Robert A. Johnson, PhD

Robert A. Johnson, PhD is a principal investigator at The Research Institute at Nationwide Children’s Hospital and an Assistant Professor of Pediatrics at The Ohio State University College of Medicine. The primary focus of the Johnson laboratory is the development of novel therapies for the treatment of ependymoma, the third most common pediatric brain tumor, by identifying and targeting the genetic changes responsible for the formation of the disease.

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Gender:

• Male

Languages Spoken:

• English

Research Center:

• Center for Childhood Cancer and Blood Diseases

Areas of Interest:

• Ependymoma is the third most common pediatric brain tumor (supratentorial (ST) and posterior fossa (PF)) and the most common adult spinal tumor (SP). Surgery and irradiation are the predominant treatments since chemotherapy is ineffective in most patients; consequently, ependymoma is incurable in up to 40% of cases. Ependymomas from different regions of the CNS display disparate prognoses, transcriptional profiles and genetic alterations, suggesting they represent distinct molecular disease subgroups. This heterogeneity confounds efforts to study, model and treat these tumors. My previous project described a novel interspecies genomic approach that meticulously matched subgroup specific driver mutations, Ephb2 overexpression, with the appropriate cell of origin, embryonic neural stem cells (NSC), to model human ependymoma subgroups (Nature. 2010 Jul 29;466(7306):632-6). Building upon these studies, my laboratory is elucidating the mechanism by which Ephb2 transforms cerebral NSCs. Using a combination of stem cell culture assays and a mouse intracranial implantation model system we are dissecting the molecular pathways involved in disease development. This is a critical next step in understanding the biology and treatment of ependymoma. Consequently, we are undertaking a series of studies that will test the central hypothesis: ‘key components of the Ephb2 signaling system play a critical role in the transformation of cerebral NSCs into ependymoma’. We are testing this hypothesis by addressing two key questions: 1. Which Ephb2 domains are required for transformation? 2. What is the role of forward and reverse signaling in transformation? In order to answer these questions we are taking advantage of established Ephb2 point mutations as well as domain deletion constructs and evaluating their effects on NSC transformation using our stem cell culture and intracranial implant systems.

Undergraduate School

• The Johns Hopkins University, Department of Biology
  Date Completed: 06/30/1992

Graduate School

• New York University, Department of Biology
  Date Completed: 06/30/1995

Post Doctoral

• Weill Graduate School of Medical Science of Cornell University
  Date Completed: 06/30/2001

2010–present

• Principal Investigator, Center for Childhood Cancer, The Research Institute at Nationwide Children's Hospital, Columbus, OH

2006–2010

• Postdoctoral Fellow Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN

2005–2006

• Postdoctoral Fellow Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN

2004–2005

• Postdoctoral Fellow Department of Pharmacology, Cancer Institute of New Jersey, New Brunswick, NJ

2002–2004

• Postdoctoral Fellow Department of Pharmacology, Fox Chase Cancer Center, Philadelphia, PA

• Atkinson JM, Shelat AA, Carcaboso AM, Kranenburg TA, Arnold LA, Boulos N, Wright K, Johnson RA, Poppleton H, Mohankumar KM, Féau C, Phoenix T, Gibson P, Zhu L, Tong Y, Eden C, Ellison DW, Priebe W, Koul D, Yung WK, Gajjar A, Stewart CF, Guy RK, Gilbertson RJ. 2011. An integrated in vitro and in vivo high-throughput screen identifies treatment leads for ependymoma.  Cancer Cell. Vol. 20, no. 3. (September): 384-399.
• Pounds S, Gao CL, Johnson RA, Wright KD, Poppleton H, Finkelstein D, Leary SE, Gilbertson RJ. 2011. A procedure to statistically evaluate agreement of differential expression for cross-species genomics.  Bioinformatics. Vol. 27, no. 15. (August): 2098-2103.
• Johnson RA, Wright KD, Poppleton H, Mohankumar M, Finkelstein D, Pounds SB, Rand V, Leary SE, White E, Eden C, Hogg T, Northcott P, Mack S, Neale G, Wang YD, Coyle B, Atkinson J, DeWire M, Kranenburg TA, Gillespie Y, Allen JC, Merchant T, Boop FA, Sanford RA, Gajjar A, Ellison DW, Taylor MD, Grundy RG, Gilbertson RJ. 2010. Cross-species genomics matches driver mutations and cell compartments to model ependymoma.  Nature. Vol. 466, no. 7306. (July): 632-636.
• Johnson R, Wright KD, Gilbertson RJ. 2009. Molecular profiling of pediatric brain tumors: insight into biology and treatment.  Curr Oncol Rep. Vol. 11, no. 1. (January): 68-72.
• Johnson RA, Shepard EM, Scotto KW. 2005. Differential regulation of MDR1 transcription by the p53 family members. Role of the DNA binding domain.  J Biol Chem. Vol. 280, no. 14. (April): 13213-13219.
• Johnson RA, Ince TA, Scotto KW. 2001. Transcriptional repression by p53 through direct binding to a novel DNA element.  J Biol Chem. Vol. 276, no. 29. (July): 27716-27720.
• Scotto KW, Johnson RA. 2001. Transcription of the multidrug resistance gene MDR1: a therapeutic agent.  Mol Interv.. Vol. 1, no. 2. (June): 117-125.
• Stockhammer G, Manley GT, Johnson R, Rosenblum MK, Samid D, Lieberman FS. 1995. Inhibition of proliferation and induction of differentiation in medulloblastoma- and astrocytoma-derived cell lines with phenylacetate.  J Neurosurg. Vol. 83, no. 4. (October): 672-681.