Julian Walfridsson group

Our knowledge of the genes and regulatory pathways that are involved in initiation, maintenance and development of acute myeloid leukemia (AML) remains incompletely understood. As a consequence, the development of more efficient treatments against AML has been limited and the prognosis remains unsatisfactory.

The main focus of our research is to discover factors and pathways that can serve as potential drug targets in AML and to delineate the underlying molecular mechanisms by which these effectors are involved in pathogenesis. With this objective we use functional genomic techniques, in vivo models, patient derived cells and cell- and molecular biology techniques. 

Keywords: AML, RNAi screening, functional genomics, epigenetics, in vivo cancer models, molecular mechanisms


Julian Walfridsson,Group Leader, Ph.D., Assistant Professor

Dr. Walfridsson was recruited to Karolinska Institutet as an assistant professor in 2011. He holds a Ph.D. degree in Cell and Molecular Biology at Karolinska Institutet, Sweden (2000) and did a postdoc at the Biotech Research Innovation Centre (BRIC), University of Copenhagen, Denmark (2007-2010).

Yaser Heshmati, Doctoral student

He was awarded a Master of Science in Human Genetics at the University of  Social Welfare and Rehabilitation Sciences, Teheran, Iran, in 2010.

Phone: +46 (08) 585 83623

Aditya Harisankar, Doctoral student

He was awarded a Master of Science in Applied Biotechnology, at Uppsala University, Uppsala, in 2012.

Phone: +46 (08) 585 83623

Gözde Türköz, Doctoral student

She was awarded a Master of Science in Health Sciences, at Mersin University, Mersin, Turkey, in 2009.

Phone: +46 (08) 585 83623

Esmat Kamali Dolatabadi, PhD, Postdoc

She was awarded a PhD in Cellular and Molecular Biology at Teheran Islamic Azad University, Tehran, Iran, in 2013.

Phone: +46 (08) 585 83623


Acute myeloid leukemia (AML) is an aggressive blood cancer and less than 20% of adults and only about 60% of the children are cured of their disease, highlighting the urgent need of more effective treatment strategies.

Although the mechanisms of the disease remain incompletely understood, it is well established that cooperating genetic and epigenetic alterations contribute to AML pathogenesis. Various studies have demonstrated that individual AML tumor samples contain several hundreds to thousands of different gene mutations. The consequence of these genetic and epigenetic alterations is a widespread transcriptional deregulation of gene expression that give the cancer cells a proliferative growth advantage compared to normal cells. For the vast majority of these abnormalities it is not known which genes or downstream regulatory pathways that contribute to the initiation, maintenance and development of AML.

Current projects in our research group aims to identify and characterize novel biologically and clinically relevant genes with a role in AML pathogenesis and maintenance.

Specifically the projects aims to:

  1. Identify and characterize novel “druggable” epigenetic target genes that can serve as potential therapeutic targets to battle AML.
  2.  Functionally annotate the causative mutations that are involved in AML pathogenesis.
  3. Determine the underlying molecular mechanisms by which the identified target genes contribute to AML pathogenesis and tumor expansion.

Towards these goals, we have established a cutting-edge technical and methodological platform, including flow cytometry, genome-wide mapping and analysis of epigenetic modifications (ChIP-sequencing and MeDIP-Seq), large-scale genetic screening systems, patient-derived AML cells and in vivo AML model systems.

The ultimate aim is that the proposed strategy can lead to the discovery of relevant drug targets that can facilitate the development of novel therapeutic interventions in AML treatment.

Financial support

  • Wallenberg Institute for Regenerative Medicine (WIRM)

  • Cancerfonden

  • Åke Wibergs Stiftelse

  • Magnus Bergvalls Stiftelse

  • Åke Olssons Stiftelse

Selected publications

Vulnerability of glioblastoma cells to catastrophic vacuolization and death induced by a small molecule.
Kitambi S, Toledo E, Usoskin D, Wee S, Harisankar A, Svensson R, et al
Cell 2014 Apr;157(2):313-28

shRNA screening identifies JMJD1C as being required for leukemia maintenance.
Sroczynska P, Cruickshank V, Bukowski J, Miyagi S, Bagger F, Walfridsson J, et al
Blood 2014 Mar;123(12):1870-82

The FUN30 chromatin remodeler, Fft3, protects centromeric and subtelomeric domains from euchromatin formation.
Strålfors A, Walfridsson J, Bhuiyan H, Ekwall K
PLoS Genet. 2011 Mar;7(3):e1001334

A chromatin-remodeling protein is a component of fission yeast mediator.
Khorosjutina O, Wanrooij P, Walfridsson J, Szilagyi Z, Zhu X, Baraznenok V, et al
J. Biol. Chem. 2010 Sep;285(39):29729-37

Characterization of an antagonistic switch between histone H3 lysine 27 methylation and acetylation in the transcriptional regulation of Polycomb group target genes.
Pasini D, Malatesta M, Jung H, Walfridsson J, Willer A, Olsson L, et al
Nucleic Acids Res. 2010 Aug;38(15):4958-69

JARID2 regulates binding of the Polycomb repressive complex 2 to target genes in ES cells.
Pasini D, Cloos P, Walfridsson J, Olsson L, Bukowski J, Johansen J, et al
Nature 2010 Mar;464(7286):306-10

ATAD2 is a novel cofactor for MYC, overexpressed and amplified in aggressive tumors.
Ciró M, Prosperini E, Quarto M, Grazini U, Walfridsson J, McBlane F, et al
Cancer Res. 2009 Nov;69(21):8491-8

A genome-wide role for CHD remodelling factors and Nap1 in nucleosome disassembly.
Walfridsson J, Khorosjutina O, Matikainen P, Gustafsson C, Ekwall K
EMBO J. 2007 Jun;26(12):2868-79

Interaction of Epe1 with the heterochromatin assembly pathway in Schizosaccharomyces pombe.
Isaac S, Walfridsson J, Zohar T, Lazar D, Kahan T, Ekwall K, et al
Genetics 2007 Apr;175(4):1549-60

Genome-wide studies of histone demethylation catalysed by the fission yeast homologues of mammalian LSD1.
Opel M, Lando D, Bonilla C, Trewick S, Boukaba A, Walfridsson J, et al
PLoS ONE 2007 Apr;2(4):e386

The CHD remodeling factor Hrp1 stimulates CENP-A loading to centromeres.
Walfridsson J, Bjerling P, Thalen M, Yoo E, Park S, Ekwall K
Nucleic Acids Res. 2005 ;33(9):2868-79

Dicer is required for chromosome segregation and gene silencing in fission yeast cells.
Provost P, Silverstein R, Dishart D, Walfridsson J, Djupedal I, Kniola B, et al
Proc. Natl. Acad. Sci. U.S.A. 2002 Dec;99(26):16648-53

HematologyRegenerative Medicine