Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human AML1-ETO transduced cord blood cells, CD34 selected, compared to normal cord blood cells, CD34 selected


ABSTRACT: AML1-ETO expression in normal human umbilical cord blood CD34+ cells leads to long-term proliferation of an early self-renewing primitive progenitor cell with multilineage potential and stem cell ability, but these cells do not induce leukemia in immunodeficient mice. This comparative microarray study was initiated to determine the differences in the transcriptome of AML-ETO-expressing CD34+ cells after extended culture in vitro, using normal cord blood cells expanded for 6-8 weeks in vitro and subsequently purified for the CD34+ population as the control comparison. Experiment Overall Design: We have established a culture system whereby we retrovirally transduce human CD34+ cells, obtained from cord blood, with the leukemia fusion gene AML1-ETO. Cells expressing this fusion protein are able to proliferate long-term in vitro in a cytokine dependent manner. AML1-ETO-expressing cord blood cells have a large population of primitive self-renewing CD34+ cells with continued abnormal differentiation. We grow these cells in serum-free conditions using the BIT supplement from Stem Cell Technologies. For the current experiments we used cell cultures that had been proliferating in vitro for 8-12 weeks, in a cytokine cocktail of SCF, TPO, FLT3L, IL-6 all at 20 ng/mL and IL-3 at 10 ng/mL. Control cord blood samples that were CD34 purified were expanded for 5-8 weeks in the same culture media as used for AML1-ETO cells. All samples were magnetically selected for the CD34+ population, returned to culture, and one week later again selected for CD34+ cells and then lysed for RNA isolation.

ORGANISM(S): Homo sapiens

SUBMITTER: James Mulloy 

PROVIDER: E-GEOD-8023 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death.

Krejci Ondrej O   Wunderlich Mark M   Geiger Hartmut H   Chou Fu-Sheng FS   Schleimer David D   Jansen Michael M   Andreassen Paul R PR   Mulloy James C JC  

Blood 20071101 4


Chromosomal translocation (8;21) is present in 10% to 15% of patients with acute myeloid leukemia. Expression of the AML1-ETO (AE) fusion protein alone is not sufficient to induce leukemia, but the nature of the additional genetic alterations is unknown. It is unclear whether AE facilitates acquisition of these cooperating events. We show that AE down-regulates genes involved in multiple DNA repair pathways, potentially through a mechanism involving direct binding at promoter elements, and incre  ...[more]

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