Consequences of widespread deregulation of the c-myc gene in transgenic mice: multiple neoplasms and normal development

Cell. 1986 May 23;45(4):485-95. doi: 10.1016/0092-8674(86)90280-1.


We have constructed a transgenic mouse strain in which a mammary tumor virus LTR/c-myc fusion gene is anomalously expressed in a wide variety of tissues. The deregulated c-myc transgene, now glucocorticoid inducible, contributes to an increased incidence of a variety of tumors, including those of testicular, breast, lymphocytic (B cell and T cell), and mast cell origin. The deregulated gene does not, however, otherwise disturb cell proliferation, nor does it interfere with normal development in these animals. Moreover, since not all tissues that express the transgene develop neoplasms, these results begin to define the transforming spectrum of the c-myc oncogene. They also extend to several organ systems the notion that elements in addition to an activated c-myc gene are required to induce malignancy in the living organism.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenocarcinoma / genetics
  • Animals
  • Dexamethasone / pharmacology
  • Female
  • Gene Expression Regulation* / drug effects
  • Genes, Synthetic
  • Genetic Engineering
  • Genetic Vectors
  • Lymphoma / genetics
  • Male
  • Mammary Neoplasms, Experimental / genetics
  • Mammary Tumor Virus, Mouse / genetics
  • Mast-Cell Sarcoma / genetics
  • Mice / genetics
  • Mice / growth & development
  • Neoplasms, Experimental / genetics*
  • Organ Specificity
  • Pedigree
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins c-myc
  • Proto-Oncogenes*
  • Sertoli Cell Tumor / genetics
  • Testicular Neoplasms / genetics


  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-myc
  • Dexamethasone