ReviewBlood2009
Therapeutic targeting of MLL.
Review in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
67 citing papers in PubMed, 126 citations in OpenAlex.
- Synthesis, Structure-Activity Relationships, and Antitumor Activities of Quinoxiline-Containing Inhibitors of the Protein-Protein Interactions between Transcription Coactivator AF9/ENL and DOT1L/AF4.Journal of medicinal chemistry · 2025Article
- Molecular profiling of head and neck squamous cell carcinomas in North-eastern Italy identifies possible tumour cell vulnerabilities.Translational oncology · 2025Article
- Cytokine-induced memory-like NK cells combined with Tafasitamab demonstrate efficacy against B-cell acute lymphoblastic leukemia.Immunotherapy advances · 2025Article
- Sequential drug treatment targeting cell cycle and cell fate regulatory programs blocks non-genetic cancer evolution in acute lymphoblastic leukemia.Genome biology · 2024Article
- Three-dimensional chromatin landscapes in MLLr AML.Experimental hematology & oncology · 2024Article
- Multi-omic analysis of longitudinal acute myeloid leukemia patient samples reveals potential prognostic markers linked to disease progression.Frontiers in genetics · 2024Article
- The Biological Significance of AFF4: Promoting Transcription Elongation, Osteogenic Differentiation and Tumor Progression.Combinatorial chemistry & high throughput screening · 2024Review
- Article
- Enhancer remodeling drives MLL oncogene-dependent transcriptional dysregulation in leukemia stem cells.Blood advances · 2023Article
- Defined Human Leukemic CD34+ Liquid Cultures to Study HDAC/Transcriptional Repressor Complexes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Downregulation of SETD5 Suppresses the Tumorigenicity of Hepatocellular Carcinoma Cells.Molecules and cells · 2022Article
- A proteolysis-targeting chimera molecule selectively degrades ENL and inhibits malignant gene expression and tumor growth.Journal of hematology & oncology · 2022Article
- LEDGF/p75-mediated chemoresistance of mixed-lineage leukemia involves cell survival pathways and super enhancer activators.Cancer gene therapy · 2022Review
- Allosteric regulation of histone lysine methyltransferases: from context-specific regulation to selective drugs.Biochemical Society transactions · 2021Review
- Small-molecule inhibitor of AF9/ENL-DOT1L/AF4/AFF4 interactions suppresses malignant gene expression and tumor growth.Theranostics · 2021Article
- KMT2A/C mutations function as a potential predictive biomarker for immunotherapy in solid tumors.Biomarker research · 2020Article
- Aberrant Activity of Histone-Lysine N-Methyltransferase 2 (KMT2) Complexes in Oncogenesis.International journal of molecular sciences · 2020Review
- CCAAT enhancer binding protein alpha (CEBPA) biallelic acute myeloid leukaemia: cooperating lesions, molecular mechanisms and clinical relevance.British journal of haematology · 2020Review
- H3K4 methylation at active genes mitigates transcription-replication conflicts during replication stress.Nature communications · 2020Article
- CDKI-73: an orally bioavailable and highly efficacious CDK9 inhibitor against acute myeloid leukemia.Investigational new drugs · 2019Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Treatment of hematologic malignancies is evolving from a uniform approach to targeted therapies directed at the underlying molecular abnormalities of disease. The mixed lineage leukemia (MLL) proto-oncogene is a recurrent site of genetic rearrangements in acute leukemias; and since its discovery in 1992, many advances have been made in understanding its role in leukemogenesis. A variety of MLL translocation partners have been described, and detailed structure/function studies have identified functional domains that are required for transformation. Proteins associated with the MLL core complex or its fusion partners have been isolated and characterized for their critical roles in leukemia pathogenesis. Downstream mediators of MLL transcriptional regulation and multiple collaborating signaling pathways have been described and characterized. These advances in our understanding of MLL-related leukemogenesis provide a foundation for ongoing and future efforts to develop novel therapeutic strategies that will hopefully result in better treatment outcomes.
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.