ArticleBlood2005
The MLL partial tandem duplication: evidence for recessive gain-of-function in acute myeloid leukemia identifies a novel patient subgroup for molecular-targeted therapy.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.
- A systematic review and meta-analysis of the impact of WT1 polymorphism rs16754 in the effectiveness of standard chemotherapy in patients with acute myeloid leukemia.The pharmacogenomics journal · 2016Pooled it
- Trial
- Prognostic impact of KMT2A-PTD in acute myeloid leukemia in the NGS era: a multicenter retrospective study.Annals of hematology · 2026Observational
- Review
- Article
- Article
- Bacterial DNA involvement in carcinogenesis.Frontiers in cellular and infection microbiology · 2022Review
- Targeting BRD4 in acute myeloid leukemia with partial tandem duplication of theHaematologica · 2021Article
- Review
- DNMT3A mutants provide proliferating advantage with augmentation of self-renewal activity in the pathogenesis of AML in KMT2A-PTD-positive leukemic cells.Oncogenesis · 2020Article
- Review
- Direct and Indirect Targeting of HOXA9 Transcription Factor in Acute Myeloid Leukemia.Cancers · 2019Review
- The Landscape ofHemaSphere · 2019Article
- Targeted next generation sequencing can serve as an alternative to conventional tests in myeloid neoplasms.PloS one · 2019Article
- A novel regimen for relapsed/refractory adult acute myeloid leukemia using aHaematologica · 2018Article
- Partial tandem duplication ofHaematologica · 2018Article
- Molecular and cellular issues of KMT2A variants involved in Wiedemann-Steiner syndrome.European journal of human genetics : EJHG · 2018Article
- Amplification of mixed lineage leukemia gene perturbs hematopoiesis and cooperates with partial tandem duplication to induce acute myeloid leukemia.Haematologica · 2017Article
- Whole-exome sequencing identified a homozygous BRDT mutation in a patient with acephalic spermatozoa.Oncotarget · 2017Article
- Article
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
MLL (ALL-1) chimeric fusions and MLL partial tandem duplications (PTD) may have mechanistically distinct contributions to leukemogenesis. Acute myeloid leukemia (AML) blasts with the t(9;11)(p22; q23) express MLL-AF9 and MLL wild-type (WT) transcripts, while normal karyotype AML blasts with the MLL(PTD/WT) genotype express MLL PTD but not the MLL WT. Silencing of MLL WT in MLL(PTD/WT) blasts was reversed by DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors, and MLL WT induction was associated with selective sensitivity to cell death. Reduction of MLL PTD expression induced MLL WT and reduced blast colony-forming units, supporting opposing functions for MLL PTD and MLL WT whereby the MLL PTD contributes to the leukemic phenotype via a recessive gain-of-function. The coincident suppression of the MLL WT allele with the expression of the MLL PTD allele, along with the functional data presented here, supports the hypothesis that loss of WT MLL function via monoallelic repression contributes to the leukemic phenotype by the remaining mutant allele. These data from primary AML and the pharmacologic reversal of MLL WT silencing associated with a favorable alteration in the threshold for apoptosis suggest that these patients with poor prognosis may benefit from demethylating or histone deacetylase inhibitor therapy, or both.
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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.