ReviewExperimental hematology2014
Two decades of leukemia oncoprotein epistasis: the MLL1 paradigm for epigenetic deregulation in leukemia.
Review in Experimental hematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Combining menin and MEK inhibition to target poor prognosis KMT2A-rearranged RAS pathway-mutant acute myeloid leukemia.Blood advances · 2026Article
- CRISPR-based functional genomics for dissecting therapeutic dependency in primary acute myeloid leukemia samples.Molecular cell · 2026Article
- Role of MNX1-mediated histone modifications and PBX gene family in MNX1-induced leukemogenesis.Scientific reports · 2026Article
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- Fusion-specific chromatin profiles mediate transcriptional heterogeneity in MLL-rearranged acute lymphoblastic leukemia.Blood advances · 2025Article
- Engineering an inducible leukemia-associated fusion protein enables large-scale ex vivo production of functional human phagocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Progenitor-like cell type of an MLL-EDC4 fusion in acute myeloid leukemia.Blood advances · 2023Article
- Does lineage plasticity enable escape from CAR-T cell therapy? Lessons from MLL-r leukemia.Experimental hematology · 2021Review
- A chromatin perspective on metabolic and genotoxic impacts on hematopoietic stem and progenitor cells.Cellular and molecular life sciences : CMLS · 2020Review
- Article
- Menin inhibitor MI-3454 induces remission in MLL1-rearranged and NPM1-mutated models of leukemia.The Journal of clinical investigation · 2020Article
- CPSF3-dependent pre-mRNA processing as a druggable node in AML and Ewing's sarcoma.Nature chemical biology · 2020Article
- Antitumor immunity augments the therapeutic effects of p53 activation on acute myeloid leukemia.Nature communications · 2019Article
- Transcriptional addiction in mixed lineage leukemia: new avenues for target therapies.Blood science (Baltimore, Md.) · 2019Review
- Molecular characterization of an MLL1 fusion and its role in chromosomal instability.Molecular oncology · 2019Article
- Rewiring the Epigenetic Networks inFrontiers in cell and developmental biology · 2019Review
- Turning Stem Cells Bad: Generation of Clinically Relevant Models of Human Acute Myeloid Leukemia through Gene Delivery- or Genome Editing-Based Approaches.Molecules (Basel, Switzerland) · 2018Review
- WDR5 supports colon cancer cells by promoting methylation of H3K4 and suppressing DNA damage.BMC cancer · 2018Article
- Article
- The Cks1/Cks2 axis fine-tunes Mll1 expression and is crucial for MLL-rearranged leukaemia cell viability.Biochimica et biophysica acta. Molecular cell research · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
MLL1, located on human chromosome 11, is disrupted in distinct recurrent chromosomal translocations in several leukemia subsets. Studying the MLL1 gene and its oncogenic variants has provided a paradigm for understanding cancer initiation and maintenance through aberrant epigenetic gene regulation. Here we review the historical development of model systems to recapitulate oncogenic MLL1-rearrangement (MLL-r) alleles encoding mixed-lineage leukemia fusion proteins (MLL-FPs) or internal gene rearrangement products. These largely mouse and human cell/xenograft systems have been generated and used to understand how MLL-r alleles affect diverse pathways to result in a highly penetrant, drug-resistant leukemia. The particular features of the animal models influenced the conclusions of mechanisms of transformation. We discuss significant downstream enablers, inhibitors, effectors, and collaborators of MLL-r leukemia, including molecules that directly interact with MLL-FPs and endogenous mixed-lineage leukemia protein, direct target genes of MLL-FPs, and other pathways that have proven to be influential in supporting or suppressing the leukemogenic activity of MLL-FPs. The use of animal models has been complemented with patient sample, genome-wide analyses to delineate the important genomic and epigenomic changes that occur in distinct subsets of MLL-r leukemia. Collectively, these studies have resulted in rapid progress toward developing new strategies for targeting MLL-r leukemia and general cell-biological principles that may broadly inform targeting aberrant epigenetic regulators in other cancers.
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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.