Leukemic transformation in mice expressing a NUP98-HOXD13 transgene is accompanied by spontaneous mutations in Nras, Kras, and Cbl

Slape, Christopher, Liu, Leah Y., Beachy, Sarah and Aplan, Peter D. (2008) Leukemic transformation in mice expressing a NUP98-HOXD13 transgene is accompanied by spontaneous mutations in Nras, Kras, and Cbl. Blood, 112 5: 2017-2019. doi:10.1182/blood-2008-01-135186


Author Slape, Christopher
Liu, Leah Y.
Beachy, Sarah
Aplan, Peter D.
Title Leukemic transformation in mice expressing a NUP98-HOXD13 transgene is accompanied by spontaneous mutations in Nras, Kras, and Cbl
Formatted title
Leukemic transformation in mice expressing a NUP98-HOXD13 transgene is accompanied by spontaneous mutations in Nras, Kras, and Cbl
Journal name Blood   Check publisher's open access policy
ISSN 0006-4971
1528-0020
Publication date 2008-09
Sub-type Article (original research)
DOI 10.1182/blood-2008-01-135186
Open Access Status Not yet assessed
Volume 112
Issue 5
Start page 2017
End page 2019
Total pages 3
Place of publication Washington, DC, United States
Publisher American Society of Hematology
Language eng
Formatted abstract
The NUP98-HOXD13 (NHD13) fusion gene occurs in patients with myelodysplastic syndrome (MDS) and acute nonlymphocytic leukemia (ANLL). We reported that transgenic mice expressing NHD13 develop MDS, and that more than half of these mice eventually progress to acute leukemia. The latency period suggests a requirement for at least 1 complementary event before leukemic transformation. We conducted a candidate gene search for complementary events focused on genes that are frequently mutated in human myeloid leukemia. We investigated 22 ANLL samples and found a high frequency of Nras and Kras mutations, an absence of Npm1, p53, Runxl, Kit and Flt3 mutations, and a single Cbl mutation. Our findings support a working hypothesis that predicts that ANLL cases have one mutation which inhibits differentiation, and a complementary mutation which enhances proliferation or inhibit apoptosis. In addition, we provide the first evidence for spontaneous collaborating mutations in a genetically engineered mouse model of ANLL.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Diamantina Institute Publications
 
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