Genetic manipulation of AML1-ETO–induced expansion of hematopoietic precursors in a Drosophila model
Blood, ISSN: 0006-4971, Vol: 116, Issue: 22, Page: 4612-4620
2010
- 47Citations
- 76Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations47
- Citation Indexes47
- 47
- CrossRef44
- Captures76
- Readers76
- 76
Article Description
Among mutations in human Runx1/AML1 transcription factors, the t(8;21)(q22;q22) genomic translocation that creates an AML1-ETO fusion protein is implicated in etiology of the acute myeloid leukemia. To identify genes and components associated with this oncogene we used Drosophila as a genetic model. Expression of AML1-ETO caused an expansion of hematopoietic precursors in Drosophila, which expressed high levels of reactive oxygen species (ROS). Mutations in functional domains of the fusion protein suppress the proliferative phenotype. In a genetic screen, we found that inactivation of EcRB1 or activation of Foxo and superoxide dismutase-2 ( SOD2 ) suppress the AML1-ETO–induced phenotype by reducing ROS expression in the precursor cells. Our studies indicate that ROS is a signaling factor promoting maintenance of normal as well as the aberrant myeloid precursors and suggests the importance of antioxidant enzymes and their regulators as targets for further study in the context of leukemia.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S000649712031017X; http://dx.doi.org/10.1182/blood-2010-03-276998; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=78649463826&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/20688956; https://ashpublications.org/blood/article/116/22/4612/107818/Genetic-manipulation-of-AML1ETOinduced-expansion; https://facultyopinions.com/prime/4831966#eval4802060; http://dx.doi.org/10.3410/f.4831966.4802060; https://dx.doi.org/10.1182/blood-2010-03-276998; https://ashpublications.org/blood/article/116/22/4612/107818/Genetic-manipulation-of-AML1-ETO-induced-expansion; http://europepmc.org/abstract/med/20688956; http://europepmc.org/articles/PMC2996118; http://f1000.com/4831966#eval4802060; http://www.bloodjournal.org/content/116/22/4612; http://www.bloodjournal.org/content/116/22/4612.abstract; http://www.bloodjournal.org/content/116/22/4612.full.pdf; https://ashpublications.org/blood/article-pdf/116/22/4612/1495962/zh804810004612.pdf; http://www.bloodjournal.org/content/116/22/4612?sso-checked=true; http://www.bloodjournal.org/cgi/doi/10.1182/blood-2010-03-276998
American Society of Hematology
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