ArticleGenes & development2009
Mouse models of human AML accurately predict chemotherapy response.
Article in Genes & development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 1 of them a synthesis that pooled it.
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Who cites it
185 citing papers in PubMed, 1 synthesis or guideline pooled it, 277 citations in OpenAlex.
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- The pathogenesis of therapy-related myeloid neoplasms from TP53-mutant clonal hematopoiesis.Leukemia · 2026Article
- An Isoform-Specific RUNX1C-BTG2 Axis Governs AML Quiescence and Chemoresistance.Blood cancer discovery · 2025Article
- Inhibition of the minor spliceosome restricts the growth of a broad spectrum of cancers.EMBO reports · 2025Article
- A niche driven mechanism determines response and a mutation-independent therapeutic approach for myeloid malignancies.Cancer cell · 2025Article
- MutantProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Conventional chemotherapy: millions of cures, unresolved therapeutic index.Nature reviews. Cancer · 2025Review
- Germline Single-Nucleotide PolymorphismBiomedicines · 2025Article
- The E3 ubiquitin ligase Herc1 modulates the response to nucleoside analogs in acute myeloid leukemia.Blood advances · 2024Article
- Spatial metabolomics highlights metabolic reprogramming in acute myeloid leukemia mice through creatine pathway.Acta pharmaceutica Sinica. B · 2024Article
- Mutational cooperativity of RUNX1::RUNX1T1 isoform 9a and oncogenic NRAS in zebrafish myeloid leukaemia.Biology open · 2024Article
125 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
The genetic heterogeneity of cancer influences the trajectory of tumor progression and may underlie clinical variation in therapy response. To model such heterogeneity, we produced genetically and pathologically accurate mouse models of common forms of human acute myeloid leukemia (AML) and developed methods to mimic standard induction chemotherapy and efficiently monitor therapy response. We see that murine AMLs harboring two common human AML genotypes show remarkably diverse responses to conventional therapy that mirror clinical experience. Specifically, murine leukemias expressing the AML1/ETO fusion oncoprotein, associated with a favorable prognosis in patients, show a dramatic response to induction chemotherapy owing to robust activation of the p53 tumor suppressor network. Conversely, murine leukemias expressing MLL fusion proteins, associated with a dismal prognosis in patients, are drug-resistant due to an attenuated p53 response. Our studies highlight the importance of genetic information in guiding the treatment of human AML, functionally establish the p53 network as a central determinant of chemotherapy response in AML, and demonstrate that genetically engineered mouse models of human cancer can accurately predict therapy response in patients.
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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.