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Leukemia associated mutant Wilms' tumor gene 1 protein promotes expansion of human hematopoietic progenitor cells.

Author

Summary, in English

The transcription factor Wilms' tumor gene 1 (WT1) is highly expressed in the majority of leukemias, suggesting a role in leukemogenesis. Acquired WT1 mutations are reported as an independent predictor of poor clinical outcome, and mutations resulting in deletion of the entire DNA-binding zinc-finger domain (WT1delZ), is the most common type. The aim of this study was to study cellular effects of WT1(delZ) that may contribute to an oncogenic phenotype. We found that expression of WT1(delZ) supported proliferation of human hematopoietic CD34(+) progenitor cells. Moreover, WT1(delZ) transduced cells expressed erythroid markers, including raised levels of STAT5, independently of addition of erythropoietin. At the global gene expression level, WT1(delZ) caused upregulation of genes related to cell division and genes associated with erythroid maturation, in the absence of added erythropoietin. Our results indicate that WT1(delZ) promotes cell proliferation and expansion of progenitor cells, consistent with a possible role in leukemogenesis.

Department/s

Publishing year

2013

Language

English

Pages

1341-1349

Publication/Series

Leukemia Research: A Forum for Studies on Leukemia and Normal Hemopoiesis

Volume

37

Issue

10

Document type

Journal article

Publisher

Elsevier

Topic

  • Cancer and Oncology

Status

Published

Research group

  • Transcriptional mechanisms for the Wilms’ tumor gene 1 (WT1) oncoprotein

ISBN/ISSN/Other

  • ISSN: 1873-5835