Postdoctoral scientists nanotechnology

October 25, 2007

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Nanoparticles have recently been introduced as a novel therapeutic approach to deliver siRNAs or small-molecule inhibitors for the treatment of cancer. Nanoparticles can be specifically targeted to tumor cells by coating them with antibodies that recognize surface antigens expressed on the target cells. The Leukemia Research Program at Childrens Hospital Los Angeles has initiated the development of nanoparticles that are coated with an anti-CD19 antibody to target CD19+ B cell lineage tumor cells in childhood leukemia. The nanoparticles carry siRNAs that are directed against oncogenic fusion molecules that drive malignant transformation of the leukemia but are not present in normal B cells.

Applications from motivated postdoctoral scientists with a strong background in basic science and interest in clinical translation are invited. The position is available immediately. Applications should be sent by E-mail in PDF format and include a personal statement of research and career goals, a CV and publication list and the coordinates of three references. Inquiries and applications (PDF format only) should be sent by November 15th to Prof. Markus Muschen, Director, Leukemia Research Program, Childrens Hospital Los Angeles at: mmuschen@chla.usc.edu

More Information:http://www.usc.edu/programs/pibbs/site/faculty/muschen_m.htm http://www.lymphocytes.deRecent publications from the laboratory:1. Klein F, Feldhahn N, Harder L, Wang H, Wartenberg M, Hofmann WK, Wernet P, Siebert R, Müschen M. The BCR-ABL1 kinase bypasses selection for the expression of a pre-B cell receptor in pre-B acute lymphoblastic leukemia cells. J Exp Med 199:673-685, 2004.2. Klein F, Feldhahn N, Mooster JL, Sprangers M, Hofmann WK, Wernet P, Wartenberg M, Müschen M. Tracing the pre-B to immature B cell transition in human leukemia cells reveals a coordinated sequence of primary and secondary IGK gene rearrangement, IGK deletion, and IGL gene rearrangement. J Immunol 174:367-375, 2005.3. Feldhahn N, Klein F, Mooster JL, Hadweh P, Sprangers M, Wartenberg M, Bekhite MM, Hofmann WK, Herzog S, Jumaa H, Rowley JD, Müschen M. Mimicry of a constitutively active pre-B cell receptor in acute lymphoblastic leukemia cells. J Exp Med 201:1837-1852, 2005.4. Feldhahn N, Rio P, Soh BN, Liedtke S, Sprangers M, Klein F, Wernet P, Jumaa H, Hofmann WK, Hanenberg H, Rowley JD, Müschen M. Deficiency of Bruton’s tyrosine kinase in B cell precursor leukemia cells. Proc Natl Acad Sci USA 102:13266-13271, 2005.5. Klein F, Feldhahn N, Herzog S, Sprangers M, Mooster JL, Jumaa H, Müschen M. BCR-ABL1 induces aberrant splicing of IKAROS and lineage infidelity in pre-B lymphoblastic leukemia cells. Oncogene 25:1118-1124, 2006.6. Sprangers M, Feldhahn N, Herzog S, Hansmann ML, Reppel M, Hescheler J, Jumaa H, Siebert R, Müschen M. The SRC family kinase LYN redirects B cell receptor signaling in human SLP65-deficient B cell lymphoma cells. Oncogene 25:5056-5062, 2006.7. Sprangers M, Feldhahn N, Liedtke S, Jumaa H, Siebert R, Müschen M. SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells. Oncogene 25:5180-5186, 2006.8. Feldhahn N, Henke N, Melchior K, Duy C, Soh BN, Klein F, von Levetzow G, Giebel B, Li A, Hofmann WK, Jumaa H, Müschen M. Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1-transformed acute lymphoblastic leukemia cells. J Exp Med 204:1157-1166, 2007.9. Meixlsperger S, Kohler F, Wossning T, Reppel M, Müschen M, Jumaa H. Conventional light chains inhibit the autonomous signaling capacity of the B cell receptor. Immunity 26:323-333, 2007
Prof. Dr. Markus Müschenmmuschen@chla.usc.eduUniversity of Southern CaliforniaLos Angeles, CAAnsprechpartner: mmuschen@chla.usc.edu

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