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Epigenetic agent treatment through reactivation of repressed, haploinsufficient tumour suppressor genes in high-risk AML (C04)

Subject Area Hematology, Oncology
Term since 2012
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 192904750
 
Patients with adverse-genetics AML show remarkable responses to DNA-hypomethylating agents such as decitabine (DAC). We hypothesised that haploinsufficiency of tumour suppressor genes in monosomal AML is compounded by epigenetic silencing. We identified several genes, including Endogenous Retrovirus (ERV)3-1, that are preferentially de-repressed by DAC in AML cell lines. We will conduct a systematic analysis of endogenous retroviruses and other transposable elements regulated by DAC in our cell models. We aim to identify predictors of response to this treatment and to unravel non-genetic resistance mechanisms operative in AML blasts.
DFG Programme Collaborative Research Centres
Applicant Institution Albert-Ludwigs-Universität Freiburg
 
 

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