Cookie Settings

We use cookies to optimize our website. These include cookies that are necessary for the operation of the site, as well as those that are only used for anonymous statistic. You can decide for yourself which categories you want to allow. Further information can be found in our data privacy protection .


These cookies are necessary to run the core functionalities of this website and cannot be disabled.

Name Webedition CMS
Purpose This cookie is required by the CMS (Content Management System) Webedition for the system to function correctly. Typically, this cookie is deleted when the browser is closed.
Name econda
Purpose Session cookie emos_jcsid for the web analysis software econda. This runs in the “anonymized measurement” mode. There is no personal reference. As soon as the user leaves the site, tracking is ended and all data in the browser are automatically deleted.

These cookies help us understand how visitors interact with our website by collecting and analyzing information anonymously. Depending on the tool, one or more cookies are set by the provider.

Name econda
Purpose Statistics
External media

Content from external media platforms is blocked by default. If cookies from external media are accepted, access to this content no longer requires manual consent.

Name YouTube
Purpose Show YouTube content
Name Twitter
Purpose activate Twitter Feeds

Division of Experimental Hematology

Dr. Michael Milsom

Long-term effects of inflammatory exposure on HSC functional activity as a likely driver of hematologic aging
Picture: Cell Press

Advancing age is amongst the highest risk factors for development of most major cancer entities and also strongly correlates with poor response to therapy. The Division of Experimental Hematology uses the hematopoietic system as an experimentally tractable model tissue to investigate the fundamental biological principles underlying the process of aging, including age-associated malignant transformation. Our work encompasses the study of molecular events that mediate cellular aging; the environmental factors that impact upon the aging process; and the interplay between hematopoietic and non-hematopoietic cells that lead to age-associated diseases of the blood system and other organs. In addition to furthering our understanding of this complex multi-factorial process, our goal is to identify potential new strategies to delay, prevent or treat some of the clinically relevant features of aging.

Typical features of aged hematopoiesis that are of relevance to age-associated disease include increased likelihood of developing hematologic malignancies, anemia, dysregulated immune function (both immune suppression and pro-inflammatory hyperactivation), elevated platelet activation, decreased reserves of functional hematopoietic stem cells (HSCs), and a progression towards the development of “clonal hematopoiesis”. Our work focusses on gaining insight into the genetic, environmental and stochastic processes that drive the age-related evolution of these clinically-relevant processes in some individuals. To these ends, our research can be broadly divided into three research topics, which generally investigate the role that HSC exhaustion plays in mediating hematopoietic aging:

Dr. Milsom is also a group leader at the Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM), a public-private partnership between the DKFZ and the Dietmar Hopp Foundation. Further detail can be found here.


Dr. Michael Milsom
Experimental Hematology (A012)

Deutsches Krebsforschungszentrum and Heidelberg Institut für Stammzelltechnologie und experimentelle Medizin (HI-STEM GmbH)
Im Neuenheimer Feld 280
69120 Heidelberg

Tel.: +49 6221 42 3901

Selected Publications

  • Bogeska R., et al. Inflammatory exposure drives long-lived impairment of hematopoietic stem cell self-renewal activity and accelerated aging. Cell Stem Cell 29:1273-1284 (2022).
  • Cagan A., et al. Somatic mutation rates scale with lifespan across mammals. Nature 604:517-524 (2022).
  • Scheller M., et al. DNMT3AR882 mutations in Clonal Hematopoiesis and Acute Myeloid Leukemia specifically sensitize cells to Azacytidine via endogenous retrovirus and Interferon network activation. Nat. Cancer. 2:527-544 (2021)
  • Malehmir M., et al. Platelet-derived GP1b? is a mediator and potential interventional target for NASH and subsequent liver cancer. Nat. Med. 25:641-655 (2019)
to top
powered by webEdition CMS