Julian Walfridsson group - Acute myeloid leukemia (AML)

Acute myeloid leukemia (AML) is an aggressive hematological disorder with dismal prognosis. Consequently, there is an unmet medical need to achieve increased understanding of factors and effectors that drives the disease and to develop effective and targeted treatments with acceptable side effects.

About our research

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


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

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.

The projects aim 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.


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

Group leader

Julian Walfridsson

Principal researcher
H7 Department of Medicine, Huddinge

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). He did a postdoc at the Biotech Research Innovation Centre (BRIC), University of Copenhagen, Denmark (2007-2010).

Group members

I work in the Walfridsson group as an Industrial PhD Student, in collaboration with Sprint Bioscience. The project aims to identify novel drug targets for treatment of Acute Myeloid Leukemia, and it is funded by Stiftelsen för Strategisk Forskning (SSF).

I have a background in Biotechnologies from University of Parma, Italy.

Former group member:

  • Dr. Joanna Zawacka-Pankau, Senior Researcher / Team Leader

Research support

  • Wallenberg Institute for Regenerative Medicine (WIRM)
  • Cancerfonden
  • Åke Wibergs Stiftelse
  • Magnus Bergvalls Stiftelse
  • Åke Olssons Stiftelse

Selected publications

Link to all publications on PubMed

  1. Critical role of Lama4 for hematopoiesis regeneration and acute myeloid leukemia progression. Cai H, Kondo M, Sandhow L, Xiao P, Johansson AS, Sasaki T, Zawacka-Pankau J, Tryggvason K, Ungerstedt J, Walfridsson J, Ekblom M, Qian H. Blood. 2022 May 19;139(20):3040-3057. doi: 10.1182/blood.2021011510.
  2. MTH1 Inhibitor TH1579 Induces Oxidative DNA Damage and Mitotic Arrest in Acute Myeloid Leukemia. Sanjiv K, Calderón-Montaño JM, Pham TM, Erkers T, Tsuber V, Almlöf I, Höglund A, Heshmati Y, Seashore-Ludlow B, Nagesh Danda A, Gad H, Wiita E, Göktürk C, Rasti A, Friedrich S, Centio A, Estruch M, Våtsveen TK, Struyf N, Visnes T, Scobie M, Koolmeister T, Henriksson M, Wallner O, Sandvall T, Lehmann S, Theilgaard-Mönch K, Garnett MJ, Östling P, Walfridsson J, Helleday T, Warpman Berglund U. Cancer Res. 2021 Nov 15;81(22):5733-5744. doi: 10.1158/0008-5472.CAN-21-0061. Epub 2021 Sep 30. 
  3. The histone chaperone NAP1L3 is required for haematopoietic stem cell maintenance and differentiation. Heshmati Y, Kharazi S, Türköz G, Chang D, Kamali Dolatabadi E, Boström J, Krstic A, Boukoura T, Wagner E, Kadri N, Månsson R, Altun M, Qian H, Walfridsson J. Sci Rep. 2018 Jul 25;8(1):11202. doi: 10.1038/s41598-018-29518-z. 
  4. Distinct roles of mesenchymal stem and progenitor cells during the development of acute myeloid leukemia in mice. Xiao P, Sandhow L, Heshmati Y, Kondo M, Bouderlique T, Dolinska M, Johansson AS, Sigvardsson M, Ekblom M, Walfridsson J, Qian H. Blood Adv. 2018 Jun 26;2(12):1480-1494. doi: 10.1182/bloodadvances.2017013870.  
  5. The chromatin-remodeling factor CHD4 is required for maintenance of childhood acute myeloid leukemia. Heshmati Y, Türköz G, Harisankar A, Kharazi S, Boström J, Dolatabadi EK, Krstic A, Chang D, Månsson R, Altun M, Qian H, Walfridsson J. Haematologica. 2018 Jul;103(7):1169-1181. doi: 10.3324/haematol.2017.183970. Epub 2018 Mar 29.  
Content reviewer: