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Research Article

Genetic Deletion of the Desmosomal Component Desmoplakin Promotes Tumor Microinvasion in a Mouse Model of Pancreatic Neuroendocrine Carcinogenesis

  • Matthew G. H. Chun,

    Affiliations: Department of Biochemistry and Biophysics, Helen Diller Family Comprehensive Cancer Center, and Diabetes Center, University of California San Francisco, San Francisco, California, United States of America, Program in Biological Sciences, University of California San Francisco, San Francisco, California, United States of America

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  • Douglas Hanahan mail

    dh@ucsf.edu

    Affiliations: Department of Biochemistry and Biophysics, Helen Diller Family Comprehensive Cancer Center, and Diabetes Center, University of California San Francisco, San Francisco, California, United States of America, Swiss Institute for Experimental Cancer Research (ISREC), Swiss Federal Institute of Technology Lausanne (EPFL), Lausanne, Switzerland

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  • Published: September 16, 2010
  • DOI: 10.1371/journal.pgen.1001120

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Summary published in UCSF newspaper

Posted by alexmgreer on 13 Oct 2010 at 18:21 GMT

(This short summary was published in the column "UCSF Journal Club" in Synapse on 9/30/10)

The development of cancer requires multiple cell changes; for example, uncontrolled replication, inhibition of apoptosis in the face of serious genetic mutations, an ability to promote vascularization, immune cell evasion, and development of the capacity for movement and invasion. Cell movement requires a loss of adhesion to the local environment, which allows the cell to move more freely through tissues. Desmosomes are one component of ‘tight junctions’ that facilitate adherence to neighboring epithelial or muscle cells. In this paper, researchers compared the expressed genes in invasive and non-invasive pancreatic tumors and found that some components of desmosomes were expressed much less in the invasive tumors. Furthermore, they demonstrated in mice that targeted mutation of desmoplakin, a desmosome component, resulted in increased invasion of pancreatic tumors.

No competing interests declared.