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Suppression of Myc-induced apoptosis in beta cells exposes multiple oncogenic properties of Myc and triggers carcinogenic progression.

To explore the role of c-Myc in carcinogenesis, we have developed a reversible transgenic model of pancreatic beta cell oncogenesis using a switchable form of the c-Myc protein. Activation of c-Myc in adult, mature beta cells induces uniform beta cell proliferation but is accompanied by overwhelming apoptosis that rapidly erodes beta cell mass. Thus, the oncogenic potential of c-Myc in beta cells is masked by apoptosis. Upon suppression of c-Myc-induced beta cell apoptosis by coexpression of Bcl-x(L), c-Myc triggers rapid and uniform progression into angiogenic, invasive tumors. Subsequent c-Myc deactivation induces rapid regression associated with vascular degeneration and beta cell apoptosis. Our data indicate that highly complex neoplastic lesions can be both induced and maintained in vivo by a simple combination of two interlocking molecular lesions.

Pubmed ID: 12015982


  • Pelengaris S
  • Khan M
  • Evan GI



Publication Data

May 3, 2002

Associated Grants


Mesh Terms

  • 3T3 Cells
  • Animals
  • Apoptosis
  • Cadherins
  • Cell Division
  • Cell Line
  • Cell Nucleus
  • Estrogen Antagonists
  • Genes, myc
  • Humans
  • Insulinoma
  • Islets of Langerhans
  • Mice
  • Mice, Inbred Strains
  • Mice, Transgenic
  • Mutation
  • Pancreatic Neoplasms
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • Receptors, Estrogen
  • Tamoxifen
  • bcl-X Protein