ArticleHaematologica2014
Potent co-operation between the NUP98-NSD1 fusion and the FLT3-ITD mutation in acute myeloid leukemia induction.
Article in Haematologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
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- Application of Optical Genome Mapping for the Diagnosis and Risk Stratification of Myeloid and Lymphoid Malignancies.International journal of molecular sciences · 2025Article
- Review
- From low remission to hope: the efficacy of targeted therapies in NUP98-R positive pediatric acute myeloid leukemia.World journal of pediatrics : WJP · 2025Article
- DistinctInternational journal of molecular sciences · 2024Article
- NUP98 oncofusions in myeloid malignancies: An update on molecular mechanisms and therapeutic opportunities.HemaSphere · 2024Review
- Clinical features and prognosis of patients with myeloid neoplasms harboring t(7;11)(p15;p15) translocation: a single-center retrospective study.BMC cancer · 2024Article
- Article
- The Nup98::Nsd1 fusion gene induces CD123 expression in 32D cells.International journal of hematology · 2023Article
- The MLL-Menin Interaction is a Therapeutic Vulnerability inHemaSphere · 2023Article
- Article
- Layered immunity and layered leukemogenicity: Developmentally restricted mechanisms of pediatric leukemia initiation.Immunological reviews · 2023Review
- Article
- Upfront Screening by Quantitative Real-Time PCR Assay Identifies NUP98::NSD1 Fusion Transcript in Indian AML Patients.Diagnostics (Basel, Switzerland) · 2022Article
- SMARCA5 interacts with NUP98-NSD1 oncofusion protein and sustains hematopoietic cells transformation.Journal of experimental & clinical cancer research : CR · 2022Article
- Murine Models of Acute Myeloid Leukemia.Frontiers in oncology · 2022Review
- Review
- Combination Therapy of Navitoclax with Chemotherapeutic Agents in Solid Tumors and Blood Cancer: A Review of Current Evidence.Pharmaceutics · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NUP98-NSD1 fusion, product of the t(5;11)(q35;p15.5) chromosomal translocation, is one of the most prevalent genetic alterations in cytogenetically normal pediatric acute myeloid leukemias and is associated with poor prognosis. Co-existence of an FLT3-ITD activating mutation has been found in more than 70% of NUP98-NSD1-positive patients. To address functional synergism, we determined the transforming potential of retrovirally expressed NUP98-NSD1 and FLT3-ITD in the mouse. Expression of NUP98-NSD1 provided mouse strain-dependent, aberrant self-renewal potential to bone marrow progenitor cells. Co-expression of FLT3-ITD increased proliferation and maintained self-renewal in vitro. Transplantation of immortalized progenitors co-expressing NUP98-NSD1 and FLT3-ITD into mice resulted in acute myeloid leukemia after a short latency. In contrast, neither NUP98-NSD1 nor FLT3-ITD single transduced cells were able to initiate leukemia. Interestingly, as reported for patients carrying NUP98-NSD1, an increased Flt3-ITD to wild-type Flt3 mRNA expression ratio with increased FLT3-signaling was associated with rapidly induced disease. In contrast, there was no difference in the expression levels of the NUP98-NSD1 fusion or its proposed targets HoxA5, HoxA7, HoxA9 or HoxA10 between animals with different latencies to develop disease. Finally, leukemic cells co-expressing NUP98-NSD1 and FLT3-ITD were very sensitive to a small molecule FLT3 inhibitor, which underlines the significance of aberrant FLT3 signaling for NUP98-NSD1-positive leukemias and suggests new therapeutic approaches that could potentially improve patient outcome.
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