Raúl Rabadan

Raul Rabadàn is an Associate Professor in the Department of Systems Biology and Biomedical Informatics at Columbia University. He is the director of the Center for Topology of Cancer Evolution and Heterogeneity. From 2001 to 2003, Dr. Rabadan was a fellow at the Theoretical Physics Division at CERN, the European Organization for Nuclear Research, in Geneva, Switzerland. In 2003 he joined the Physics Group of the School of Natural Sciences at the Institute for Advanced Study. During 2006-2008, Dr. Rabadan was the Martin A. and Helen Chooljian Member at The Simons Center for Systems Biology at the Institute for Advanced Study in Princeton, New Jersey. He has been named one of Popular Science's Brilliant 10 (2010), a Stewart Trust Fellow (2013), and he received the Harold and Golden Lamport Award at Columbia University (2014). At Columbia, he has put together a highly interdisciplinary lab with researchers from the fields of mathematics, physics, computer science, engineering, and medicine, with the common goal of solving pressing biomedical problems through quantitative computational models. Dr. Rabadan’s current interest focuses on uncovering patterns of evolution in biological systems—in particular, RNA viruses and cancer.

Career

Dr. Rabadan is an expert on string theory phenomenology, specifically the physics of intersecting D-brane configurations. In his more recent research in physics he has studied the information paradox of black holes in the context of the Anti-de Sitter/Conformal Field Theory duality, and has proposed several experiments to search for axions. In the last 10 years he has focused his research program on theoretical and computational problems in biology.

Dr. Rabadan scientific interests lie in modeling and understanding the dynamics of biological systems through the lens of genomics. He has focused his research on the evolution of two of such biological systems: cancer and infectious diseases. In particular, he has been working in the identification of driver mechanisms of evolutionary processes, characterize key process dynamics and elucidate epistasic interactions. Dr. Rabadan is interested in understanding the evolution of infectious agents through the analysis of their genome, in particular influenza viruses including elucidating the origin of the influenza A virus subtype H1N1.[1][2] Dr. Rabadan's work in cancer genetics has led to the identification of driver alterations in hairy cell leukemia,[3] diffuse large B-cell lymphoma,[4][5] T-cell acute lymphoblastic leukemia,[6][7] chronic lymphocytic leukemia,[8][9][10] splenic marginal zone lymphoma[11] and glioblastoma multiforme;[12][13] and to the identification of recurrent alterations, which lead to therapy resistance, using longitudinal data in T-cell acute lymphoblastic leukemia7. Recently, he has been working on the application of topological data analysis to large scale genomic data.[14][15]

Dr. Rabadan’s scientific work has led to more than 100 peer-reviewed scientific publications, including in high impact factor journals (New England Journal of Medicine, Nature, Science, Nature Genetics, Nature Medicine, Cell, among others). Several of his results have been featured by the international press, including CNN, the New York Times, the Wall Street Journal, the Associated Press, Reuters International, and The Economist.

References

  1. ↑ Trifonov, V., Khiabanian, H., Greenbaum, B. & Rabadan, R. The origin of the recent swine influenza A(H1N1) virus infecting humans. Euro Surveill 14 (2009).
  2. ↑ Trifonov, V., Khiabanian, H. & Rabadan, R. Geographic dependence, surveillance, and origins of the 2009 influenza A (H1N1) virus. N Engl J Med 361, 115-119, doi:10.1056/NEJMp0904572 (2009).
  3. ↑ Tiacci, E. et al. BRAF mutations in hairy-cell leukemia. New Engl J Med 364, 2305-2315, doi:10.1056/NEJMoa1014209 (2011).
  4. ↑ Pasqualucci, L. et al. Inactivating mutations of acetyltransferase genes in B-cell lymphoma. Nature 471, 189-195, doi:10.1038/nature09730 (2011).
  5. ↑ Pasqualucci, L. et al. Analysis of the coding genome of diffuse large B-cell lymphoma. Nat Genet 43, 830-837, doi:10.1038/ng.892 (2011).
  6. ↑ Van Vlierberghe, P. et al. PHF6 mutations in T-cell acute lymphoblastic leukemia. Nat Genet 42, 338-342, doi:10.1038/ng.542 (2010).
  7. ↑ Tzoneva, G. et al. Activating mutations in the NT5C2 nucleotidase gene drive chemotherapy resistance in relapsed ALL. Nat Med 19, 368-371, doi:10.1038/nm.3078 (2013).
  8. ↑ Rossi, D. et al. Mutations of NOTCH1 are an independent predictor of survival in chronic lymphocytic leukemia. Blood 119, 521-529, doi:10.1182/blood-2011-09-379966 (2012).
  9. ↑ Rossi, D. et al. Integrated mutational and cytogenetic analysis identifies new prognostic subgroups in chronic lymphocytic leukemia. Blood 121, 1403-1412, doi:10.1182/blood-2012-09-458265 (2013).
  10. ↑ Rossi, D. et al. Mutations of the SF3B1 splicing factor in chronic lymphocytic leukemia: association with progression and fludarabine-refractoriness. Blood 118, 6904-6908, doi:10.1182/blood-2011-08-373159 (2011).
  11. ↑ Rossi, D. et al. The coding genome of splenic marginal zone lymphoma:activation of NOTCH2 and other pathways regulating marginal zone development. J Exp Med 209, 1537-1551, doi:10.1084/jem.20120904 (2012).
  12. ↑ Singh, D. et al. Transforming Fusions of FGFR and TACC Genes in Human Glioblastoma. Science, doi:10.1126/science.1220834 (2012).
  13. ↑ Singh, D. et al. Transforming fusions of FGFR and TACC genes in human glioblastoma. Science 337, 1231-1235, doi:10.1126/science.1220834 (2012).
  14. ↑ Chan, J. M., Carlsson, G. & Rabadan, R. Topology of viral evolution. Proc Natl Acad Sci U S A 110, 18566-18571, doi:10.1073/pnas.1313480110 (2013).
  15. ↑ K. Emmett, R. R. Characterizing Scales of Genetic Recombination and Antibiotic Resistance in Pathogenic Bacteria Using Topological Data Analysis. Lecture Notes in Computer Science (LNCS) (2014).

External links

To be distinguished from a blues guitar player, from Barcelona (1979), also called T-Bonski.
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