H
Hanna S. Radomska
Researcher at Ohio State University
Publications - 52
Citations - 4448
Hanna S. Radomska is an academic researcher from Ohio State University. The author has contributed to research in topics: Cellular differentiation & Myeloid leukemia. The author has an hindex of 27, co-authored 51 publications receiving 4204 citations. Previous affiliations of Hanna S. Radomska include Beth Israel Deaconess Medical Center & Harvard University.
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Journal ArticleDOI
Dominant-negative mutations of CEBPA , encoding CCAAT/enhancer binding protein-α (C/EBPα), in acute myeloid leukemia
Thomas Pabst,Beatrice U. Mueller,Pu Zhang,Hanna S. Radomska,Sailaja Narravula,Susanne Schnittger,Gerhard Behre,Wolfgang Hiddemann,Daniel G. Tenen +8 more
TL;DR: This is the first report of CEBPA mutations in human neoplasia, and such mutations are likely to induce the differentiation block found in AML.
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CCAAT/enhancer binding protein alpha is a regulatory switch sufficient for induction of granulocytic development from bipotential myeloid progenitors
TL;DR: It is shown that C/EBPα serves as a myeloid differentiation switch acting on bipotential precursors and directing them to mature to granulocytes and is specifically upregulated during granulocytic differentiation.
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Negative cross-talk between hematopoietic regulators: GATA proteins repress PU.1.
Pu Zhang,Gerhard Behre,Jing Pan,Atsushi Iwama,Nawarat Wara-aswapati,Hanna S. Radomska,Philip E. Auron,Daniel G. Tenen,Zijie Sun +8 more
TL;DR: Interactions between PU.1 and GATA proteins play a critical role in the decision of stem cells to commit to erythroid vs. myeloid lineages, suggesting that normal hematopoietic lineage development is under threat.
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The polymorphism rs944289 predisposes to papillary thyroid carcinoma through a large intergenic noncoding RNA gene of tumor suppressor type
Jarosław Jendrzejewski,Huiling He,Hanna S. Radomska,W. G. Li,Jerneja Tomsic,Sandya Liyanarachchi,Ramana V. Davuluri,Rebecca Nagy,Albert de la Chapelle +8 more
TL;DR: The data suggest that SNP rs944289 predisposes to PTC through a previously uncharacterized, long intergenic noncoding RNA gene (PTCSC3) that has the characteristics of a tumor suppressor.
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Block of C/EBPα function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations
Hanna S. Radomska,Daniela S. Basseres,Rui Zheng,Pu Zhang,Tajhal Dayaram,Yukiya Yamamoto,David W. Sternberg,Nathalie Lokker,Neill A. Giese,Stefan K. Bohlander,Susanne Schnittger,Marie Helene Delmotte,Roger J. Davis,Donald Small,Wolfgang Hiddemann,D. Gary Gilliland,Daniel G. Tenen +16 more
TL;DR: It is found that activation of FLT3 in human AML inhibits CCAAT/enhancer binding protein α (C/EBPα) function by ERK1/2-mediated phosphorylation, which may explain the differentiation block of leukemic blasts.