Michael A. Dyer, Ph.D.
Department of Developmental Neurobiology
St. Jude Children's Research Hospital
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
- Ph.D. Institution: Harvard University, Cambridge, Massachusetts
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.
- 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 Sep 26. pii: 2468. [Epub ahead of print] PubMed PMID: 25338120.
- 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 Aug 6. pii: e201488057. [Epub ahead of print] PubMed PMID: 25100735.
- Dyer MA, Arvold ND, Chen YH, Pinnell NE, Mitin T, Lee EQ, Hodi FS, Ibrahim N, Weiss SE, Kelly PJ, Floyd SR, Mahadevan A, Alexander BM. The role of whole brain radiation therapy in the management of melanoma brain metastases. Radiat Oncol. 2014 Jun 22;9:143. doi: 10.1186/1748-717X-9-143. PubMed PMID: 24954062; PubMed Central PMCID: PMC4132230.
- Pritchard EM, Stewart E, Zhu F, Bradley C, Griffiths L, Yang L, Suryadevara PK, Zhang J, Freeman BB 3rd, Guy RK, Dyer MA. Pharmacokinetics and Efficacy of the Spleen Tyrosine Kinase Inhibitor R406 after Ocular Delivery for Retinoblastoma. Pharm Res. 2014 Jun 7. [Epub ahead of print] PubMed PMID: 24906597.
- Valle-GarcĂa D, Griffiths LM, Dyer MA, Bernstein E, Recillas-Targa F. The ATRX cDNA is prone to bacterial IS10 element insertions that alter its structure. Springerplus. 2014 May 2;3:222. doi: 10.1186/2193-1801-3-222. eCollection 2014. PubMed PMID: 24834375; PubMed Central PMCID: PMC4021028.
- Chen X, Bahrami A, Pappo A, Easton J, Dalton J, Hedlund E, Ellison D, Shurtleff S, Wu G, Wei L, Parker M, Rusch M, Nagahawatte P, Wu J, Mao S, Boggs K, Mulder H, Yergeau D, Lu C, Ding L, Edmonson M, Qu C, Wang J, Li Y, Navid F, Daw NC, Mardis ER, Wilson RK, Downing JR, Zhang J, Dyer MA; St. Jude Childrenâ€™s Research Hospitalâ€“Washington University Pediatric Cancer Genome Project. Recurrent somatic structural variations contribute to tumorigenesis in pediatric osteosarcoma. Cell Rep. 2014 Apr 10;7(1):104-12. doi: 10.1016/j.celrep.2014.03.003. Epub 2014 Apr 3. PubMed PMID: 24703847; PubMed Central PMCID: PMC4096827.