Predisposition to lymphomagenesis in pim-1 transgenic mice: cooperation with c-myc and N-myc in murine leukemia virus-induced tumors

Cell. 1989 Feb 24;56(4):673-82. doi: 10.1016/0092-8674(89)90589-8.


Transgenic mice bearing the pim-1 gene supplemented with an upstream immunoglobulin enhancer and a downstream murine leukemia virus long terminal repeat express pim-1 mRNA at high levels in both B and T cells. Between 5% and 10% of the pim-1 transgenic mice develop clonal T cell lymphomas before 7 months of age, whereas none of the age-matched control mice do, providing direct evidence for the oncogenic potential of pim-1. Histological examination and FACS analysis revealed no abnormalities in hematopoietic tissues of disease-free pim-1 transgenic mice. When newborn pim-1 transgenic mice are infected with MuLV, T cell lymphomas develop much faster (latency 7-8 weeks) than in nontransgenic mice (latency 22 weeks). In all these T cell lymphomas either c-myc or N-myc was activated by proviral insertion, suggesting strong cooperation between pim-1 and myc in lymphomagenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Cell Transformation, Viral*
  • Gene Expression Regulation
  • Hematopoietic Stem Cells / physiology
  • Leukemia Virus, Murine / genetics
  • Lymphoma, Non-Hodgkin / genetics*
  • Mice
  • Mice, Transgenic
  • Protein Serine-Threonine Kinases*
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-myc
  • Proto-Oncogene Proteins c-pim-1
  • T-Lymphocytes / physiology


  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-myc
  • Pim1 protein, mouse
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-pim-1