SUPR
Epigenetic regulation of AML
Dnr:

sens2017542

Type:

SNIC SENS

Principal Investigator:

Andreas Lennartsson

Affiliation:

Karolinska Institutet

Start Date:

2017-12-08

End Date:

2024-08-01

Primary Classification:

30202: Hematology

Allocation

  • Castor /proj/nobackup at UPPMAX: 4000 GiB
  • Castor /proj at UPPMAX: 4000 GiB
  • Cygnus /proj at UPPMAX: 4000 GiB
  • Cygnus /proj/nobackup at UPPMAX: 4000 GiB
  • Bianca at UPPMAX: 2 x 1000 core-h/month

Abstract

Acute myeloid leukemia (AML) has a poor prognosis in both adults and children, with a long-term survival of only 20% and 60% respectively. No major development has occurred of the treatment the last decades and the majority of treatments for AML consist of cytotoxic drugs with low specificity. Most patients respond well to the treatment, but commonly relapse. The relapse is frequently caused by dormant leukemic stem cells (LSC) that survive the cytotoxic treatment. AML is associated with perturbed epigenetic regulation, with early mutations in and chromosomal translocations of different epigenetic regulators, that create leukemic stem cells. Therefore, epigenetic drugs that target the leukemic stem cells are very likely to increase the survival of AML patients. To be able to chose appropriate epigenetic treatment the epigenetic landscape in AML patients first needs to be thoroughly characterized. This project aims to dissect the genome-wide epigenetic landscape in AML patients using ChIP-seq, ATAC-seq, WGBS and RNA-seq.