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 Prepublished online as a Blood First Edition Paper on June 19, 2003; DOI 10.1182/blood-2003-01-0090.

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Blood, 1 October 2003, Vol. 102, No. 7, pp. 2593-2596

NEOPLASIA

NF-{kappa}B activation in premalignant mouse tal-1/scl thymocytes and tumors

Jennifer O'Neil, Juan-Jose Ventura, Nicole Cusson, and Michelle Kelliher

From the Department of Cancer Biology and the Interdisciplinary Graduate Program, Program in Molecular Medicine, University of Massachusetts Medical School, Worcester.

TAL-1/SCL activation is a common genetic event in pediatric T-cell acute lymphoblastic leukemia (T-ALL). Expression of tal-1/scl or a DNA binding mutant of tal-1/scl induces arrest of thymocyte development, resulting in decreases in double-positive and single-positive CD4 thymocytes. Moreover, nuclear p65/p50 heterodimers are detected in premalignant tal-1/scl and mut tal-1/scl thymocytes, suggesting that E2A depletion may induce developmental arrest and stimulate NF-{kappa}B activation. Increased NF-{kappa}B activity is also observed in tal-1/scl tumors and bcl-2 is overexpressed. To examine the contribution of NF-{kappa}B to tal-1/scl tumor growth in vivo, we expressed a mutant form of I{kappa}B{alpha} in tal-1/scl tumor cells. Although expression of mutant I{kappa}B{alpha} inhibited the tumor necrosis factor alpha (TNF-{alpha})-induced NF-{kappa}B response, it had no effect on tumor growth in mice. These data suggest that NF-{kappa}B activation is an early event in tal-1/scl-induced leukemogenesis, associated with arrest of thymocyte development, and does not appear to contribute to tal-1/scl-induced tumor growth. (Blood. 2003;102:2593-2596)


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