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TP53 subclones in AML
ly address the impact of subclonal TP53 mutations in such an AML cohort.
In conclusion, we have shown that subclonal TP53 muta-
tions represent an adverse prognostic marker in AML, inde-
pendently of the clone size. Our data further corroborate
the use of next-generation sequencing technologies for risk
stratification of patients with AML. Future work will assess
the clonal architecture of these specimens and investigate
whether TP53-mutated subclones exhibit DFG-Forschergruppe FOR 2674 ‚Aging-related epigenetic preleukemic/leukemic stem cell properties which may remodeling in acute myeloid leukemia’, subproject A02, and explain their persistence following cytotoxic therapies. Österreichische Nationalbank (16917).
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Acknowledgments
Funding
We thank Ms. Daniela Weber, Ulm, Germany, for excellent assistance and Dr. Karl Kashofer, Graz, Austria, for providing DNA for sequencing analysis.
This work was supported by the Austrian Science Fund FWF (P31430-B26 and P28949-B28), Leukämiehilfe Steiermark,
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