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• W2078396391 abstract "Abstract B‐cell chronic lymphocytic leukemia (B‐CLL), 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‐CLL. While deregulation of TCL1 alone caused a B‐CLL 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. J. Cell. Biochem. 100: 1109–1118, 2007. © 2006 Wiley‐Liss, Inc." @default.
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• W2078396391 date "2006-11-27" @default.
• W2078396391 modified "2023-10-13" @default.
• W2078396391 title "Animal models for chronic lymphocytic leukemia" @default.
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• W2078396391 doi "https://doi.org/10.1002/jcb.21147" @default.
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