Abstract
Abstract The t(12;21)(p13;q22) translocation is the most common chromosomal abnormality in pediatric leukemia, present in up to 25% of children with pre-B cell Acute Lymphoblastic Leukemia (ALL). This translocation involves two transcription factors, TEL(ETV6) and AML(RUNX1), both of which have crucial roles in regulating hematopoiesis. Our lab has previously established a list of TEL-AML1 transcriptional target genes using Affymetrix GeneChip global gene expression analysis of mouse fetal liver hematopoietic progenitor cells (HPC) over-expressing the fusion cDNA. This analysis demonstrated deregulated expression of genes associated with STAT3 signaling, known to be one of the most important pathways required for proliferation and maintenance of multipotency in cancer stem cells. In this study, we analyze the importance of STAT3 activity in a mouse model of TEL-AML1 overexpression, in human TEL-AML1 positive leukemia cells and primary human leukemic samples. Our results show that activation STAT3, via RAC1 induction, is necessary for the survival, proliferation and self-renewal of TEL-AML1 positive leukemia through transcriptional regulation of MYC expression. In conclusion we show a novel signaling pathway important for the maintenance of TEL-AML1 leukemia that constitutes a promising novel therapeutic strategy for the treatment of TEL-AML1 leukemia. Citation Format: Maurizio Mangolini, Jasper de Boer, Vanessa Walf-Vorderwülbecke, Rob Pieters, Monique den Boer, Owen Williams. TEL-AML1-induced STAT3 activation is essential for t(12;21)-associated childhood leukemia. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3818. doi:10.1158/1538-7445.AM2013-3818
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