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

Associate Professor

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

  • 314 286-0032

  • 314 286-2893

  • 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:

The Magee lab is working to answer several important questions that surround the causes of childhood leukemia. How do childhood leukemias arise from normal blood forming stem cells? How do leukemia cells hijack normal stem cell programs? Why do childhood and adult leukemias have different mutations? Can we identify and target vulnerabilities that are unique to childhood leukemia? To address these questions, we have created new pediatric leukemia models in mice. We have identified normal developmental switches that contribute to childhood leukemia formation, and we are now studying how to modify these switches to prevent leukemia. Furthermore, we have identified mechanisms that cause some children develop leukemia after they receive chemotherapy for an unrelated malignancy, such as a lymphoma or a neuroblastoma. Our studies will ultimately lead to new methods to treat and even prevent childhood leukemia.

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:

1. Li Y, Kong W, Yang W, Patel RM, Casey EB, Okeyo-Owuor T, White JM, Porter SN, Morris SA, Magee JA. Single-cell analysis of neonatal HSC ontogeny reveals gradual and uncoordinated transcriptional reprogramming that begins before birth Cell Stem Cell. 2020. PMID:32822583 DOI: 10.1016/j.stem.2020.08.001

2. Okeyo-Owuor T, Patel RM, Li Y, Yang W, Casey EB, Cluster AS, Porter SN, Bryder D, Magee JA. The efficiency of murine MLL-ENL driven leukemia initiation changes with age and peaks during neonatal development. Blood Advances. 2019. 3:2388-2399. PMID: 31405949 PMCID: PMC6693010 DOI: 10.1182/bloodadvances.2019000554

3. Porter SN, Cluster AS, Yang W, Busken KA, Patel RM, Ryoo J, Magee JA. Fetal and neonatal hematopoietic progenitors are functionally and transcriptionally resistant to Flt3-ITD mutations. eLife. 2016. 5:e18882. PMID: 27879203 PMCID: PMC5153248 DOI: 10.7554/eLife.18882

4. 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 PMCID: PMC6731097 DOI: 10.1016/j.exphem.2017.05.006

5. 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 PMCID: PMC4911494 DOI: 10.1016/j.stemcr.2016.04.008

Last Updated: 9/10/2020 2:11:19 PM

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