Michael A. Dyer, Ph.D.

Michael A. Dyer, Ph.D.

Associate Member
Department of Developmental Neurobiology
St. Jude Children's Research Hospital

Affiliated Professor
Department of Anatomy and Neurobiology


St. Jude Children's Research Hospital
DTRC Room D2025C
332 N. Lauderdale
Memphis, TN 38105
Tel: (901) 495-2257
Fax: (901) 495-3143
Email: Michael A. Dyer



Education

  • Ph.D. Institution: Harvard University, Cambridge, Massachusetts

Links

St. Jude Faculty - Michael A. Dyer

Research Interests

My laboratory studies the regulation of growth during neural development and disease. Cell division must be carefully regulated during brain development to ensure that the resulting tissue is the appropriate size and contains the correct proportion of each specialized cell type. If the precise balance of cell types were altered in the brain, then the different neurons and glia would not be able to work together to process information. Many of the genes that control growth during development are also involved in regulating cell division following brain injury or in certain degenerative processes. In addition, these genes are often mutated in cancer cells. Therefore, by studying the regulation of growth during development, we can learn about the cause and progression of a variety of diseases in the central nervous system. This may ultimately lead to the design of better treatments for neural injury, degeneration and cancer.

The retina is a specialized region of the central nervous system that receives and processes visual information. Like the rest of the central nervous system, injury, degeneration and cancer involve changes in the growth properties of retinal cells. We use a wide range of experimental approaches to study how cell division is controlled during retinal development and disease. Methods currently being used in the lab include genetically engineered mice, replication incompetent retroviral vectors suitable for in vivo studies, explant culture systems, microarray hybridization, and to extended our observations to human retinopathies we use normal and diseased human tissue and monkey samples. Experimental approaches that are under development include retinal physiology (ERG), electron microscopy, cell sorting, in vivo mouse models of retinoblastoma, and computational modeling of proliferation during development.

Representative Publications

  • Chen X, Pappo A, Dyer MA. Pediatric solid tumor genomics and developmental pliancy. Oncogene. 2015 Feb 2. doi: 10.1038/onc.2014.474. [Epub ahead of print] Review. PubMed PMID: 25639868.
  • Benavente CA, Dyer MA. Genetically engineered mouse and orthotopic human tumor xenograft models of retinoblastoma. Methods Mol Biol. 2015;1267:307-17. doi: 10.1007/978-1-4939-2297-0_15. PubMed PMID: 25636476.
  • Benavente CA, Dyer MA. Genetics and epigenetics of human retinoblastoma. Annu Rev Pathol. 2015 Jan 24;10:547-62. doi: 10.1146/annurev-pathol-012414-040259. PubMed PMID: 25621664.
  • Stewart E, Goshorn R, Bradley C, Griffiths LM, Benavente C, Twarog NR, Miller GM, Caufield W, Freeman BB 3rd, Bahrami A, Pappo A, Wu J, Loh A, Karlström Ã…, Calabrese C, Gordon B, Tsurkan L, Hatfield MJ, Potter PM, Snyder SE, Thiagarajan S, Shirinifard A, Sablauer A, Shelat AA, Dyer MA. Targeting the DNA repair pathway in Ewing sarcoma. Cell Rep. 2014 Nov 6;9(3):829-41. doi: 10.1016/j.celrep.2014.09.028. Epub 2014 Oct 23. PubMed PMID: 25437539.
  • Benavente CA, Finkelstein D, Johnson DA, Marine JC, Ashery-Padan R, Dyer MA. Chromatin remodelers HELLS and UHRF1 mediate the epigenetic deregulation of genes that drive retinoblastoma tumor progression. Oncotarget. 2014 Oct 30;5(20):9594-608. PubMed PMID: 25338120; PubMed Central PMCID: PMC4259422.
  • Miles WO, Korenjak M, Griffiths LM, Dyer MA, Provero P, Dyson NJ. Post-transcriptional gene expression control by NANOS is up-regulated and functionally important in pRb-deficient cells. EMBO J. 2014 Oct 1;33(19):2201-15. doi: 10.15252/embj.201488057. Epub 2014 Aug 6. PubMed PMID: 25100735; PubMed Central PMCID: PMC4282507.

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