Partners MS Center
Simon N. Willis, Ph.D

Fellow in Neurology

Center for Neurologic Diseases
Brigham and Women's Hospital
Harvard Medical School, NRB641
77 Avenue Louis Pasteur
Boston, MA 02115

Tel: (617) 525-5330
Fax: (617) 525-5333

Email:snwillis@partners.org

__________________________________________________________________________

Education

  • 1996-1999 Bachelor of Science, The University of Melbourne (Honours) Major: Biochemistry
  • 2001-2005  Doctor of Philosophy, The Walter and Eliza Hall Institute of Medical Research at The University of Melbourne

Postdoctoral Training:

  • 2005-2006 The Walter and Eliza Hall Institute of Medical Research at The University of Melbourne
  • 2006- Harvard Medical School, Boston, MA

Research interests:

  • Cancer Research/Apoptosis
  • Autoimmune disease/Multiple Sclerosis

Publications:

  1. Willis SN, Hutchins A, Hammet F, Ciciulla J, Soo W, White D, van der Spek P, Henderson MA, Gish K, Venter DJ, Armes JE. Detailed gene copy number and RNA expression analysis of the 17q12-23 region in primary breast cancers. Genes Chromosomes and Cancer 2003; 36: 382-92.
  2. Willis SN, Day CL, Hinds MG, Huang DCS. The Bcl-2-regulated apoptotic pathway. Journal of Cell Science 2003; 116: 4053-6.
  3. Chen L†, Willis SN†, Wei A†, Smith BJ, Fletcher JI, Hinds MG, Colman PM, Day CL, Adams JM and Huang DCS. Differential targeting of pro-survival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. Molecular Cell 2005; 17: 393-403. †Co-first author
  4. Willis SN, Chen L, Dewson G, Wei A, Naik E, Fletcher JI, Adams JM, Huang DCS. Pro-apoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. Genes and Development 2005; 19: 1294-1305.
  5. Willis SN, Adams JM. Life in the balance: how BH3-only proteins induce apoptosis. Current Opinion in Cell Biology 2005; 6: 617-625.
  6. Huntington ND, Xu Y, Puthalakath H, Light A, Willis SN, Strasser A, Tarlinton DM. CD45 links the B cell receptor with cell survival and is required for the persistence of germinal centers. Nature Immunology 2006;7: 190-198.
  7. Adams JM, Huang DC, Strasser A, Willis SN, Chen L, Wei A, van Delft M, Fletcher JI, Puthalakath H, Kuroda J, Michalak EM, Kelly PN, Bouillet P, Villunger A, O'Reilly L, Bath ML, Smith DP, Egle A, Harris AW, Hinds M, Colman P, Cory S. Subversion of the Bcl-2 life/death switch in cancer development and therapy. Cold Spring Harbor Symposium on Quantitative Biology. 2005; 70:469-77.
  8. van Delft MF, Wei AH, Mason KD, Vandenberg CJ, Chen L, Czabotar PE, Willis SN, Scott CL, Day CL, Cory S, Adams JM, Roberts AW, Huang DC. The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized. Cancer Cell. 2006; 10(5): 389-99.
  9. Willis SN, Fletcher JI, Kaufmann T, van Delft MF, Chen L, Czabotar PE, Ierino H, Lee EF, Fairlie WD, Bouillet P, Strasser A, Kluck RM, Adams JM, Huang DC. Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak. Science. 2007; 315(5813): 856-9.
  10. Huntington ND, Puthalakath H, Gunn P, Naik E, Michalak EM, Smyth MJ, Tabarias H, Degli-Esposti MA, Dewson G, Willis SN, Motoyama N, Huang DC, Nutt SL, Tarlinton DM, Strasser A. Interleukin 15-mediated survival of natural killer cells is determined by interactions among Bim, Noxa and Mcl-1. Nat Immunol. 2007 Aug;8(8):856-63.

Patents

  1. Huang DCS, Colman PM, Day CL, Adams JM, Willis SN, Wei A, Smith B, Hinds MG. Therapeutic molecules and methods for generating and/or selecting same (PCT/AU05/0000140).
  2. Huang DCS, Adams JM, Willis SN, Chen L, Wei A. Apoptosis induction by interruption of Bak-Mcl-1/Bcl-xL interaction (provisional).


 
 
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