Maria Wieske

ORCID: 0000-0003-4485-8802
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About
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Research Areas
  • Acute Myeloid Leukemia Research
  • Protein Degradation and Inhibitors
  • Histone Deacetylase Inhibitors Research
  • RNA Research and Splicing
  • Nuclear Structure and Function
  • Chronic Myeloid Leukemia Treatments

Goethe University Frankfurt
2018-2022

The WHO classifies t(6;9)-positive acute myeloid leukemia (AML) as a subgroup of high-risk AML because its clinical and biological peculiarities, such young age therapy resistance. t(6;9) encodes the DEK/NUP214 fusion oncoprotein that targets only small subpopulation bone marrow progenitors for leukemic transformation. This distinguishes from other oncoproteins, PML/RARα, RUNX1/ETO, or MLL/AF9, which have broad target population they block differentiation increase stem cell capacity. A...

10.1371/journal.pgen.1010463 article EN cc-by PLoS Genetics 2022-10-26

Summary Acute myeloid leukemias (AML) are characterized by recurrent genomic alterations, often in transcriptional regulators, which form the basis on current prognostication and therapeutic intervention is overlaid. In AML transformation can be attributed to single chromosomal aberrations encoding oncogenes, such as t(15;17)-PML/RARα or t(6;9)-DEK/CAN but it unclear how these aberrant transcription factors drive leukemic signaling influence cellular responses targeted therapies. Here we...

10.1101/464958 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-11-07

Acute myeloid leukemias (AML) are characterized by recurrent genomic alterations, often in transcriptional regulators, which form the basis on current prognostication and therapeutic intervention is overlaid. In AML transformation can be attributed to single chromosomal aberrations encoding oncogenes, such as t(15;17)-PML/RARα or t(6;9)-DEK/CAN but it unclear how these aberrant transcription factors drive leukemic signaling influence cellular responses targeted therapies. Here we show that...

10.2139/ssrn.3305572 article EN SSRN Electronic Journal 2018-01-01

Patients within the WHO-subgroup of t(6;9)-positive acute myeloid leukemia (AML) differ from other AML subgroups as they are characterised by younger age and a grim prognosis. Leukemic transformation can often be attributed to single chromosomal aberrations encoding oncogenes, in case t(6;9)-AML fusion protein DEK-CAN (also called DEK-NUP214). As being rare disease there is urgent need for models t(6;9)-AML. The only cell line derived patient currently available FKH1. By using...

10.1007/s00277-022-04905-9 article EN cc-by Annals of Hematology 2022-08-08
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