Study

Oncogenic fate conversion by PRDM16s causes acute myeloid leukemia

Study ID Alternative Stable ID Type
EGAS00001003235 Other

Study Description

Oncogenic mutations confer aberrant replicative capacity to cells with little or no replicative capacity, generating cancer stem cells that perpetuate the tumor through extensive self-replication and differentiation blockade. However, whether oncogenes disrupt the cellular identity ofcancer stem cell by altering the developmental potential is unknown. Fate conversion has been demonstrated by ectopic expression of master transcriptional regulators, such as PU.1 and C/EBP alpha that confers myeloid cell fate to other cell types, and PRDM16 that confers brown adipose fate to white adipocytes or myoblasts. Here we show that a transcriptional regulator overexpressed in human myeloid malignancies, PRDM16s, causes oncogenic fate conversion, by transforming cells fated to form platelets and erythrocytes into myeloid leukemia-initiating cells (LICs). Prdm16s expression in hematopoietic progenitor cells caused a myelodysplastic syndrome (MDS)-like disease that progressed to acute myelogenous leukemia (AML). The myeloid diseases caused by Prdm16s exhibited expansion of megakaryocyte-erythroid ... (Show More)

Study Datasets 2 datasets.

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Dataset ID Description Technology Samples
EGAD00001004359
4 WGS bam files for 4 cases with fusion
Illumina HiSeq 2000 4
EGAD00001004360
10 RNA-Seq bam files including 4 cases with fusion and 6 controls without fusion.
Illumina HiSeq 2000 10

Who archives the data?

There are no publications available