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Blood, 19 March 2009, Vol. 113, No. 12, pp. 2791-2794. Prepublished online as a Blood First Edition Paper on January 23, 2009; DOI 10.1182/blood-2008-06-160713. This Article Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2008-06-160713v1 113/12/2791    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Holler, C. Articles by Egle, A. Search for Related Content PubMed PubMed Citation Articles by Holler, C. Articles by Egle, A. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 2, 2008 Accepted January 7, 2009 PKC is essential for the development of CLL in the TCL1 transgenic mouse model: Validation of PKC as a therapeutic target in CLL Claudia Holler, Josefina D Pinon, Ursula Denk, Christoph Heyder, Sebastian Hofbauer, Richard Greil, and Alexander Egle* 3rd Medical Department for Hematology, Oncology, Hemostasiology, Infectious diseases and Rheumatology, University Hospital Salzburg, Salzburg, Austria * Corresponding author; email: a.egle{at}salk.at. The development and the propagation of chronic lymphocytic leukemia (CLL) has been linked to signalling via the B-cell receptor (BCR). Protein kinase C (PKC) is an essential signalling element of the BCR and was recently shown to be overexpressed in human CLL. We used the TCL1 transgenic mouse model to directly target PKC in the development of murine CLL. TCL1 overexpression did restore the CD5+ B cell population that is absent in PKC deficient mice. However, PKC deleted TCL1 transgenic mice did not develop a CLL disease, suggesting a role of PKC in the establishment of the malignant clone. Moreover, targeting of PKC with the specific inhibitor Enzastaurin led to killing of human CLL samples in vitro. We thus propose that PKC may be a relevant target for the treatment of CLL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Herling, K. A. Patel, N. Weit, N. Lilienthal, M. Hallek, M. J. Keating, and D. Jones High TCL1 levels are a marker of B-cell receptor pathway responsiveness and adverse outcome in chronic lymphocytic leukemia Blood, November 19, 2009; 114(21): 4675 - 4686. [Abstract] [Full Text] [PDF]

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