Jeffrey Magee, M.D., Ph.D.

Assistant Professor

Developmental, Regenerative and Stem Cell Biology Program
Molecular Genetics and Genomics Program
Molecular Cell Biology Program

  • 314 286-0032

  • 314 286-2893

  • 8208

  • 4304 MPRB (4th floor in the office suites)



  • Cancer biology, stem cell, hematopoiesis, leukemia, developmental biology

  • Developmental context and genetic variation as underlying mechanisms of childhood cancer

Research Abstract:

We are interested in understanding why children get cancer. Childhood cancers are different from adult cancers - they are not caused by mutations accumulated over decades of time. They are usually not associated with environmental exposures (e.g. smoking), chronic inflammation or Mendelian syndromes. Yet they are the most common cause of death due to disease among children in developed countries. This suggests that normal mechanisms of development may contribute to the process of transformation, as might non-Mendelian genetic predispositions.

We are using mouse models of leukemia to understand how developmental programs in the blood system can influence the effects of mutations. For example, we are using single cell RNA-sequencing to understand how transcriptional programs change with age in developing hematopoietic stem cells. Furthermore, we are characterizing the epigenetic programs that guide these transcriptional changes, and that shape the response to specific mutations. All of our models focus on mutations found in human patients, and our goal is to relate our findings to critical, targetable pathways in human leukemias (i.e. bedside to bench to bedside).

Trainees in the Magee lab will gain experience in mouse models of human blood cancers, hematopoietic stem cell biology, developmental biology, genomics and translational research.

Selected Publications:

Porter SN and Magee JA. PRKCH regulates hematopoietic stem cell function and predicts poor prognosis in acute myeloid leukemia. Experimental Hematology. 2017. 53:43-47. PMID: 28596089

Porter SN, Cluster AS, Yang W, Busken KA, Patel RM, Ryoo JA, Magee JA. Fetal and neonatal hematopoietic progenitors are functionally and transcriptionally resistant to Flt3-ITD mutations. eLife. 2016. 5:e18882. PMID: 27879203

Porter SN, Cluster AS, Singer RAJ, Voigtmann J, Monlish DA, Schuettpelz LG, Magee JA. Pten cell autonomously modulates the HSC response to inflammatory cytokines. Stem Cell Reports. 2016. 6:806-814. PMID: 27185281

Kraus M, Dolinski B, Rosahl TW, Magee JA. Protein kinase N3 deficiency impedes PI3-Kinase pathway driven leukemogenesis without affecting normal hematopoiesis. Leukemia. 2015. 29:255-258. PMID: 25234167

Magee JA. Comment on: Genomics of primary chemoresistance and remission induction failure in pediatric and adult acute myeloid leukemia. British Journal of Haematology. 2017. 176:5 PMID: 27766614

Magee JA. Sleepwalking stem cells. Blood. 2017. 129:1887-1888. PMID: 28385766

Last Updated: 7/18/2018 4:08:35 PM

Changes in normal developmental programs determine whether mutations, in this case FLT3-ITD, are able to initiate leukemia development
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