The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Mouse models of human AML accurately predict chemotherapy response
Open accessAbstract
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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RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia
Zuber, J., Shi, J., Wang, E., Rappaport, A. R., Herrmann, H., Sison, E. A., Magoon, D., Qi, J., Blatt, K., Wunderlich, M., et al. (2011) · Nature · doi:10.1038/nature10334 · Cited by 1,870
Self-citationAn inhibitor of oxidative phosphorylation exploits cancer vulnerability
Molina, J. R., Sun, Y., Protopopova, M., Gera, S., Bandi, M., Bristow, C., McAfoos, T., Morlacchi, P., Ackroyd, J., Agip, A.-N. A., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0052-4 · Cited by 928
In vivo engineering of oncogenic chromosomal rearrangements with the CRISPR/Cas9 system
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Self-citationSykes, D. B., Kfoury, Y. S., Mercier, F. E., Wawer, M. J., Law, J. M., Haynes, M. K., Lewis, T. A., Schajnovitz, A., Jain, E., Lee, D., et al. (2016) · Cell · doi:10.1016/j.cell.2016.08.057 · Cited by 500
Transcriptional plasticity promotes primary and acquired resistance to BET inhibition
Rathert, P., Roth, M., Neumann, T., Muerdter, F., Roe, J.-S., Muhar, M., Deswal, S., Cerny-Reiterer, S., Peter, B., Jude, J., et al. (2015) · Nature · doi:10.1038/nature14898 · Cited by 499
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Metadata
- Authors
- Zuber, J., Radtke, I., Pardee, T. S., Zhao, Z., Rappaport, A. R., Luo, W., McCurrach, M. E., Yang, M.-M., Dolan, M. E., Kogan, S. C., Downing, J. R., & Lowe, S. W.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2009-04-01
- Volume
- 23
- Issue
- 7
- Pages
- 877-889
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2122659245
- Cited by
- 279
- References
- 6
- Type
- posted content
- Language
- en
- Open access
- diamond
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- Zuber, J., Radtke, I., Pardee, T. S., Zhao, Z., Rappaport, A. R., Luo, W., McCurrach, M. E., Yang, M.-M., Dolan, M. E., Kogan, S. C., Downing, J. R., & Lowe, S. W. (2009). Mouse models of human AML accurately predict chemotherapy response. Genes & Development. https://doi.org/10.1101/gad.1771409
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