5 years, 48 males and 7 females) had the history of gastric resection.
  • The mean age of gastric resection was 50.2 +/- 16.6 years, and the mean interval from gastrectomy to pulmonary tuberculosis was 13.6 +/- 11.0 years.
  • Gastrectomy was done due to carcinoma of the stomach in 31 cases, gastric and/or duodenal ulcer in 21 cases, adenomatous polyp in two cases, and accidental injury in one case.
  • No one had recurrence of carcinoma of the stomach.
  • I calculated the odds of tuberculosis among gastrectomy patients to be 3.8 times that of appropriate controls.
  • It is easy to stay in the leaching lesion so that anti-tuberculosis drugs are much effective, and the patients recover easily.
  • However, if the treatment is delayed, it is fatally because hematogenous metastasis are easy to occur and become miliary tuberculosis.
  • With AIDS patients with tuberculosis, there are the following problems on the treatment. (1) The adverse reactions by antituberculosis drugs tend to occur in AIDS patients.
  • Eleven of 33 AIDS patients with tuberculosis had the adverse reactions (skin rash, fever, liver dysfunction) considered to be due to antituberculosis drugs.
  • It is a very large burden for the HIV infected persons to take simultaneously antituberculosis drugs, medicines for opportunistic infections, and anti-HIV medicines.
  • Since many medicines are taken, it is difficult to determine which drug is the cause once an adverse reaction occurs and all medicines should be often stopped. (2) The combined use with rifampicin (RFP) is difficult for the protease inhibitors and nonnuclear acid reverse transcriptase inhibitors.
  • RFP induces cytochrome P-450 in liver, accelerates the metabolism of some concomitant drug agents, and reduces blood concentration them remarkably.
  • When starting the two above-mentioned medicines during tuberculosis treatment, RFP should be changed to rifabutin (RFB) which has less induction of P-450 than RFP.
  • So, the treatment with EFV and RFP is recently chosen.
  • However, the monitor of the blood concentration of EFV is required, and the dose of EFV should be increased if it is a low value. (3) When a highly active antiretroviral therapy (HAART) is given to AIDS patients with tuberculosis, transient worsening of tuberculosis may develop after about two weeks. (ABSTRACT TRUNCATED)

  • Genetic Alliance. consumer health - Tuberculosis.
  • MedlinePlus Health Information. consumer health - Tuberculosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14672050.001).
  • [ISSN] 0022-9776
  • [Journal-full-title] Kekkaku : [Tuberculosis]
  • [ISO-abbreviation] Kekkaku
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


5. Kawajiri H, Yashiro M, Shinto O, Nakamura K, Tendo M, Takemura S, Node M, Hamashima Y, Kajimoto T, Sawada T, Ohira M, Hirakawa K: A novel transforming growth factor beta receptor kinase inhibitor, A-77, prevents the peritoneal dissemination of scirrhous gastric carcinoma. Clin Cancer Res; 2008 May 1;14(9):2850-60
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel transforming growth factor beta receptor kinase inhibitor, A-77, prevents the peritoneal dissemination of scirrhous gastric carcinoma.
  • PURPOSE: Transforming growth factor beta receptor (TGFbeta-R) is reported to correlate with the malignant potential of scirrhous gastric carcinoma.
  • The aim of the current study is to clarify the possibility of molecular target therapy with a TGFbeta-R inhibitor, A-77, for the treatment of peritoneal dissemination of scirrhous gastric cancer.
  • EXPERIMENTAL DESIGN: Three scirrhous gastric cancer cell lines and two fibroblasts were used.
  • For in vivo experiments, the A-77 was administered i.p. to mouse models of peritoneal dissemination.
  • RESULTS: The A-77 administration resulted in a significantly (P < 0.01) better prognosis for the mice with peritoneal dissemination (median survival time, 51 days), compared with the control (median survival time, 25 days).
  • A-77 decreased the expression of alpha(2), alpha(3), and alpha(5) integrins in gastric cancer cells.
  • CONCLUSION: The TGFbeta-R inhibitor, A-77, decreased the expression of integrins in cancer cells and the proliferation of fibroblasts, which resulted in the decreased adhesive and invasive abilities of scirrhous gastric cancer cells to peritoneum.
  • A-77 is thus considered to be useful for the inhibition of peritoneal dissemination of scirrhous gastric carcinoma.
  • [MeSH-major] Adenocarcinoma, Scirrhous / drug therapy. Antineoplastic Agents / therapeutic use. Neoplasm Metastasis / prevention & control. Peritoneal Neoplasms / secondary. Pyrazoles / therapeutic use. Quinolines / therapeutic use. Receptors, Transforming Growth Factor beta / antagonists & inhibitors. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Integrins / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Invasiveness. Phosphorylation. RNA, Small Interfering / metabolism. Smad2 Protein / metabolism

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18451253.001).
  • [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 / A-77 compound; 0 / Antineoplastic Agents; 0 / Integrins; 0 / Pyrazoles; 0 / Quinolines; 0 / RNA, Small Interfering; 0 / Receptors, Transforming Growth Factor beta; 0 / Smad2 Protein
  •  go-up   go-down


6. Abe H, Kuroki M, Tachibana K, Li T, Awasthi A, Ueno A, Matsumoto H, Imakiire T, Yamauchi Y, Yamada H, Ariyoshi A, Kuroki M: Targeted sonodynamic therapy of cancer using a photosensitizer conjugated with antibody against carcinoembryonic antigen. Anticancer Res; 2002 May-Jun;22(3):1575-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted sonodynamic therapy of cancer using a photosensitizer conjugated with antibody against carcinoembryonic antigen.
  • To this end, a photoimmunoconjugate (PIC) was prepared between ATX-70, a photosensitizer of a gallium-porphyrin analogue, and F11-39, a high affinity monoclonal antibody (MAb) against carcinoembryonic antigen (CEA), which is often overexpressed in various carcinoma cells.
  • The cytotoxicity of F39/ATX-70 against CEA-expressing human gastric carcinoma cells in vitro was found to be greater than that of ATX-70 when applied in combination with ultrasound irradiation.
  • When in vivo anti-tumor effects in a mouse xenograft model were assessed, intravenous administration of F39/ATX-70 followed by ultrasonic irradiation produced a marked growth inhibition of tumor compared with irradiation alone or irradiation after administration of ATX-70.
  • These results suggest that the PIC between anti-CEA MAb and ATX-70 may have applications in sonodynamic therapy where destruction of CEA-expressing tumor is required.
  • [MeSH-major] Carcinoembryonic Antigen / immunology. Immunoconjugates / pharmacology. Photosensitizing Agents / pharmacology. Porphyrins / pharmacology. Ultrasonic Therapy / methods
  • [MeSH-minor] Animals. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / metabolism. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / toxicity. Antibody Specificity. Mice. Mice, Inbred BALB C. Mice, Nude. Stomach Neoplasms / drug therapy. Stomach Neoplasms / immunology. Stomach Neoplasms / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12168839.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Carcinoembryonic Antigen; 0 / Immunoconjugates; 0 / Photosensitizing Agents; 0 / Porphyrins; 135099-39-7 / ATX 70
  •  go-up   go-down


7. Coburger C, Lage H, Molnár J, Langner A, Hilgeroth A: Multidrug resistance reversal properties and cytotoxic evaluation of representatives of a novel class of HIV-1 protease inhibitors. J Pharm Pharmacol; 2010 Dec;62(12):1704-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: P-Glycoprotein (P-gp) plays a central role in the development of resistance against cytostatics in anticancer therapy and against human immunodeficiency virus (HIV) therapeutics of the HIV-1 protease inhibitor type.
  • An approach to reverse the so-called multidrug resistance (MDR) phenomenon by the use of P-gp inhibiting agents is a challenge in the therapy of cancer and AIDS.
  • METHODS: Novel HIV-1 protease inhibitors (H17, JW41, JW33 and JW46) have been evaluated in comparison with ritonavir as P-gp inhibiting agents, in the exclusively P-gp overexpressing model cell line mouse T lymphoma using flow cytometry.
  • The cytotoxic properties against various cell lines were characterized in the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay to estimate potential toxic effects in therapeutically relevant concentrations in metabolically active HepG2 cells, drug-sensitive Jurkat cells and in gastric carcinoma cells.
  • CONCLUSIONS: The novel compounds have been shown to be prospective AIDS therapeutics, acting as effective and nontoxic P-gp inhibitors compared with ritonavir, which is a known P-gp inhibitor with unfavourable toxic and P-gp substrate properties.
  • [MeSH-major] Cell Survival / drug effects. Drug Resistance, Multiple / drug effects. HIV Protease Inhibitors / pharmacology. P-Glycoprotein / antagonists & inhibitors. Ritonavir / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Hep G2 Cells. Humans. Jurkat Cells. Lymphoma, T-Cell. Mice. Mitochondria / drug effects. Mitochondria / metabolism

  • Genetic Alliance. consumer health - HIV.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 The Authors. JPP © 2010 Royal Pharmaceutical Society of Great Britain.
  • (PMID = 21054396.001).
  • [ISSN] 2042-7158
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIV Protease Inhibitors; 0 / P-Glycoprotein; O3J8G9O825 / Ritonavir
  •  go-up   go-down


8. Kirikoshi H, Katoh M: Expression and regulation of WNT10B in human cancer: up-regulation of WNT10B in MCF-7 cells by beta-estradiol and down-regulation of WNT10B in NT2 cells by retinoic acid. Int J Mol Med; 2002 Oct;10(4):507-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have previously cloned and characterized the human orthologue of mouse proto-oncogene Wnt-10b using bioinformatics and cDNA-PCR.
  • Human WNT10B is moderately expressed in MKN45 and MKN74 cells derived from human gastric cancer, and is up-regulated by tumor necrosis factor alpha (TNFalpha) in MKN45 cells.
  • Here, expression and regulation of WNT10B in human cancer other than gastric cancer were investigated using cDNA-PCR.
  • WNT10B mRNA was expressed in the majority of squamous cell carcinoma cell lines derived from esophageal cancer and cervical cancer.
  • [MeSH-major] Estradiol / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Proto-Oncogene Proteins / genetics. Tretinoin / pharmacology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Cell Line. Down-Regulation. Humans. Neoplasms, Germ Cell and Embryonal / drug therapy. Up-Regulation. Wnt Proteins

  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12239602.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / WNT10B protein, human; 0 / Wnt Proteins; 4TI98Z838E / Estradiol; 5688UTC01R / Tretinoin
  •  go-up   go-down


9. Han Z, Hong Z, Chen C, Gao Q, Luo D, Fang Y, Cao Y, Zhu T, Jiang X, Ma Q, Li W, Han L, Wang D, Xu G, Wang S, Meng L, Zhou J, Ma D: A novel oncolytic adenovirus selectively silences the expression of tumor-associated STAT3 and exhibits potent antitumoral activity. Carcinogenesis; 2009 Dec;30(12):2014-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Consequently, the STAT3 protein is emerging as an ideal target for cancer therapy.
  • This paper reports the generation of an oncolytic adenovirus (M4), which selectively blocks STAT3 signaling in tumor cells as a novel therapeutic strategy.
  • Systemic administration of M4 significantly inhibited tumor growth in an orthotopic gastric carcinoma mouse model, eliminated abdominal cavity metastases and prolonged survival time.
  • In summary, M4 has low toxicity and great potential as a therapeutic agent for different types of cancers.
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Collagen / chemistry. Drug Combinations. Humans. Laminin / chemistry. Male. Mice. Mice, Inbred BALB C. Models, Genetic. Mutation. Neoplasm Metastasis. Neovascularization, Pathologic. Oligonucleotides, Antisense / genetics. Proteoglycans / chemistry. Signal Transduction

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19843641.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Combinations; 0 / Laminin; 0 / Oligonucleotides, Antisense; 0 / Proteoglycans; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 119978-18-6 / matrigel; 9007-34-5 / Collagen
  •  go-up   go-down


10. Ding L, Chen XP, Zhang ZW, Guan J, Zhang WG, Wang HP, Wang ZH, Li CL: Synergistic effect of bromocriptine and tumor necrosis factor-alpha on reversing hepatocellular carcinoma multidrug resistance in nude mouse MDR1 model of liver neoplasm. World J Gastroenterol; 2005 Sep 28;11(36):5621-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synergistic effect of bromocriptine and tumor necrosis factor-alpha on reversing hepatocellular carcinoma multidrug resistance in nude mouse MDR1 model of liver neoplasm.
  • AIM: To investigate the effect of bromocriptine (BCT) and tumor necrosis factor-alpha (TNF-alpha) on hepatocellular carcinoma (HCC) multidrug resistance (MDR) in nude mouse MDR model of liver neoplasm.
  • METHODS: Human hepatocarcinoma cell line HepG(2), drug resistant hepatocarcinoma cell line HepG(2)/adriamycin (ADM) and hepatocarcinoma cell line transfected with TNF-alpha gene HepG(2)/ADM/TNF were injected into the liver of nude mice via orthotopic implantation and MDR model of liver neoplasm in vivo was established (HepG(2), ADM, TNF, BCT groups).
  • Among these groups, BCT group and TNF group were treated with BCT through gastric canal.
  • Each group was divided into control group and chemotherapy group.
  • RESULTS: The nude mouse model of each cell line was inoculated successfully.
  • After chemotherapy, abdominal cavity tumor growth inhibition rate was higher in BCT group (67%) compared to ADM and TNF groups, and similar to HepG(2) group (54%).
  • CONCLUSION: BCT and TNF-alpha can reverse HCC MDR in nude mouse MDR1 model of liver neoplasm.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bromocriptine / pharmacology. Drug Resistance, Neoplasm / drug effects. Liver Neoplasms / drug therapy. P-Glycoprotein / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Drug Synergism. Female. Gene Expression Regulation, Neoplastic. Genes, MDR / genetics. Genes, MDR / physiology. Humans. Mice. Mice, Nude. Neoplasm Transplantation. RNA, Messenger / metabolism

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16237754.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 3A64E3G5ZO / Bromocriptine
  • [Other-IDs] NLM/ PMC4481477
  •  go-up   go-down


11. Yamada N, Ohira M, Hirakawa K: [COX and study of cancer therapy]. Gan To Kagaku Ryoho; 2004 Aug;31(8):1147-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [COX and study of cancer therapy].
  • The increased expression of COX-2 in carcinoma tissue is found in gastric cancer, lung cancer and breast cancer as well as colon cancer.
  • It was shown that COX-2 played an important role in carcinogenesis by an experiment using a cultured cell and an animal experiment using a knockout mouse.
  • Food and Drug Administration (FDA) approved administration of a COX-2 inhibitor to FAP patients.
  • [MeSH-major] Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / biosynthesis. Neoplasms / enzymology. Prostaglandin-Endoperoxide Synthases / biosynthesis
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Animals. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Breast Neoplasms / enzymology. Colonic Neoplasms / enzymology. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Female. Humans. Lung Neoplasms / enzymology. Male. Membrane Proteins. Mice. Mice, Knockout. Neoplastic Cells, Circulating / drug effects. Stomach Neoplasms / enzymology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15332534.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 27
  •  go-up   go-down


12. Yoshida T, Endo Y, Obata T, Kosugi Y, Sakamoto K, Sasaki T: Influence of cytidine deaminase on antitumor activity of 2'-deoxycytidine analogs in vitro and in vivo. Drug Metab Dispos; 2010 Oct;38(10):1814-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To elucidate the relationship between the chemosensitivity to antitumor dCyd nucleosides and CDA expression, we established a stable line of human gastric carcinoma TMK-1 cells constitutively overexpressing CDA (TMK-1/CDA) and examined its chemosensitivity to antitumor dCyd analogs in vitro and in vivo.
  • We observed comparable reactivity for dFdC and Ara-C, and the substrate reactivity of CNDAC to recombinant human CDA was more than 10 times less efficient than those of Ara-C and dFdC.
  • In addition, we transplanted TMK-1/CDA cells into a nude mouse xenograft model and examined their in vivo chemosensitivity to CNDAC.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Female. Humans. Mice. Mice, Nude. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / enzymology. Neoplasms, Experimental / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Substrate Specificity. Transfection. Xenograft Model Antitumor Assays

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20587622.001).
  • [ISSN] 1521-009X
  • [Journal-full-title] Drug metabolism and disposition: the biological fate of chemicals
  • [ISO-abbreviation] Drug Metab. Dispos.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 0W860991D6 / Deoxycytidine; EC 3.5.4.5 / Cytidine Deaminase
  •  go-up   go-down


13. Nakahara C, Nakamura K, Yamanaka N, Baba E, Wada M, Matsunaga H, Noshiro H, Tanaka M, Morisaki T, Katano M: Cyclosporin-A enhances docetaxel-induced apoptosis through inhibition of nuclear factor-kappaB activation in human gastric carcinoma cells. Clin Cancer Res; 2003 Nov 1;9(14):5409-16
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclosporin-A enhances docetaxel-induced apoptosis through inhibition of nuclear factor-kappaB activation in human gastric carcinoma cells.
  • PURPOSE: We sought to determine whether cyclosporin-A (CsA) enhances docetaxel [Taxotere (TXT)]- induced apoptosis in human gastric carcinoma cells, and, if so, to determine the relation between this apoptosis and nuclear factor-kappaB (NF-kappaB) activation.
  • EXPERIMENTAL DESIGN: Two human gastric carcinoma cell lines (GCTM-1 and MK-1), a human embryonic pulmonary fibroblast cell line, and human umbilical vein endothelial cells were used as drug targets.
  • The therapeutic effects of a combination of TXT and CsA were assessed in a mouse peritoneal dissemination model.
  • RESULTS: A combination of CsA (5 micro M) and TXT (10 nM) significantly enhanced apoptotic cell death in both carcinoma cell lines but not in nonmalignant cell lines in comparison with the single-agent treatment alone.
  • This effect was not related to drug uptake, efflux, or MDR1 expression.
  • These effects were also observed in freshly obtained TXT-resistant gastric carcinoma cells isolated from a patient with malignant ascites.
  • TXT alone induced NF-kappaB activation in both carcinoma cell types, and this activation was suppressed by CsA.
  • A combination of TXT and NF-kappaB decoy, a well-known NF-kappaB inhibitor, also enhanced apoptotic cell death in the carcinoma cells.
  • CONCLUSIONS: Treatment with CsA and TXT in combination may be an effective therapeutic strategy for patients with gastric carcinoma.
  • [MeSH-major] Apoptosis / drug effects. Colonic Neoplasms / drug therapy. Cyclosporine / pharmacology. NF-kappa B / antagonists & inhibitors. Stomach Neoplasms / drug therapy. Taxoids / pharmacology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Animals. Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. Caspase Inhibitors. Caspases / metabolism. Chromatography, High Pressure Liquid. Drug Combinations. Enzyme Inhibitors / pharmacology. Female. Humans. Mice. Mice, Inbred BALB C. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / prevention & control. Peritoneal Neoplasms / secondary. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14614027.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Caspase Inhibitors; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Taxoids; 15H5577CQD / docetaxel; 83HN0GTJ6D / Cyclosporine; EC 3.4.22.- / Caspases
  •  go-up   go-down


14. Lu Y, Lin P, Lu B, Wang J, Zhang J, Huang X: [Studies on release characteristics and cytotoxicity of 5-fluorouracil loaded polylactide microspheres on lung cancer cell lines]. Zhongguo Fei Ai Za Zhi; 2000 Dec 20;3(6):432-4
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The antitumor activities of 5-FU-PLA microspheres against human and mouse lung, gastric and hepatocellular carcinoma cell lines were detected byMTT colorimetric assay.
  • The lung and gastric cancer cell lines were more sensitive than hepatocellular cancer cell line to 5-FU-PLA microspheres.
  • The antitumor activity significantly correlated with the time of drug action and the dose of 5-FU released from the microspheres.
  • It can keep the antitumor activities for a relatively long time.
  • The current study provides an experimental basis for interventional therapy of tumors.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21029576.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


15. Wang Y, Adachi Y, Imsumran A, Yamamoto H, Piao W, Li H, Ii M, Arimura Y, Park MY, Kim D, Lee CT, Carbone DP, Imai K, Shinomura Y: Targeting for insulin-like growth factor-I receptor with short hairpin RNA for human digestive/gastrointestinal cancers. J Gastroenterol; 2010 Feb;45(2):159-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We constructed a recombinant adenovirus expressing short hairpin RNA targeting IGF-IR (shIGF-IR) and assessed its effect on signal transduction, proliferation, and survival in digestive/gastrointestinal cancer cell lines representing colorectal, gastric, and pancreatic adenocarcinoma, esophageal squamous cell carcinoma, and hepatoma.
  • We analyzed the effects of shIGF-IR alone and with chemotherapy in vitro and in nude mouse xenografts, as well as on insulin signaling and hybrid receptor formation between IGF-IR and insulin receptor.
  • RESULTS: shIGF-IR blocked expression and autophosphorylation of IGF-IR and downstream signaling by the IGFs, but not by insulin. shIGF-IR suppressed proliferation and carcinogenicity in vitro and up-regulated apoptosis in a dose-dependent fashion. shIGF-IR augmented the effects of chemotherapy on in vitro growth and apoptosis induction.
  • Moreover, the combination of shIGF-IR and chemotherapy was highly effective against tumors in mice. shIGF-IR reduced hybrid receptor formation without effect on expression of insulin receptor.
  • CONCLUSIONS: shIGF-IR may have therapeutic utility in human digestive/gastrointestinal cancers, both alone and in combination with chemotherapy.
  • [MeSH-major] Gastrointestinal Neoplasms / therapy. RNA, Small Interfering / administration & dosage. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, Insulin / metabolism
  • [MeSH-minor] Adenoviridae / genetics. Animals. Antineoplastic Agents / pharmacology. Apoptosis. Cell Line, Tumor. Cell Proliferation. Combined Modality Therapy. Dose-Response Relationship, Drug. Female. Gene Targeting / methods. Genetic Vectors. Humans. Insulin / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Signal Transduction. Xenograft Model Antitumor Assays

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 1994 Dec 16;79(6):927-30 [8001140.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23 ):11118-28 [16322262.001]
  • [Cites] J Clin Invest. 1988 Apr;81(4):976-81 [2832449.001]
  • [Cites] Cancer Res. 1998 Jul 1;58(13):2825-31 [9661897.001]
  • [Cites] Physiol Rev. 1990 Jul;70(3):591-614 [1694588.001]
  • [Cites] Int J Cancer. 1994 Aug 1;58(3):452-9 [8050827.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):391-7 [17210722.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6432-41 [14559833.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):806-11 [9486653.001]
  • [Cites] Cancer Res. 1991 Apr 1;51(7):1898-903 [2004373.001]
  • [Cites] Nature. 2002 Jul 11;418(6894):244-51 [12110901.001]
  • [Cites] Carcinogenesis. 2007 May;28(5):947-56 [17183068.001]
  • [Cites] Int J Cancer. 1992 Dec 2;52(6):910-7 [1281142.001]
  • [Cites] Gut. 2005 May;54(5):591-600 [15831900.001]
  • [Cites] J Natl Cancer Inst. 2000 Sep 20;92 (18):1472-89 [10995803.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10123-7 [16287993.001]
  • [Cites] Mol Cancer Ther. 2008 Jun;7(6):1483-93 [18566219.001]
  • [Cites] J Biol Chem. 2003 May 2;278(18):15991-7 [12604614.001]
  • [Cites] Gut. 1999 May;44(5):704-8 [10205209.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8912-21 [14695208.001]
  • [Cites] J Natl Cancer Inst. 1999 Apr 7;91(7):620-5 [10203281.001]
  • [Cites] Cancer Gene Ther. 2005 Jan;12 (1):90-100 [15499378.001]
  • [Cites] Gastroenterology. 2005 Aug;129(2):464-75 [16083703.001]
  • [Cites] Cancer Res. 2009 Feb 15;69(4):1350-7 [19190347.001]
  • [Cites] Mol Cancer Ther. 2005 Aug;4(8):1214-21 [16093437.001]
  • [Cites] J Pathol. 2005 Jan;205(2):145-53 [15641016.001]
  • [Cites] Cancer Res. 1995 Jan 15;55(2):249-52 [7812953.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7372-6 [12499282.001]
  • [Cites] Clin Cancer Res. 2005 Mar 1;11(5):2063-73 [15756033.001]
  • [Cites] Gastroenterology. 2002 Oct;123(4):1191-204 [12360481.001]
  • [Cites] EMBO J. 1986 Oct;5(10):2503-12 [2877871.001]
  • [Cites] J Biol Chem. 2002 Oct 18;277(42):39684-95 [12138094.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):11217-21 [8248231.001]
  • [Cites] Cell. 1993 Oct 8;75(1):59-72 [8402901.001]
  • [Cites] Br J Cancer. 1992 Mar;65(3):341-6 [1558785.001]
  • [Cites] Endocrinology. 1990 Jun;126(6):3033-42 [1693565.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):1940-8 [16488992.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 19;93(24):1852-7 [11752009.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10238-46 [19074892.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2007-11 [7743492.001]
  • [Cites] Nature. 2003 Jan 16;421(6920):220-1 [12529623.001]
  • [Cites] Cancer Res. 2009 Jan 1;69(1):161-70 [19117999.001]
  • [Cites] Hepatogastroenterology. 2001 Nov-Dec;48(42):1788-92 [11813625.001]
  • [Cites] Cell Mol Life Sci. 2000 Jul;57(7):1050-93 [10961344.001]
  • [Cites] Cancer Res. 1996 Aug 15;56(16):3831-6 [8706031.001]
  • [Cites] Am J Physiol. 1999 Apr;276(4 Pt 1):G817-27 [10198323.001]
  • [Cites] Lung Cancer. 2007 Mar;55(3):279-86 [17134788.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):3038-41 [8674059.001]
  • [Cites] Acta Biochim Biophys Sin (Shanghai). 2008 Jun;40(6):497-504 [18535748.001]
  • (PMID = 19902140.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Insulin; 0 / RNA, Small Interfering; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptor, Insulin
  •  go-up   go-down


16. Saukkonen K, Rintahaka J, Sivula A, Buskens CJ, Van Rees BP, Rio MC, Haglund C, Van Lanschot JJ, Offerhaus GJ, Ristimaki A: Cyclooxygenase-2 and gastric carcinogenesis. APMIS; 2003 Oct;111(10):915-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase-2 and gastric carcinogenesis.
  • Epidemiological studies have shown that the use of nonsteroid anti-inflammatory drugs (NSAIDs) is associated with reduced risk of gastric cancer.
  • Two Cox genes have been cloned, of which Cox-2 has been connected with gastric carcinogenesis.
  • Expression of Cox-2 is elevated in gastric adenocarcinomas, which correlates with several clinicopathological parameters, including depth of invasion and lymph node metastasis.
  • Cox-2 expression is especially prominent in intestinal-type gastric carcinoma and it is already present in dysplastic precursor lesions of this disease, which suggests that Cox-2 contributes to gastric carcinogenesis already at the preinvasive stage.
  • Our most recent data show that Cox-2 is expressed in gastric adenomas of trefoil factor 1 deficient mice.
  • Treatment of these mice with a Cox-2 selective inhibitor, celecoxib, reduced the size of the adenomas.
  • Taken together these data support efforts to initiate clinical studies to investigate the effect of Cox-2 inhibitors as chemotherapeutic agents and as adjuvant treatment modalities against gastric neoplasias.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / therapeutic use. Gene Expression. Humans. Membrane Proteins. Mice. Mice, Knockout. Models, Biological. Peptides / deficiency. Peptides / genetics

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14616542.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Peptides; 0 / Tff1 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 76
  •  go-up   go-down


17. Lee CW, Rickman B, Rogers AB, Ge Z, Wang TC, Fox JG: Helicobacter pylori eradication prevents progression of gastric cancer in hypergastrinemic INS-GAS mice. Cancer Res; 2008 May 1;68(9):3540-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Helicobacter pylori eradication prevents progression of gastric cancer in hypergastrinemic INS-GAS mice.
  • Helicobacter pylori infection results in chronic gastritis, which may progress to gastric cancer.
  • In this study, we investigated the efficacy of H. pylori eradication in preventing the progression of gastritis to gastric cancer in H. pylori-infected transgenic INS-GAS mice. H. pylori infection induced severe dysplasia and gastric cancer classified as high-grade and low-grade gastrointestinal intraepithelial neoplasia (GIN) in INS-GAS mice at 28 weeks postinfection (WPI). H. pylori eradication therapy using omeprazole, metronidazole, and clarithromycin was administered p.o. at 8, 12, or 22 WPI.
  • Although not as effective as early antimicrobial treatment, prevention of progression to high-grade GIN was achieved by H. pylori eradication at 12 and 22 WPI (P < 0.05).
  • Consistent with reduced gastric pathology, H. pylori eradication at all time points significantly down-regulated gastric Interferon-gamma, tumor necrosis factor-alpha, inducible nitric oxide synthase, and Reg 1 mRNA levels (P < 0.05) and reduced epithelial proliferation in the corpus (P < 0.01) compared with untreated infected mice.
  • We concluded that H. pylori eradication prevented gastric cancer to the greatest extent when antibiotics are given at an early point of infection, but that eradication therapy given at a later time point delayed the development of severe dysplastic lesions.

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. OMEPRAZOLE .
  • Hazardous Substances Data Bank. Clarithromycin .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Natl Cancer Inst. 1995 Jan 4;87(1):28-33 [7666459.001]
  • [Cites] J Natl Cancer Inst. 2000 Dec 6;92(23):1881-8 [11106679.001]
  • [Cites] J Clin Invest. 1996 Oct 15;98(8):1918-29 [8878444.001]
  • [Cites] Gastroenterology. 1997 Apr;112(4):1386-97 [9098027.001]
  • [Cites] Gastroenterology. 1998 Dec;115(6):1483-93 [9834276.001]
  • [Cites] Am J Physiol. 1999 Oct;277(4 Pt 1):G773-84 [10516143.001]
  • [Cites] Cancer Sci. 2004 Nov;95(11):872-7 [15546504.001]
  • [Cites] Infect Immun. 2005 Mar;73(3):1664-70 [15731067.001]
  • [Cites] Lab Invest. 2005 May;85(5):702-15 [15765119.001]
  • [Cites] Gastroenterology. 2005 Jun;128(7):1937-52 [15940628.001]
  • [Cites] Gastroenterology. 2005 Jun;128(7):1965-83 [15940630.001]
  • [Cites] Gut. 2005 Nov;54(11):1536-40 [15985559.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10709-15 [16322215.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Jan;290(1):G175-82 [16109843.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):732-7 [16407106.001]
  • [Cites] J Natl Cancer Inst. 2006 Jul 19;98(14):974-83 [16849680.001]
  • [Cites] J Natl Cancer Inst. 2006 Oct 4;98(19):1426 [17018791.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):60-9 [17200707.001]
  • [Cites] Infect Immun. 2007 Jun;75(6):2699-707 [17353283.001]
  • [Cites] Gut. 2007 Jun;56(6):772-81 [17170018.001]
  • [Cites] Am J Pathol. 2007 Nov;171(5):1520-8 [17982128.001]
  • [Cites] Carcinogenesis. 2007 Dec;28(12):2597-604 [17724378.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1994;61:1-241 [7715068.001]
  • [Cites] J Antimicrob Chemother. 1999 Nov;44(5):629-40 [10552979.001]
  • [Cites] Gastroenterology. 2000 Jan;118(1):36-47 [10611152.001]
  • [Cites] Gastroenterology. 2000 Jul;119(1):7-14 [10889149.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6376-80 [11103800.001]
  • [Cites] N Engl J Med. 2001 Sep 13;345(11):829-32 [11556306.001]
  • [Cites] Infect Immun. 2002 May;70(5):2630-9 [11953405.001]
  • [Cites] Aliment Pharmacol Ther. 2002 Aug;16(8):1449-56 [12182744.001]
  • [Cites] Gastroenterology. 2003 Mar;124(3):762-77 [12612914.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):942-50 [12615707.001]
  • [Cites] Gastroenterology. 2003 Jun;124(7):1879-90 [12806621.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Jul;47(7):2249-55 [12821476.001]
  • [Cites] JAMA. 2004 Jan 14;291(2):187-94 [14722144.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jan;13(1):4-10 [14744726.001]
  • [Cites] Appl Environ Microbiol. 2004 May;70(5):2791-800 [15128534.001]
  • [Cites] Gut. 2004 Sep;53(9):1244-9 [15306578.001]
  • [Cites] Lancet. 1984 Jun 16;1(8390):1311-5 [6145023.001]
  • [Cites] Cancer Res. 1988 Jul 1;48(13):3554-60 [3288329.001]
  • [Cites] Ital J Gastroenterol. 1991 Jan;23(1):24-8 [1747497.001]
  • [Cites] J Cell Biochem Suppl. 1992;16G:73-8 [1469907.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3671-6 [8631979.001]
  • (PMID = 18441088.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI037750-12; United States / NIEHS NIH HHS / ES / P30ES02109; United States / NIEHS NIH HHS / ES / ES002109-299010; United States / NIAID NIH HHS / AI / AI037750-12; United States / NCI NIH HHS / CA / R01 CA093405; United States / NIAID NIH HHS / AI / R01 AI037750-13; United States / NIAID NIH HHS / AI / AI037750-13; United States / NIAID NIH HHS / AI / R01AI37750; United States / NCI NIH HHS / CA / R01 CA093405-07A1; United States / NCI NIH HHS / CA / CA093405-07A1; United States / NIAID NIH HHS / AI / R01 AI037750; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / P01 CA026731-299002; United States / NIEHS NIH HHS / ES / P30 ES002109-299010; United States / NCI NIH HHS / CA / P01 CA026731; United States / NCI NIH HHS / CA / P01CA26731; United States / NCI NIH HHS / CA / CA026731-299002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Anti-Ulcer Agents; 0 / Lithostathine; 0 / Reg1 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole
  • [Other-IDs] NLM/ NIHMS95242; NLM/ PMC2653414
  •  go-up   go-down


18. Lane HA, Motoyama AB, Beuvink I, Hynes NE: Modulation of p27/Cdk2 complex formation through 4D5-mediated inhibition of HER2 receptor signaling. Ann Oncol; 2001;12 Suppl 1:S21-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The molecular mechanisms mediating the anti-proliferative effects of the murine anti-HER2 monoclonal antibody (4D5) were investigated in HER2-overexpressing human carcinoma cell lines.
  • Treatment with 4D5 resulted in a dramatic accumulation of BT-474 breast carcinoma cells in G1; concomitant with reduced expression of proteins involved in sequestration of the cyclin E/Cdk2 inhibitor protein p27, increased association of p27 with Cdk2 complexes and Cdk2 inactivation.
  • No equivalent effects were observed in BT-474 cells treated with a control, non-inhibitory HER2 monoclonal antibody (FRP5) or in a HER2-overexpressing cell line insensitive to 4D5 treatment (MKN7 gastric carcinoma cells), confirming the relationship between these molecular changes and 4D5-mediated inhibition of proliferation.
  • HER2-overexpressing breast tumor line (SKBR3), and suggests that the dependency of a given tumor cell on elevated HER2-receptor signaling for the maintenance of p27 sequestration proteins may determine the clinical response to treatment with the humanized anti-HER2 monoclonal antibody Herceptin (trastuzumab).

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. Trastuzumab .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11521716.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Cdkn1b protein, mouse; 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.22 / Cyclin-Dependent Kinases; P188ANX8CK / Trastuzumab
  • [Number-of-references] 5
  •  go-up   go-down


19. Koshikawa N, Mizushima H, Minegishi T, Iwamoto R, Mekada E, Seiki M: Membrane type 1-matrix metalloproteinase cleaves off the NH2-terminal portion of heparin-binding epidermal growth factor and converts it into a heparin-independent growth factor. Cancer Res; 2010 Jul 15;70(14):6093-103
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Membrane type 1-matrix metalloproteinase cleaves off the NH2-terminal portion of heparin-binding epidermal growth factor and converts it into a heparin-independent growth factor.
  • Epidermal growth factor (EGF) receptors (ErbB) and EGF family members represent promising targets for cancer therapy.
  • Heparin-binding EGF (HB-EGF) is a member of the EGF family and is an important target for therapy in some types of human cancers.
  • Here, we show that membrane type 1-matrix metalloproteinase (MT1-MMP; MMP14), a potent invasion-promoting protease, markedly enhances HB-EGF-dependent tumor formation in mice.
  • The ErbB family of receptors expressed in human gastric carcinoma cells play a role in mediating enhanced HB-EGF activity by MT1-MMP during invasive cell growth in collagen.
  • Thus, we shed light on a new mechanism whereby HB-EGF activity is regulated that should be considered when designing HB-EGF-targeted cancer therapy.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line. Cell Line, Tumor. Dogs. Fibroblasts / cytology. Fibroblasts / drug effects. Gene Knockdown Techniques. Heparin-binding EGF-like Growth Factor. Humans. Mice. Molecular Sequence Data. Neoplasm Invasiveness. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Small Interfering / genetics. Rats. Rats, Inbred BUF. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology. Transfection

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c)2010 AACR.
  • (PMID = 20587521.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HBEGF protein, human; 0 / Hbegf protein, mouse; 0 / Hbegf protein, rat; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.4.24.80 / Matrix Metalloproteinase 14
  •  go-up   go-down


20. Kamata S, Kishimoto T, Kobayashi S, Miyazaki M, Ishikura H: Possible involvement of persistent activity of the mammalian target of rapamycin pathway in the cisplatin resistance of AFP-producing gastric cancer cells. Cancer Biol Ther; 2007 Jul;6(7):1036-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possible involvement of persistent activity of the mammalian target of rapamycin pathway in the cisplatin resistance of AFP-producing gastric cancer cells.
  • AFP-producing gastric carcinoma (AFPGC) is a highly malignant variant of gastric cancer.
  • An effective chemotherapy is needed to improve on the poor outcome of this disease.
  • We investigated the role of a pivotal kinase pathway, the mammalian target of rapamycin complex 1 (mTORC1) pathway, in the effectiveness of chemotherapeutic agents in three AFPGC cell lines (GCIY, FU97 and Takigawa) as well as in four cell lines of conventional-type gastric carcinoma (CGC).
  • Finally, combined treatment of rapamycin and cisplatin significantly suppressed the subcutaneously implanted GCIY cells.
  • In conclusion rapamycin may be a potential supplemental agent for the treatment of AFPGC when used in combination with cisplatin.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cisplatin / pharmacology. Protein Kinases / physiology. Signal Transduction / physiology. Stomach Neoplasms / drug therapy. alpha-Fetoproteins / biosynthesis
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. Male. Mice. Mice, Inbred BALB C. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Transcription Factors / physiology. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / analysis

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17568186.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CRTC1 protein, human; 0 / Transcription Factors; 0 / alpha-Fetoproteins; 0 / bcl-2-Associated X Protein; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; Q20Q21Q62J / Cisplatin; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


21. Kinoshita J, Fushida S, Harada S, Yagi Y, Fujita H, Kinami S, Ninomiya I, Fujimura T, Kayahara M, Yashiro M, Hirakawa K, Ohta T: Local angiotensin II-generation in human gastric cancer: correlation with tumor progression through the activation of ERK1/2, NF-kappaB and survivin. Int J Oncol; 2009 Jun;34(6):1573-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Local angiotensin II-generation in human gastric cancer: correlation with tumor progression through the activation of ERK1/2, NF-kappaB and survivin.
  • Angiotensin II is a main effector peptide in renin-angiotensin system, acting as a growth promoter via angiotensin II type 1 (AT1) receptor.
  • The present study examined intrinsic angiotensin II generating system in gastric cancer and potential roles of angiotensin II in cellular proliferation and survival.
  • The expression of AT1 receptor was examined in gastric cancer cell lines and tissues.
  • In addition, we measured angiotensin II concentration in tissues from twenty gastric cancer and corresponding normal region using the florisil method.
  • In vitro, we investigated the potential roles of angiotensin II in cellular proliferation and cell survival in cultured human gastric cancer cell line.
  • The effects of AT1 receptor blocker candesartan were evaluated in a mouse model of peritoneal carcinomatosis.
  • AT1 receptor protein was expressed in gastric cancer cell lines and tissues.
  • Angiotensin II stimulates the cell proliferation in the AT1 receptor-positive OCUM2MD3 gastric cancer cell line and this proliferative effect of angiotensin II was inhibited by a specific AT1 receptor antagonist, candesartan.
  • Candesartan significantly prolonged survival time in a mouse model of peritoneal carcinomatosis compared with control group (p=0.0.197, log-rank test).
  • Our data provide in vivo evidence of intrinsic angiotensin II generating system in gastric cancer and indicate locally formed angiotensin II is involved in cellular proliferation and survival.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adenocarcinoma, Clear Cell / drug therapy. Adenocarcinoma, Clear Cell / metabolism. Adenocarcinoma, Clear Cell / secondary. Adenocarcinoma, Mucinous / drug therapy. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / secondary. Adult. Aged. Angiotensin II Type 1 Receptor Blockers / pharmacology. Animals. Apoptosis / drug effects. Benzimidazoles / pharmacology. Blotting, Western. Carcinoma, Medullary / drug therapy. Carcinoma, Medullary / metabolism. Carcinoma, Medullary / secondary. Case-Control Studies. Cell Proliferation / drug effects. Disease Progression. Electrophoretic Mobility Shift Assay. Female. Humans. Immunoenzyme Techniques. Inhibitor of Apoptosis Proteins. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / metabolism. Peritoneal Neoplasms / pathology. Receptor, Angiotensin, Type 1 / chemistry. Receptor, Angiotensin, Type 1 / drug effects. Receptor, Angiotensin, Type 1 / metabolism. Stomach / metabolism. Stomach / pathology. Survival Rate. Tetrazoles / pharmacology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Hazardous Substances Data Bank. CANDESARTAN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19424575.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / BIRC5 protein, human; 0 / Benzimidazoles; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Receptor, Angiotensin, Type 1; 0 / Tetrazoles; 11128-99-7 / Angiotensin II; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; S8Q36MD2XX / candesartan
  •  go-up   go-down






Advertisement