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Defining the Molecular Nexus of Cancer, Type 2 Diabetes and Cardiovascular Disease

  1. Author:
    Cabarcas, S. M.
    Hurt, E. M.
    Farrar, W. L.

  2. Author Address

    [Cabarcas, S. M.; Farrar, W. L.] NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21702 USA. [Hurt, E. M.] MedImmune LLC, Gaithersburg, MD USA.;Farrar, WL, NCI, Canc Stem Cell Sect, Lab Canc Prevent, Ctr Canc Res, 1050 Boyles St,Bldg 560,Room 21-78, Frederick, MD 21702 USA.;farrarw@mail.nih.gov
    1. Year: 2010
    2. Date: Nov
  2. Journal: Current Molecular Medicine
    1. 10
    2. 8
    3. Pages: 741-755
  4. Type of Article: Review
  5. ISSN: 1566-5240
  1. Abstract:

    The metabolic syndrome is characterized by a state of metabolic dysfunction resulting in the development of several chronic diseases that are potentially deadly. These metabolic deregulations are complex and intertwined and it has been observed that many of the mechanisms and pathways responsible for diseases characterizing the metabolic syndrome such as type 2 diabetes and cardiovascular disease are linked with cancer development as well. Identification of molecular pathways common to these diverse diseases may prove to be a critical factor in disease prevention and development of potential targets for therapeutic treatments. This review focuses on several molecular pathways, including AMPK, PPARs and FASN that interconnect cancer development, type 2 diabetes and cardiovascular disease. AMPK, PPARs and FASN are crucial regulators involved in the maintenance of key metabolic processes necessary for proper homeostasis. It is critical to recognize and identify common pathways deregulated in interrelated diseases as it may provide further information and a much more global picture in regards to disease development and prevention. Thus, this review focuses on three key metabolic regulators, AMPK, PPARs and FASN, that may potentially serve as therapeutic targets.

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External Sources

  1. View record in Web of Science®
  2. WOS: 000284623000005

Library Notes

  1. Fiscal Year: FY2010-2011
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