ArticleMolecular cancer2013
POU1F1 is a novel fusion partner of NUP98 in acute myeloid leukemia with t(3;11)(p11;p15).
Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Comprehensive mutational profiling and clinical outcome of adult acute myeloid leukemia patients with NUP98 rearrangement.Leukemia · 2026Article
- NUP98 rearrangements in adult AML patients: evaluation of clinical implications and identification of novel fusion partners.Leukemia · 2026Article
- Abnormal PLK2 expression is associated with specific subtypes and may help risk stratification in acute myeloid leukemia.Discover oncology · 2026Article
- NUP98 oncofusions in myeloid malignancies: An update on molecular mechanisms and therapeutic opportunities.HemaSphere · 2024Review
- Article
- Mechanistic insights and potential therapeutic approaches for NUP98-rearranged hematologic malignancies.Blood · 2020Review
- NUP98 is rearranged in 3.8% of pediatric AML forming a clinical and molecular homogenous group with a poor prognosis.Leukemia · 2017Article
- Over-Expression of POU Class 1 Homeobox 1 Transcription Factor (Pit-1) Predicts Poor Prognosis for Breast Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- NUP98-PHF23 is a chromatin-modifying oncoprotein that causes a wide array of leukemias sensitive to inhibition of PHD histone reader function.Cancer discovery · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNUP98 gene rearrangements have been reported in acute myeloid leukemia, giving rise to fusion proteins that seem to function as aberrant transcription factors, and are thought to be associated with poor prognosis.
findingsA patient with treatment-related acute myeloid leukemia presented a t(3;11)(p11;p15) as the only cytogenetic abnormality. FISH and molecular genetic analyses identified a class 1 homeobox gene, POU1F1, located on chromosome 3p11, as the fusion partner of NUP98. In addition, we have found that the patient harbored an FLT3-ITD mutation, which most likely collaborated with the NUP98-POU1F1 fusion gene in malignant transformation.
conclusionsWe have identified POU1F1 as the NUP98 fusion partner in therapy-related AML with a t(3;11)(p11;p15). This is the first POU family member identified as a fusion partner in human cancer.
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