Review
Oncogene (2004) 23, 2275–2286. doi:10.1038/sj.onc.1207410 Published online 2 February 2004
The c-Rel transcription factor and B-cell proliferation: a deal with the devil
Thomas D Gilmore1, Demetrios Kalaitzidis1, Mei-Chih Liang1 and Daniel T Starczynowski1
1Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215, USA
Correspondence: TD Gilmore, E-mail: gilmore@bu.edu
Received 6 November 2003; Revised 30 November 2003; Accepted 1 December 2003; Published online 2 February 2004.
Abstract
Activation of the Rel/NF-
B signal transduction pathway has been associated with a variety of animal and human malignancies. However, among the Rel/NF-
B family members, only c-Rel has been consistently shown to be able to malignantly transform cells in culture. In addition, c-rel has been activated by a retroviral promoter insertion in an avian B-cell lymphoma, and amplifications of REL (human c-rel) are frequently seen in Hodgkin's lymphomas and diffuse large B-cell lymphomas, and in some follicular and mediastinal B-cell lymphomas. Phenotypic analysis of c-rel knockout mice demonstrates that c-Rel has a normal role in B-cell proliferation and survival; moreover, c-Rel nuclear activity is required for B-cell development. Few mammalian model systems are available to study the role of c-Rel in oncogenesis, and it is still not clear what features of c-Rel endow it with its unique oncogenic activity among the Rel/NF-
B family. In any event, REL may provide an appropriate therapeutic target for certain human lymphoid cell malignancies.
Keywords:
c-Rel, Rel, NF-
B, B cell, lymphoma, gene amplification
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