Animal models for chronic lymphocytic leukemia

Yuri Pekarsky*, Nicola Zanesi, Rami I. Aqeilan, Carlo M. Croce

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

42 Scopus citations

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.

Original languageAmerican English
Pages (from-to)1109-1118
Number of pages10
JournalJournal of Cellular Biochemistry
Volume100
Issue number5
DOIs
StatePublished - 1 Apr 2007
Externally publishedYes

Keywords

  • B-cell
  • Mouse model
  • Tcl1

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