Modeling myeloid leukemia tumor suppressor gene inactivation in the mouse

Kevin M. Shannon, Michelle M. Le Beau, David A. Largaespada, Nigel Killeen

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Introducing dominant oncogenic alterations uncovered in human myeloid malignancies into the mouse germline provides a powerful approach for studying leukemogenesis. However, little is known about how gene inactivation contributes to the development of myeloid malignancies. We describe how Nf1 mutant mice provide one example in which disrupting a tumor suppressor gene has been used to generate an informative murine leukemia model. We also discuss how chromosome engineering technologies are being harnessed to model the segmental deletions found in myeloid malignancies, and how these approaches can be combined with retrovirally medicated insertional mutagenesis to generate new models and for gene discovery.

Original languageEnglish (US)
Pages (from-to)191-199
Number of pages9
JournalSeminars in Cancer Biology
Issue number3
StatePublished - 2001

Bibliographical note

Funding Information:
The work in our laboratories described in this article was supported, in part, by NIH grants U01 CA84221, PO1 CA40046, and RO1 CA72614. We are indebted to our collaborators Tyler Jacks and Wade Clapp for advice and assistance in the studies of Nf1 mutant mice, and to Allan Bradley for providing reagents for the chromosomal engineering studies. Due to space constraints, the literature cited represents only a fraction of the original research in some of the areas discussed and emphasizes review articles.


  • Chromosome engineering
  • Mouse models
  • Myeloid leukemia
  • Nuerofibromatosis
  • Tumor suppressor genes


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