ArticleCancer research2011
Common and overlapping oncogenic pathways contribute to the evolution of acute myeloid leukemias.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 68 citations in OpenAlex.
- Acute myeloid leukemia associated RUNX1 variants induce aberrant expression of transcription factor TCF4.Leukemia · 2025Article
- Cell of origin epigenetic priming determines susceptibility to Tet2 mutation.Nature communications · 2024Article
- Studying the potential of upregulated PTGS2 and VEGF-C besides hyper-methylation of PTGS2 promoter as biomarkers of Acute myeloid leukemia.Molecular biology reports · 2022Article
- Identification of autophagy-associated genes and prognostic implications in adults with acute myeloid leukemia by integrated bioinformatics analysis.Frontiers in oncology · 2022Article
- HCK maintains the self-renewal of leukaemia stem cells via CDK6 in AML.Journal of experimental & clinical cancer research : CR · 2021Article
- Evaluation of Nrf2, Keap1 and Apoptotic Pathway Genes Expression in Acute Myeloid Leukemia Patients.Iranian journal of pharmaceutical research : IJPR · 2021Article
- Integrated Analyses of Mouse Stem Cell Transcriptomes Provide Clues for Stem Cell Maintenance and Transdifferentiation.Frontiers in genetics · 2020Article
- A Trib2-p38 axis controls myeloid leukaemia cell cycle and stress response signalling.Cell death & disease · 2018Article
- Trib2 expression in granulocyte-monocyte progenitors drives a highly drug resistant acute myeloid leukaemia linked to elevated Bcl2.Oncotarget · 2018Article
- Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells.Journal of visualized experiments : JoVE · 2018Article
- Emerging roles of transit-amplifying cells in tissue regeneration and cancer.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- Overexpression of SOX4 correlates with poor prognosis of acute myeloid leukemia and is leukemogenic in zebrafish.Blood cancer journal · 2017Article
- A quantitative proteomics approach identifies ETV6 and IKZF1 as new regulators of an ERG-driven transcriptional network.Nucleic acids research · 2016Article
- Update on acute myeloid leukemia stem cells: New discoveries and therapeutic opportunities.World journal of stem cells · 2016Review
- Targeting PI3Kδ and PI3Kγ signalling disrupts human AML survival and bone marrow stromal cell mediated protection.Oncotarget · 2016Article
- High expression of LMO2 predicts a favorable outcome in adult patients with BCR/ABL negative B-cell acute lymphoblastic leukemia.Oncology letters · 2016Article
- Targeting Aberrant Epigenetic Networks Mediated by PRMT1 and KDM4C in Acute Myeloid Leukemia.Cancer cell · 2016Article
- Stress and Non-Stress Roles of Inflammatory Signals during HSC Emergence and Maintenance.Frontiers in immunology · 2016Review
- Hematopoietic Differentiation Is Required for Initiation of Acute Myeloid Leukemia.Cell stem cell · 2015Article
- A novel mouse model identifies cooperating mutations and therapeutic targets critical for chronic myeloid leukemia progression.The Journal of experimental medicine · 2015Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 4 countries.
Funding
Abstract
Fusion oncogenes in acute myeloid leukemia (AML) promote self-renewal from committed progenitors, thereby linking transformation and self-renewal pathways. Like most cancers, AML is a genetically and biologically heterogeneous disease, but it is unclear whether transformation results from common or overlapping genetic programs acting downstream of multiple mutations or by the engagement of unique genetic programs acting cooperatively downstream of individual mutations. This distinction is important, because the involvement of common programs would imply the existence of common molecular targets to treat AML, no matter which oncogenes are involved. Here we show that the ability to promote self-renewal is a generalized property of leukemia-associated oncogenes. Disparate oncogenes initiated overlapping transformation and self-renewal gene expression programs, the common elements of which were defined in established leukemic stem cells from an animal model as well as from a large cohort of patients with differing AML subtypes, where they strongly predicted pathobiological character. Notably, individual genes commonly activated in these programs could partially phenocopy the self-renewal function of leukemia-associated oncogenes in committed murine progenitors. Furthermore, they could generate AML following expression in murine bone marrow. In summary, our findings reveal the operation of common programs of self-renewal and transformation downstream of leukemia-associated oncogenes, suggesting that mechanistically common therapeutic approaches to AML are likely to be possible, regardless of the identity of the driver oncogene involved.
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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.