ArticleBlood2005
Conditional MN1-TEL knock-in mice develop acute myeloid leukemia in conjunction with overexpression of HOXA9.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- N-MYC regulates cell survival via eIF4G1 in inv(16) acute myeloid leukemia.Science advances · 2024Article
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- Novel strategy for rapid functional in vivo validation of oncogenic drivers in haematological malignancies.Scientific reports · 2019Article
- N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer.The Journal of clinical investigation · 2019Article
- Overexpression of MN1 confers resistance to chemotherapy, accelerates leukemia onset, and suppresses p53 and Bim induction.PloS one · 2012Article
- The leukemia-associated fusion protein MN1-TEL blocks TEL-specific recognition sequences.PloS one · 2012Article
- Functional characterization of high levels of meningioma 1 as collaborating oncogene in acute leukemia.Leukemia · 2010Article
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- Meningioma 1 is required for appropriate osteoblast proliferation, motility, differentiation, and function.The Journal of biological chemistry · 2009Article
- Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics.Journal of hematology & oncology · 2009Review
- The Mn1 transcription factor acts upstream of Tbx22 and preferentially regulates posterior palate growth in mice.Development (Cambridge, England) · 2008Article
- Article
- The MN1-TEL myeloid leukemia-associated fusion protein has a dominant-negative effect on RAR-RXR-mediated transcription.Oncogene · 2007Article
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- Retroviral insertional mutagenesis identifies genes that collaborate with NUP98-HOXD13 during leukemic transformation.Cancer research · 2007Article
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- MN1, a novel player in human AML.Blood cells, molecules & diseasesReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The chromosomal translocation t(12; 22)(p13;q11) in human myeloid leukemia generates an MN1-TEL (meningioma 1-translocation-ETS-leukemia) fusion oncoprotein. This protein consists of N-terminal MN1 sequences, a transcriptional coactivator fused to C-terminal TEL sequences, an ETS (E26 transformation-specific) transcription factor. Enforced expression of MN1-TEL in multipotent hematopoietic progenitors in knock-in mice perturbed growth and differentiation of myeloid as well as lymphoid cells. Depending on obligatory secondary mutations, these mice developed T-cell lympholeukemia. Here we addressed the role of MN1-TEL in myeloid leukemogenesis using the same mouse model. Expression of MN1-TEL enhanced the growth of myeloid progenitors in an interleukin 3/stem cell factor (IL-3/SCF)-dependent manner in vitro whereas 10% of MN1-TEL-expressing mice developed altered myelopoiesis with severe anemia after long latency. Coexpression of MN1-TEL and IL-3, but not SCF, rapidly caused a fatal myeloproliferative disease rather than acute myeloid leukemia (AML). Because MN1-TEL+ AML patient cells overexpress HOXA9 (homeobox A9), we tested the effect of coexpression of MN1-TEL and HOXA9 in mice and found that 90% of MN1-TEL+/HOXA9+ mice developed AML much more rapidly than control HOXA9+ mice. Thus, the leukemogenic effect of MN1-TEL in our knock-in mice is pleiotropic, and the type of secondary mutation determines disease outcome.
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