The role of HOXB2 and HOXB3 in acute myeloid leukemia.
Lindblad, Oscar LU ; Chougule, Rohit A. LU ; Moharram, Sausan A. LU ; Kabir, Nuzhat N ; Sun, Jianmin LU ; Kazi, Julhash U. LU
and Rönnstrand, Lars
LU
(2015)
In Biochemical and Biophysical Research Communications
467(4).
p.742-747
- Abstract
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/8148844
- author
- Lindblad, Oscar
LU
; Chougule, Rohit A.
LU
; Moharram, Sausan A.
LU
; Kabir, Nuzhat N
; Sun, Jianmin
LU
; Kazi, Julhash U.
LU
and Rönnstrand, Lars
LU
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Biochemical and Biophysical Research Communications
- volume
- 467
- issue
- 4
- pages
- 742 - 747
- publisher
- Elsevier
- external identifiers
-
- pmid:26482852
- wos:000365145300022
- scopus:84946605856
- pmid:26482852
- ISSN
- 1090-2104
- DOI
- 10.1016/j.bbrc.2015.10.071
- language
- English
- LU publication?
- yes
- id
- 21bd247d-17a5-4cb7-854f-ca516ac48882 (old id 8148844)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/26482852?dopt=Abstract
- date added to LUP
- 2016-04-01 10:27:03
- date last changed
- 2025-04-04 15:25:31
@article{21bd247d-17a5-4cb7-854f-ca516ac48882,
abstract = {{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.}},
author = {{Lindblad, Oscar and Chougule, Rohit A. and Moharram, Sausan A. and Kabir, Nuzhat N and Sun, Jianmin and Kazi, Julhash U. and Rönnstrand, Lars}},
issn = {{1090-2104}},
language = {{eng}},
number = {{4}},
pages = {{742--747}},
publisher = {{Elsevier}},
series = {{Biochemical and Biophysical Research Communications}},
title = {{The role of HOXB2 and HOXB3 in acute myeloid leukemia.}},
url = {{https://lup.lub.lu.se/search/files/7283575/1854133.pdf}},
doi = {{10.1016/j.bbrc.2015.10.071}},
volume = {{467}},
year = {{2015}},
}