Skip NavigationSkip to Content
Return Return to Search Results

Induction of Metastatic Gastric Cancer by Peroxisome Proliferator-Activated Receptor delta Activation

  1. Author:
    Pollock, C. B.
    Rodriguez, O.
    Martin, P. L.
    Albanese, C.
    Li, X.
    Kopelovich, L.
    Glazer, R. I.

  2. Author Address

    [Pollock, Claire B.; Rodriguez, Olga; Albanese, Chris; Glazer, Robert I.] Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20057 USA. [Martin, Philip L.] NCI Frederick, Ctr Adv Preclin Res, SAIC, Ft Detrick, MD 21702 USA. [Li, Xin] Lombardi Comprehens Canc Ctr, Dept Biostat Bioinformat & Biomath, Washington, DC 20057 USA. [Kopelovich, Levy] NCI, Chemoprevent Agent Dev & Res Grp, Canc Prevent Div, Bethesda, MD 20814 USA.;Glazer, RI, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20057 USA.;glazerr@georgetown.edu
    1. Year: 2010
    2. Date: Dec 27
  2. Journal: Ppar Research
    1. Pages: 12
  4. Type of Article: Article
  5. Article Number: 571783
  6. ISSN: 1687-4757
  1. Abstract:

    Peroxisome proliferator-activated receptord (PPAR delta) regulates a multiplicity of physiological processes associated with glucose and lipid metabolism, inflammation, and proliferation. One or more of these processes likely create risk factors associated with the ability of PPAR delta agonists to promote tumorigenesis in some organs. In the present study, we describe a new gastric tumor mouse model that is dependent on the potent and highly selective PPARd agonist GW501516 following carcinogen administration. The progression of gastric tumorigenesis was rapid as determined by magnetic resonance imaging and resulted in highly metastatic squamous cell carcinomas of the forestomach within two months. Tumorigenesis was associated with gene expression signatures indicative of cell adhesion, invasion, inflammation, and metabolism. Increased PPAR delta expression in tumors correlated with increased PDK1, Akt, beta-catenin, and S100A9 expression. The rapid development of metastatic gastric tumors in this model will be useful for evaluating preventive and therapeutic interventions in this disease.

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1155/2010/571783
  3. View record in Web of Science®
  4. WOS: 000286264000001

Library Notes

  1. Fiscal Year: FY2010-2011
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel