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Scott J. Diede
Acting Assistant Professor
Attending Physician
Associate in Clinical Research
Attending Physician
Associate in Clinical Research
Fred Hutchinson Cancer Research Center
Summary
The goal of my research is to determine the role DNA methylation plays in the formation of pediatric cancers. Pediatric cancers are fundamentally different from adult malignancies, being less genetically complex and also embryonal in nature, a characteristic that suggests a block in the normal process of differentiation may exist. As opposed to the acquisition of genetic mutations, aberrant epigenetic regulation, such as DNA methylation, may play a crucial role in this block, and provides an attractive target for novel therapies. Attempting to correct genetic mutations that drive cancer growth is a daunting task, however reversing epigenetic changes such as abnormal DNA methylation may be much more amenable to drug development. Cancer-specific DNA methylation may also provide valuable biomarkers for cancer detection, diagnosis, and risk assessment. I have a broad background in chromatin and chromosome maintenance, with specific training and expertise in molecular biology and assay development. These skills were first honed during my Ph.D. thesis work using yeast as a model organism to study telomere biology and have subsequently been developed during my work as a clinical fellow and junior faculty member studying genomic and epigenomic changes that occur in pediatric cancer. As a practicing pediatric hematologist and oncologist, I am also able to identify challenges in the clinical setting and bring these problems back into the laboratory and attempt to solve them. In summary, I have a demonstrated record of innovative research projects in the subject of cancer biology, and my expertise and experience have prepared me to translate new discoveries made in the laboratory into new treatments for children with cancer.
| Current Institution | Fred Hutchinson Cancer Research Center |
| Current School | Division of Clinical Research |
| Disciplines | |
| Current and Past Advisor(s) | Daniel E. Gottschling, Stephen J. Tapscott |
| Address | 1100 Fairview Ave N, Mailstop c3-168 Seattle Washington 98109 United States Phone: 206-667-4286 |
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Education
The University of Chicago
B.A., Chemistry
(1988 - 1992)
The University of Chicago
M.D./Ph.D
(1992 - 2003)
Seattle Children's Hospital
Internship, General Pediatrics
(2003 - 2004)
Seattle Children's Hospital
Residency, General Pediatrics
(2004 - 2005)
Seattle Children's Hospital
Fellowship, Pediatric Hematology-Oncology
(2005 - 2008)
Work Experience
Achievements
General
Publication Summary
J.D. Roback, S.J. Diede, M. Downen, H.J. Lee, J. Kwon, T.H. Large, U.Otten, and B.H. Wainer (1992). Expression of neurotrophins and the low-affinity NGF receptor in septal and hippocampal reaggregate cultures: local physiologic effects of NGF synthesized in the septal region. Developmental Brain Research 70(1), 123-133.
S.J. Diede and D.E. Gottschling (1999). Telomerase-mediated telomere addition in vivo requires DNA primase and DNA polymerases aand d. Cell 99(7), 723-733.\
M.D. DuBois, S.J. Diede, A.E. Stellwagen, and D.E. Gottschling (2000). All things must end: telomere dynamics in yeast. Cold Spring Harbor Symposium on Quantitative Biology 65, 281-296.
S.E. Peterson, A.E. Stellwagen, S.J. Diede, M.S. Singer, Z.W. Haimberger, C.O. Johnson, M. Tzoneva, and D.E. Gottschling (2001). The function of a stem-loop in telomerase RNA is linked to the DNA repair protein Ku. Nature Genetics 27(1), 64-67.
S.J. Diede and D.E. Gottschling (2001). Exonuclease activity is required for sequence addition and Cdc13p loading at a de novo telomere. Current Biology 11(17), 1336-1340.
J.R. Tenlen, J.A. Schisa, S.J. Diede, and B.D. Page (2006). Reduced dosage of pos-1 suppresses Mex mutants and reveals complex interactions among CCCH zinc-finger proteins during Caenorhabditis elegans embryogenesis. Genetics 174(4), 1933-1945.
B.D. Page, S.J. Diede, J.R. Tenlen, and E.L. Ferguson (2007). EEL-1, a Hect E3 ubiquitin ligase, controls asymmetry and persistence of the SKN-1 transcription factor in the C. elegans embryo. Development 134(12), 2303-2314.
M.A. Knight, D. Hernandez, S.J. Diede, H.G. Dauwerse, I. Rafferty, S.M. Forrest, R.J.M. Gardner, E. Storey, G-J. B. van Ommen, S.J. Tapscott, K.H. Fischbeck, A.B. Singleton (2008). A duplication at chromosome 11q12.2-11q12.3 is associated with spinocerebellar ataxia type 20 (SCA20). Human Molecular Genetics 17(24), 3847-3853.
Z. Yang, K.L. MacQuarrie, E. Analau, A.E. Tyler, F.J. Dilworth, Y. Cao, S.J. Diede, and S.J. Tapscott (2009). MyoD and E-protein heterodimers switch rhabdomyosarcoma cells from an arrested myoblast phase to a differentiated state. Genes & Development 23(6), 694-707.
S.J. Diede, J. Guenthoer, L.N. Geng, S.E. Mahoney, M. Marotta, J.M. Olson, H. Tanaka, and S.J. Tapscott (2010). DNA methylation of developmental genes in pediatric medulloblastomas identified by denaturation analysis of methylation differences. Proceedings of the National Academy of Sciences 107(1), 234-239.
S.J. Diede, H. Tanaka, D.A. Bergstrom, M.-C. Yao, and S.J. Tapscott (2010). Genome-wide analysis of palindrome formation. Nature Genetics 42(4), 279.
J. Guenthoer, S.J. Diede, H. Tanaka, X. Chai, L. Hsu, S.J. Tapscott, and P.L. Porter (2012). Assessment of palindromes as platforms for DNA amplification in breast cancer. Genome Research 22(2), 232-245.
S.E. Mahoney, Z. Yao, C.C. Keyes, S.J. Tapscott, and S.J. Diede (2012). Genome-wide DNA methylation studies suggest distinct DNA methylation patterns in pediatric embryonal and alveolar rhabdomyosarcomas. Epigenetics 7(4), 400-408.
K.L. MacQuarrie, Z. Yao, A.P. Fong, S.J. Diede, E.R. Rudzinski, D.S. Hawkins, and S.J.Tapscott (2013). Comparison of genome-wide binding of MyoD in normal human myogenic cells and rhabdomyosarcomas identifies regional and local suppression of pro-myogenic transcription factors. Molecular and Cellular Biology 33(4), 773-784.
Books
Other Publications
