Jon Larson

E-mail: lars0327@umn.edu

Thesis Advisor: David Largaespada

Year entered: 2005

Degrees received:
B.S., Genetics and Cell Biology, University of Minnesota, Minneapolis, MN 1999

Honors and awards:

• The Arnold and Mabel Beckman Center for Transposon Research Travel Award Spring 2008
  
• MICaB Student Travel Award Fall 2008
  
• University of Minnesota Brain Tumor Program Travel Award 2008
  
• Select Poster Presentation,13th Annual Society for Neuro-Oncology Scientific Meeting 2008
  
• MICaB Golden Pipetman Award Spring 2009
• MICaB student representative 2008-2009
  

Thesis research:
Over 40,000 primary brain tumors are diagnosed and more than 10,000 brain tumor patients die each year in the United States. These tumors affect people of all ages and are categorized by their location and cell type. Gliomas are glial cell tumors common in adults, while primitive neuroectodermal tumors (PNET) are common in children and include medulloblastoma and supratentorial PNET subtypes. Current understanding of the heterogeneous genetic basis for these tumors has provided insight into their histogenesis and pathology. However, this knowledge is incomplete as distinct molecules and signaling pathways provide variable levels of disease risk and severity. To address this, I am using brain-specific Sleeping Beauty (SB) transposon-mediated insertional mutagenesis in mice. This forward genetics method directs the identification and characterization of novel genetic mutations required for tumor formation. The mutagenic transposon vector T2/Onc is capable of activating oncogenes or silencing tumor suppressor genes upon transposase-mediated mobilization and genomic re-integration within or near such genes. T2/Onc integration sites are subsequently identified by transposon-specific sequences and common integration sites throughout the genome of multiple tumors identify candidate cancer genes with altered expression. I am also using SB transposon-mediated transgenesis in the neonatal mouse brain to mimic tumor formation in vivo and further characterize candidate brain cancer genes. The SB system is, therefore, a comprehensive genetic method to better understand the genetic causes of glioma and PNET development.

Publications:

• Wiesner, S.M.*, Decker, S.A.*, Larson, J.D., Ericson, K., Forster, C., Gallardo, J., Long, C., Demorest, Z.L., Zamora, E.A., Low, W.C., SanataCruz, K., Largaespada, D.A., Ohlfest, J.R. 2009. De novo induction of genetically engineered brain tumors in mice using plasmid DNA. Cancer Research 69(2):431-439. *Co-first authors

• M.E. Robu, J.D. Larson,A. Nasevicius, S. Beiraghi, C. Brenner, S. A. Farber and S.C. Ekker. 2007. p53 activation by knockdown technologies. PLOS Genetics 3(5):e78
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