Megan A. Hatlen

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The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that(More)
t(8;21) is one of the most frequent chromosomal abnormalities observed in acute myeloid leukemia (AML). However, expression of AML1-ETO is not sufficient to induce transformation in vivo. Consistent with this observation, patients with this translocation harbor additional genetic abnormalities, suggesting a requirement for cooperating mutations. To better(More)
Multiple myeloma is a plasma cell neoplasm with an extremely variable clinical course. Animal models are needed to better understand its pathophysiology and for preclinical testing of potential therapeutic agents. Hematopoietic cells expressing the hypermorphic Rad50(s) allele show hematopoietic failure, which can be mitigated by the lack of a transcription(More)
4–12% of acute myeloid leukemia (AML) patients present with a translocation between chromosomes 8 and 21 (Müller et al., 2008). However, transgenic mice expressing AML1-ETO only develop AML after treatment with muta-genic agents, suggesting a requirement for cooperating events (Higuchi et al., 2002). Two mouse models of AML1-ETO– driven AML have been(More)
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