The focus of Dr. Donald (Will) Parsons’ research has been the development of large-scale (genomic) methods to identify and evaluate cancer-causing mutations in human tumors, with a goal of rapidly identifying genetic alterations which may serve as targets for new diagnostic tests and treatments. His work has resulted in the identification of numerous mutated genes and genetic pathways that contribute to tumor initiation and progression, providing a novel view of the genetic landscape of human cancers.
For example, an analysis of glioblastoma multiforme (GBM), the most lethal brain tumor of both adults and children, for the first time identified mutation of the isocitrate dehydrogenase genes (IDH1 and IDH2) as a common and critical event in the development of gliomas. This discovery has opened a novel and potentially clinically-useful area of brain tumor research: further work evaluating the functional relation of these mutations to glioma development and the applicability of this finding for diagnostic and therapeutic purposes is ongoing.
Dr. Will Parsons is currently engaged in similar genomic analyses of several other pediatric solid tumors, with a focus on pediatric central nervous system cancers, his area of clinical interest.
Donald W. (Will) Parsons, MD, PhD
Enrique L. Ramos
Parsons DW, Jones S et al. An integrated genomic analysis of human glioblastoma multiforme. Science 2008; 321: 1807-12. PubMed PMID: 18772396.
Yan H, Parsons DW et al. IDH1 and IDH2 mutations in gliomas. New Eng J Med 2009; 360: 765-73. PubMed PMID: 19228619.
Parsons DW, Li M, Zhang X et al. The Genetic Landscape of the Childhood Cancer Medulloblastoma. Science 2011; 331(6016):435-9. PubMed PMID: 21163964.
Parsons DW, Roy A, Plon SE et al. Clinical tumor sequencing: An incidental casualty of the American College of Medical Genetics and Genomics recommendations for reporting of incidental findings. J Clin Oncol 2014; Jun 23. [Epub] PubMed PMID: 24958819.
Chakraborty R, Hampton OA, Shen X et al. Mutually exclusive recurrent somatic mutations in MAP2K1 and BRAF support a central role for ERK activation in LCH pathogenesis. Blood 2014 Sep 8. pii: blood-2014-05-577825. [Epub] PubMed PMID: 25202140.
Scollon S, Bergstrom K, Kerstein RA et al. Obtaining informed consent for clinical tumor and germline exome sequencing of newly diagnosed childhood cancer patients. Genome Med 2014; in press.