ArticleTheranostics2018
Inactivation of PBX3 and HOXA9 by down-regulating H3K79 methylation represses NPM1-mutated leukemic cell survival.
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Article in Theranostics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
What it found
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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
25 citing papers in PubMed, 41 citations in OpenAlex.
- The landscape of gene co-expression modules correlating with prognostic genetic abnormalities in AML.Journal of translational medicine · 2021Trial
- Targeting the Menin-KMT2A interaction in leukemia: Lessons learned and future directions.International journal of cancer · 2026Review
- HOXA9 drives lymphatic metastasis by activating the c-MYC-glycolysis-lactate axis in gastric cancer.Journal of translational medicine · 2025Article
- Pbx3-mediated suppression of type I interferon response contributes to leukemia progression driven by MLL-AF9.Cancer gene therapy · 2025Article
- Targeting chromatin modifying complexes in acute myeloid leukemia.Stem cells translational medicine · 2025Review
- HOXA9 transcription factor is a double-edged sword: from development to cancer progression.Cancer metastasis reviews · 2024Review
- Induction of AML cell differentiation using HOXA9/DNA binding inhibitors as a potential therapeutic option for HOXA9-dependent AML.HemaSphere · 2024Article
- Loss of RNA-binding protein CELF2 promotes acute leukemia development via FAT10-mTORC1.Oncogene · 2024Article
- Regulation of HOX gene expression in AML.Blood cancer journal · 2024Review
- Nucleophosmin 1 cooperates with the methyltransferase DOT1L to preserve peri-nucleolar heterochromatin organization by regulating H3K27me3 levels and DNA repeats expression.Epigenetics & chromatin · 2023Article
- Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia.Cancer discovery · 2023Article
- Role of HOXA9 in solid tumors: mechanistic insights and therapeutic potential.Cancer cell international · 2022Review
- Histone methylation modification patterns and relevant M-RiskScore in acute myeloid leukemia.Heliyon · 2022Article
- HOXA9 Overexpression Contributes to Stem Cell Overpopulation That Drives Development and Growth of Colorectal Cancer.International journal of molecular sciences · 2022Article
- Emerging Targeted Therapy for Specific Genomic Abnormalities in Acute Myeloid Leukemia.International journal of molecular sciences · 2022Review
- Expression Landscape and Functional Roles of HOXA4 and HOXA5 in Lung Adenocarcinoma.International journal of medical sciences · 2022Article
- Tumour-derived small extracellular vesicles suppress CD8+ T cell immune function by inhibiting SLC6A8-mediated creatine import in NPM1-mutated acute myeloid leukaemia.Journal of extracellular vesicles · 2021Article
- Long non‑coding RNA LINC00460 serves as a potential biomarker and oncogene via regulation of the miR‑320b/PBX3 axis in acute myeloid leukemia.Molecular medicine reports · 2021Article
- LT-171-861, a novel FLT3 inhibitor, shows excellent preclinical efficacy for the treatment of FLT3 mutant acute myeloid leukemia.Theranostics · 2021Article
- PBX3 in Cancer.Cancers · 2020Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Wu ZhangState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Chen ZhaoDepartment of Hematology, the First Hospital of China Medical University, Shenyang, China.
Junmei ZhaoState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Yongmei ZhuState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Xiangqin WengState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Qiusheng ChenState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Huiping SunState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Jian-Qing MiState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Junmin LiState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Jiang ZhuState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Zhu ChenState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Pier Paolo PandolfiDivision of Genetics, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Saijuan ChenState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Xiaojing YanDepartment of Hematology, the First Hospital of China Medical University, Shenyang, China.
Jie XuState Key Laboratory for Medical Genomics, Shanghai Institute of Hematology, Rui-Jin Hospital affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Shanghai Jiao Tong University · CNFirst Hospital of China Medical University · CNBeth Israel Deaconess Medical Center · US
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) with an NPM1 mutation (NPMc+) has a distinct gene expression signature and displays molecular abnormalities similar to mixed lineage leukemia (MLL), including aberrant expression of the
Indexed as
Cell SurvivalProtein Processing, Post-TranslationalAnimalsAntineoplastic AgentsBenzimidazolesCell Line, TumorDisease Models, AnimalGene Expression ProfilingHistone-Lysine N-MethyltransferaseHistonesHomeodomain ProteinsHumansLeukemia, Myeloid, AcuteMethylationMethyltransferasesMice, TransgenicAntineoplastic AgentsBenzimidazolesDOT1L protein, humanEPZ-5676Histone-Lysine N-MethyltransferaseHistoneshomeobox protein HOXA9Homeodomain ProteinsMethyltransferasesNPM1 protein, humanNpm1 protein, mouseNuclear ProteinsNucleophosminproto-oncogene protein Pbx3Proto-Oncogene ProteinsDOT1L inhibitorH3K79 hypermethylationHOXA9NPM1 mutationPBX3
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Read underepoch 390
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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.