ArticleGenes & development2011
An integrated approach to dissecting oncogene addiction implicates a Myb-coordinated self-renewal program as essential for leukemia maintenance.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 192 papers.
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Who cites it
192 citing papers in PubMed, 278 citations in OpenAlex.
- PTBP1 controls oncogenic transcript processing and maintenance of acute myeloid leukemia.Leukemia · 2026Article
- Optimized post-GWAS analysis identifies therapeutic targets for essential thrombocythemia and polycythemia vera.Communications medicine · 2026Article
- Optical genome mapping uncovers disease-defining variants in an adult T-lymphoblastic leukemia and impacts prognosis.Molecular cytogenetics · 2026Article
- MCL1 inhibition to enhance the efficacy of MYB targeting in pediatric acute myeloid leukemia.Cell death & disease · 2026Article
- Epigenetic reactivation of the tumor suppressor ZBTB7A by KDM4 inhibition in human acute myeloid leukemia.Science translational medicine · 2026Article
- Fusion oncoproteins orchestrate tumorigenesis and sustain malignant progression via a positive feedback mechanism.Cell & bioscience · 2026Review
- FTO depletion does not alter mbioRxiv : the preprint server for biology · 2025Article
- Article
- Guanine nucleotide biosynthesis blockade impairs MLL complex formation and sensitizes leukemias to menin inhibition.Nature communications · 2025Article
- The synergistic effect of c-Myb hyperactivation and Pu.1 deficiency induces Pelger-Huët anomaly and promotes sAML.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- BPDCN MYB fusions regulate cell cycle genes, impair differentiation, and induce myeloid-dendritic cell leukemia.JCI insight · 2024Article
- The adsorption of drugs on nanoplastics has severe biological impact.Scientific reports · 2024Article
- Murine neonatal cardiac regeneration depends on Insulin-like growth factor 1 receptor signaling.Scientific reports · 2024Article
- Enhanced depletion of MLL-fusion proteins in acute leukemia: potential for improved therapeutic outcomes.Experimental hematology & oncology · 2024Article
- Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024Review
- Article
- Understanding the Multi-Functional Role of TCTP in the Regeneration Process of Earthworm, Perionyx excavatus.Tissue engineering and regenerative medicine · 2024Article
- MYB as a Critical Transcription Factor and Potential Therapeutic Target in AML.Advances in experimental medicine and biology · 2024Review
- Systematic evaluation of AML-associated antigens identifies anti-U5 SNRNP200 therapeutic antibodies for the treatment of acute myeloid leukemia.Nature cancer · 2023Article
- Reversal of MYB-dependent suppression of MAFB expression overrides leukaemia phenotype in MLL-rearranged AML.Cell death & disease · 2023Article
132 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedFellman, Christof [corrected to Fellmann, Christof]
Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
Although human cancers have complex genotypes and are genomically unstable, they often remain dependent on the continued presence of single-driver mutations-a phenomenon dubbed "oncogene addiction." Such dependencies have been demonstrated in mouse models, where conditional expression systems have revealed that oncogenes able to initiate cancer are often required for tumor maintenance and progression, thus validating the pathways they control as therapeutic targets. Here, we implement an integrative approach that combines genetically defined mouse models, transcriptional profiling, and a novel inducible RNAi platform to characterize cellular programs that underlie addiction to MLL-AF9-a fusion oncoprotein involved in aggressive forms of acute myeloid leukemia (AML). We show that MLL-AF9 contributes to leukemia maintenance by enforcing a Myb-coordinated program of aberrant self-renewal involving genes linked to leukemia stem cell potential and poor prognosis in human AML. Accordingly, partial and transient Myb suppression precisely phenocopies MLL-AF9 withdrawal and eradicates aggressive AML in vivo without preventing normal myelopoiesis, indicating that strategies to inhibit Myb-dependent aberrant self-renewal programs hold promise as effective and cancer-specific therapeutics. Together, our results identify Myb as a critical mediator of oncogene addiction in AML, delineate relevant Myb target genes that are amenable to pharmacologic inhibition, and establish a general approach for dissecting oncogene addiction in vivo.
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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.