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Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Lack of the p42 form of C/EBPα leads to spontaneous immortalization and lineage infidelity of committed myeloid progenitors

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  1. The frequency and severity of epistaxis in children with sickle cell anaemia in eastern Uganda: a case-control study

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  2. Lack of topoisomerase copy number changes in patients with de novo and relapsed diffuse large B-cell lymphoma

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  1. Mutant CEBPA directly drives the expression of the targetable tumor-promoting factor CD73 in AML

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Heterozygous loss of Srp72 in mice is not associated with major hematological phenotypes

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. A programmed wave of uridylation-primed mRNA degradation is essential for meiotic progression and mammalian spermatogenesis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. The splicing factor RBM25 controls MYC activity in acute myeloid leukemia

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. BloodSpot: a database of healthy and malignant haematopoiesis updated with purified and single cell mRNA sequencing profiles

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Acute myeloid leukemia (AML) develops via a multistep process involving several genetic and epigenetic events, which ultimately leads to the formation of a heterogeneous population of malignant cells, of which only a small subpopulation termed the leukemia initiating cell (LIC) is able to sustain the leukemia. The identity of the LIC is highly diverse and ranges from populations resembling hematopoietic stem cells or multipotent progenitors (MPPs) to more committed myeloid progenitors, and the question still remains whether this is a direct consequence of which cells are targets of the final transforming events. In this study, we use premalignant cells from a Cebpa mutant AML model, in which the LIC population resembles granulocyte-macrophage progenitors (GMPs), to show that premalignant GMPs undergo spontaneous immortalization with a high clonal frequency when cultured in vitro, suggesting that these cells constitute the target of the final transforming events. Furthermore, we show that premalignant GMPs are characterized by a distinct T cell gene expression signature correlating with an increased potential for differentiation toward the T cell lineage. These findings have implications for our understanding of the transcriptional wiring in premalignant myeloid progenitors and how this contributes to the development of AML.
OriginalsprogEngelsk
TidsskriftExperimental Hematology
Vol/bind41
Udgave nummer10
Sider (fra-til)882-93
ISSN0301-472X
DOI
StatusUdgivet - 2 jul. 2013

ID: 38945858