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Group David Bryder

Research summary

Hematopoietic (blood) stem cells (HSCs) represent a very rare - but highly potent - cell type located in the bone marrow. HSCs associate with two main attributes;

  1. their intrinsic capacity to give rise to all of the different types of blood cells, and
  2. their ability to give rise to new HSCs.

These two properties enable an individual to maintain blood cell formation over a lifetime from a relatively few number of cells. It is also these two properties that are utilized in the clinical use of bone marrow transplantation, a clinical treatment modality in which HSCs can rebuild a completely new blood system.

The research of our group focus on how the blood system, and HSCs in particular, is regulated in situations such as infections, stress, aging and leukemia (cancer of blood cells). While HSCs are associated with a fairly clear functional definition regarding their developmental and self-renewal potential, all HSCs do not behave the same.

For instance, HSCs in aged individuals have a dramatically reduced ability to develop into blood cells involved in adaptive immunity (T and B cells). It has been proposed that such preferences for differentiation, at the level of HSCs, might underlie the dramatically increased predisposition for myeloid malignancies with age. Therefore, our goal is to understand, at cellular and molecular levels, what controls the fate of HSCs.

The traditional experimental paradigm for such work is the use of transplantation-based models. However, recent studies from our laboratory have demonstrated that HSC behavior in the transplantation setting is fundamentally different from their normal behavior. We believe knowledge derived from such alternative model systems should be of relevance from both preventive and therapeutic perspectives, including for broadening of HSC transplantation as a therapy and for the development of therapies based on in situ manipulation of HSCs.

Research tools and resources

In our research, we use advanced cell sorting and a range of cellular and molecular biology techniques, including next-generation sequencing and Cas9/CRISPR-based approaches. Integral to our work is also the application and development of novel transgenic mouse models. As cellular heterogeneity is a critical parameter in our work, much of our work aims to characterize cellular responses at the single cell level.

Current group members

David Bryder, PhD, Professor
Anna Hogmalm, PhD, Lab manager
Vimala Antonydhason, PhD, Post-doc
Qinyu Zhang, PhD, Post-doc
Daniel Sjövall, MD student, Amanuens
Froste Svensson, Project Assistant

Pekka Jaako, PhD, (senior) Post-doc
Anna Staffas, PhD, (senior) Post-doc

Selected publications

  1. Hif-1α Deletion May Lead to Adverse Treatment Effect in a Mouse Model of MLL-AF9-Driven AML.
    Velasco-Hernandez T, Soneji S, Hidalgo I, Erlandsson E, Cammenga J, Bryder D. Stem Cell Reports. 2019 Jan 8;12(1):112-121.
  2. Murine HSCs contribute actively to native hematopoiesis but with reduced differentiation capacity upon aging.
    Säwen P, Eldeeb M, Erlandsson E, Kristiansen TA, Laterza C, Kokaia Z, Karlsson G, Yuan J, Soneji S, Mandal PK, Rossi DJ, Bryder D. Elife. 2018 Dec 18;7.
  3. Immunoediting is not a primary transformation event in a murine model of MLL-ENL AML.
    Dudenhöffer-Pfeifer M, Bryder D. Life Sci Alliance. 2018 Jul 10;1(4):e201800079.
  4. Critical modulation of hematopoietic lineage fate by Hepatic Leukemia Factor.
    Wahlestedt M, Ladopoulos V, Hidalgo I, Castillo MS, Hannah R, Säwén P, Wan H, Dudenhöffer-Pfeifer M, Magnusson M, Norddahl GL, Göttgens B and Bryder D.  Cell Rep. 2017 Nov 21;21(8):2251-2263.
  5. Clonal reversal of ageing-associated stem cell lineage bias via a pluripotent intermediate.
    Wahlestedt M, Erlandsson E, Kristiansen T, Lu R, Brakebusch C, Weissman IL, Yuan J, Martin-Gonzalez J, Bryder D. Nat Commun. 2017 Feb 22;8:14533.
  6. Mitotic History Reveals Distinct Stem Cell Populations and Their Contributions to Hematopoiesis.
    Säwén P, Lang S, Mandal P, Rossi DJ, Soneji S, Bryder D. Cell Rep. 2016 Mar 29;14(12):2809-18.
  7. Hematopoietic stem cells are intrinsically protected against MLL-ENL-mediated transformation.
    Ugale A*, Norddahl GL*, Wahlestedt M, Säwén P, Jaako P, Pronk CJ, Soneji S, Cammenga J, Bryder D.  Cell Rep. 2014 Nov 20;9(4):1246-55.
  8. An epigenetic component of hematopoietic stem cell aging amenable to reprogramming into a young state.
    Wahlestedt M, Norddahl GL, Sten G, Ugale A, Frisk MA, Mattsson R, Deierborg T, Sigvardsson M, Bryder D. Blood. 2013 May 23;121(21):4257-64.
  9. Accumulating mitochondrial DNA mutations drive premature hematopoietic aging phenotypes distinct from physiological stem cell aging.
    Norddahl GL, Pronk CJ, Wahlestedt M, Sten G, Nygren JM, Ugale A, Sigvardsson M, Bryder D. Cell Stem Cell. 2011 May 6;8(5):499-510.
  10. Elucidation of the phenotypic, functional, and molecular topography of a myeloerythroid progenitor cell hierarchy.
    Pronk CJ*, Rossi DJ*, Månsson R, Attema JL, Norddahl GL, Chan CK, Sigvardsson M, Weissman IL, Bryder D. Cell Stem Cell. 2007 Oct 11;1(4):428-42.


More group David Bryder publications on PubMed


Contact information

David Bryder

E-mail: David Bryder
Phone: +46 (0)31 786 6210

Visiting address:
Sahlgrenska Center
for Cancer Research,
Medicinaregatan 1F
413 90 Gothenburg

Page Manager: Yael Zukovsky Fitoussi|Last update: 7/2/2020

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