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The Capital Region of Denmark - a part of Copenhagen University Hospital
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Oncogenic fusion proteins expressed in immature hematopoietic cells fail to recapitulate the transcriptional changes observed in human AML

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

    Research output: Contribution to journalJournal articleResearchpeer-review

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

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

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

    Research output: Contribution to journalJournal articleResearchpeer-review

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

    Research output: Contribution to journalJournal articleResearchpeer-review

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Reciprocal chromosomal translocations are observed in one-third of acute myeloid leukemia (AML) cases. Targeting and understanding the effects of the resulting aberrant oncogenic fusion proteins may help developing drugs against specific leukemic subtypes, as demonstrated earlier by the use of ATRA in acute promyelocytic leukemia. Hematopoietic stem/progenitor (HSPCs) cells transduced with oncogenic fusion genes are regarded as promising in vitromodels of their corresponding AML subtypes. Here, we critically assessed the potential of such in vitro models using an integrative bioinformatics approach. Surprisingly, we found that the gene-expression profiles of CD34+ human HSPCs transformed with the potent oncogenic fusion proteins AML-ETO or MLL-AF9, only weakly resembled those derived from primary AML samples. Hence, our work raises concerns as to the relevance of the use of in vitro transduced cells to study the impact of transcriptional deregulation in human AML.

Original languageEnglish
JournalOncogenesis
Volume3
Pages (from-to)e106
ISSN2157-9024
DOIs
Publication statusPublished - 16 Jun 2014

ID: 44353160