期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 100, 期 5, 页码 1109-1118出版社
WILEY-LISS
DOI: 10.1002/jcb.21147
关键词
B-cell; mouse model; Tcl1
B-cell chronic lymphocytic leukemia (B-CLIL), the most common leukemia in the Western world, results from an expansion of a rare population of CD5+ mature B-lymphocytes. Although clinical features and genomic abnormalities in B-CLL have been studied in considerable detail, the molecular mechanisms underlying disease development has remained unclear until recently. In the last 4 years, several transgenic mouse models for B-CLL were generated. Investigations of these mouse models revealed that deregulation of three pathways, Tcl1-Akt pathway, TNF-NF-kB pathway, and Bcl2-mediated anti-apoptotic pathway, result in the development of B-CILL. While deregulation of TCL1 alone caused a B-CLIL phenotype in mice, overexpression of Bcl2 required aberrantly activated TNF-NF-kB pathway signaling to yield the disease phenotype. In this article, we present what has been learned from mice with B-CLL phenotype and how these mouse models of B-CLL were used to test therapeutic treatments for this common leukemia.
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