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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.

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LYMPHOID NEOPLASIA

Brief Report

PKCβ is essential for the development of chronic lymphocytic leukemia in the TCL1 transgenic mouse model: validation of PKCβ as a therapeutic target in chronic lymphocytic leukemia

Claudia Holler1, Josefina D. Piñón1, Ursula Denk1, Christoph Heyder1, Sebastian Hofbauer1, Richard Greil1, and Alexander Egle1

1 Laboratory for Immunological and Molecular Cancer Research, 3rd Medical Department for Hematology, Oncology, Hemostasiology, Infectious Diseases and Rheumatology, University Hospital Salzburg, Salzburg, Austria

The development and the propagation of chronic lymphocytic leukemia (CLL) has been linked to signaling via the B-cell receptor (BCR). Protein kinase C β (PKCβ) is an essential signaling element of the BCR and was recently shown to be overexpressed in human CLL. We used the TCL1 transgenic mouse model to directly target PKCβ in the development of murine CLL. TCL1 overexpression did restore the CD5+ B-cell population that is absent in PKCβ-deficient mice. However, PKCβ-deleted TCL1 transgenic mice did not develop a CLL disease, suggesting a role of PKCβ in the establishment of the malignant clone. Moreover, targeting of PKCβ with the specific inhibitor enzastaurin led to killing of human CLL samples in vitro. We thus propose that PKCβ may be a relevant target for the treatment of CLL.


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