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The role of HOXB2 and HOXB3 in acute myeloid leukemia.

Författare

Summary, in English

Acute myeloid leukemia (AML) is a heterogeneous aggressive disease and the most common form of adult leukemia. Mutations in the type III receptor tyrosine kinase FLT3 are found in more than 30% of patients. Drugs against FLT3 have been developed for the treatment of AML, but they lack specificity, show poor response and lead to the development of a resistant phenotype upon treatment. Therefore, a deeper understanding of FLT3 signaling will facilitate identification of additional pharmacological targets in FLT3-driven AML. In this report, we identify HOXB2 and HOXB3 as novel regulators of oncogenic FLT3-ITD-driven AML. We show that HOXB2 and HOXB3 expression is upregulated in a group of AML patients carrying FLT3-ITD. Overexpression of HOXB2 or HOXB3 in mouse pro-B cells resulted in decreased FLT3-ITD-dependent cell proliferation as well as decreased colony formation and increased apoptosis. Expression of HOXB2 or HOXB3 resulted in a significant decrease in FLT3-ITD-induced AKT, ERK, p38 and STAT5 phosphorylation. Our data suggest that HOXB2 and HOXB3 act as a tumor suppressors in FLT3-ITD driven AML.

Avdelning/ar

Publiceringsår

2015

Språk

Engelska

Sidor

742-747

Publikation/Tidskrift/Serie

Biochemical and Biophysical Research Communications

Volym

467

Issue

4

Dokumenttyp

Artikel i tidskrift

Förlag

Elsevier

Ämne

  • Hematology

Status

Published

ISBN/ISSN/Övrigt

  • ISSN: 1090-2104