Neuroglial Regulation of the Haematopoietic Stem Cell Niche in Acute Myeloid Leukaemia Transformation

Acute myeloid leukaemia (AML) is a highly aggressive type of cancer, where abnormal white blood cells grow fast and accumulate inside the bone cavity. AML is the most common acute leukaemia in adults, its incidence increases with age and the prognosis for the older patient remains bleak. Overcoming these problems will require better understanding of AML. It has been proposed that the presence of several lesions in the genetic information (DNA) of blood stem cells is required for AML development. This suggestion is based on the fact that some of these lesions, when present as sole alterations, are only able to induce chronic blood disorders in mouse models but not the transition to AML. Indeed, this indicates that other factors must participate in the process. These factors might comprise additional genetic lesions as previously suggested, but also specific alterations in the microenvironment that tightly controls the normal function of blood stem cells, which has received little consideration. This project will test the potential role of the bone marrow microenvironment in the transition from chronic to acute blood malignancies, and the importance of this to human AML. Thus, the results of this project have a strong translational potential. We will provide not only with insights into the basic processes that regulate blood stem cell function/dysfunction, but also with knowledge of early markers for patient diagnosis/prognosis and will apply this knowledge in search of novel therapies against AML.

Different aspects of this project have been funded by:

-UiT, University Hospital of Northern Norway (UNN) and The Regional Health Authorities of Northern Norway (Helse Nord) - Start-up package, 2014-2019

-The Research Council of Norway (Stem Cell Program) - Young Research Talent, 2015-2019

-The Norwegian Cancer Society (Kreftforeningen), 2015-2018

-The Regional Health Authorities of Northern Norway (Helse Nord), 2017-2019

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Last updated: 14.12.2016 11:08