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Blood, 1 February 2007, Vol. 109, No. 3, pp. 961-970.
Prepublished online as a Blood First Edition Paper on October 17, 2006September 28, 2006; DOI 10.1182/blood-2006-07-036640.
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Submitted July 24, 2006
Accepted September 16, 2006
Commonly dysregulated genes in murine APL cells
Wenlin Yuan, Jacqueline Payton, Matthew Holt, Daniel Link, Mark Watson, John DiPersio, and Timothy Ley*
Siteman Cancer Center, Washington University, St. Louis, MO, United States
Dept of Pathology & Immunology, Washington University, St. Louis, MO, United States
* Corresponding author; email: timley{at}im.wustl.edu.
To identify genes that are commonly dysregulated in a murine model of acute promyelocytic leukemia, we first defined gene expression patterns during normal murine myeloid development; serial gene expression profiling studies were performed with primary murine hematopoietic progenitors that were induced to undergo myeloid maturation in vitro with G-CSF. Many genes were reproducibly expressed in restricted developmental "windows," suggesting a structured hierarchy of expression that is relevant for the induction of developmental fates and/or differentiated cell functions. We compared the normal myeloid developmental transcriptome to that of APL cells derived from mice expressing PML-RAR under control of the murine cathepsin G locus. While many promyelocyte-specific genes were highly expressed in all APL samples, 116 genes were reproducibly dysregulated in many independent APL samples, including Fos, Jun, Egr-1, TNF, and VCAM-1. However, this set of commonly dysregulated genes was expressed normally in preleukemic, early myeloid cells from the same mouse model, suggesting that dysregulation occurs as a "downstream" event during disease progression. These studies suggest that the genetic events that lead to APL progression may converge on common pathways that are important for leukemia pathogenesis.
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