ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2012
Menin as a hub controlling mixed lineage leukemia.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Current perspectives on KMT2A fusion proteins and menin inhibition in paediatric acute myeloid leukaemia.The FEBS journal · 2026Review
- Review
- Menin inhibitors for the treatment of acute myeloid leukemia: challenges and opportunities ahead.Journal of hematology & oncology · 2024Review
- Menin in Cancer.Genes · 2024Review
- HOXA9 Regulome and Pharmacological Interventions in Leukemia.Advances in experimental medicine and biology · 2024Review
- Design of Inhibitors That Target the Menin-Mixed-Lineage Leukemia Interaction.Computation (Basel, Switzerland) · 2024Article
- Review
- Men1 disruption in Nkx3.1-deficient mice results in AROncogene · 2021Article
- KMT2C/D COMPASS complex-associated diseases [KClinical epigenetics · 2020Review
- Direct and Indirect Targeting of HOXA9 Transcription Factor in Acute Myeloid Leukemia.Cancers · 2019Review
- Molecular characterization of an MLL1 fusion and its role in chromosomal instability.Molecular oncology · 2019Article
- Disruption of the menin-MLL interaction triggers menin protein degradation via ubiquitin-proteasome pathway.American journal of cancer research · 2019Article
- Potential Treatment of Acute Leukemia with Inhibitors of Menin/MLL Interaction.ACS medicinal chemistry letters · 2018Article
- Targeting Transcription Factors for Cancer Treatment.Molecules (Basel, Switzerland) · 2018Review
- Menin enhances c-Myc-mediated transcription to promote cancer progression.Nature communications · 2017Article
- Article
- Differential requirement for wild-type Flt3 in leukemia initiation among mouse models of human leukemia.Experimental hematology · 2014Article
- Menin-mediated regulation of miRNA biogenesis uncovers the IRS2 pathway as a target for regulating pancreatic beta cells.Oncoscience · 2014Article
- FBP1 Is an Interacting Partner of Menin.International journal of endocrinology · 2014Article
- Targeted drug discovery for pediatric leukemia.Frontiers in oncology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Mixed lineage leukemia (MLL) fusion protein (FP)-induced acute leukemia is highly aggressive and often refractory to therapy. Recent progress in the field has unraveled novel mechanisms and targets to combat this disease. Menin, a nuclear protein, interacts with wild-type (WT) MLL, MLL-FPs, and other partners such as the chromatin-associated protein LEDGF and the transcription factor C-Myb to promote leukemogenesis. The newly solved co-crystal structure illustrating the menin-MLL interaction, coupled with the role of menin in recruiting both WT MLL and MLL-FPs to target genes, highlights menin as a scaffold protein and a central hub controlling this type of leukemia. The menin/WT MLL/MLL-FP hub may also cooperate with several signaling pathways, including Wnt, GSK3, and bromodomain-containing Brd4-related pathways to sustain MLL-FP-induced leukemogenesis, revealing new therapeutic targets to improve the treatment of MLL-FP leukemias.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.