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Activating c-KIT mutations confers oncogenic cooperativity and rescue RUNX1-ETO induced DNA-damage in human cells

ABSTRACT: REtr causes genomic instability in U937 cells. Activated forms of c-KIT, like c-KIT(N822K), rescues the Retr induced genomic instability by increasing the rate of DNA repair by homologous recombination

ORGANISM(S): Homo sapiens

PROVIDER: GSE57658 | GEO | 2014/07/29

SECONDARY ACCESSION(S): PRJNA247464

REPOSITORIES: GEO

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Activating c-KIT mutations confers oncogenic cooperativity and rescue RUNX1-ETO induced DNA-damage in human cells

Project description:REtr causes genomic instability in U937 cells. Activated forms of c-KIT, like c-KIT(N822K), rescues the Retr induced genomic instability by increasing the rate of DNA repair by homologous recombination Human U937 cells were transduced with retroviral vectors encoding REtr or c-KIT(N822K), expanded in culture and FACS selected prior to molecular analysis

2014-07-29 | E-GEOD-57658 | biostudies-arrayexpress

Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1-ETO-induced DNA damage in human cells

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Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1-ETO-induced DNA damage in human cells

Project description:REtr causes genomic instability in human CD34+ cells. Activated forms of c-KIT, like c-KIT(N822K), rescue the REtr-induced genomic instability by increasing the rate of DNA repair by homologous recombination. Human CD34+ hematopoietic progenitor cells were transduced with retroviral vectors encoding c-KIT(N822K) or mock control vectors, expanded in culture and FACS selected prior to molecular analysis.

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RUNX1/ETO and mutant KIT both contribute to programming the transcriptional and chromatin landscape in t(8;21) AML (ATAC-Seq)

Project description:Acute myeloid leukemia development occurs in a step-wise fashion whereby an original driver mutation is followed by additional mutations. The first type of mutations tends to be in genes encoding members of the epigenetic/transcription regulatory machinery (i.e. RUNX1, DNMT3, TET2), while the secondary mutations often involve genes encoding members of signalling pathways that cause uncontrolled growth of such cells such as the growth factor receptors c-KIT of FLT3. Patients usually present with both types of mutations, but it is currently unclear how both mutational events shape the epigenome in developing AML cells. To this end we generated an in vitro model of t(8;21) AML by expressing its driver oncoprotein RUNX1-ETO with or without a mutated (N822K) KIT protein. The expression of N822K–c-KIT strongly increases the self-renewal capacity of RUNX1-ETO expressing cells. Global analysis of gene expression changes and alterations in the epigenome show that N822K–c-KIT expression profoundly influences the open chromatin landscape and transcription factor binding. However, our experiments also show that double mutant cells still differ from their patient derived counterparts, highlighting the importance of studying patient cells to obtain a true picture of how gene regulatory networks have been reprogrammed during tumourigenesis.

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RUNX1/ETO and mutant KIT both contribute to programming the transcriptional and chromatin landscape in t(8;21) AML (RNA-Seq)

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RUNX1/ETO and mutant KIT both contribute to programming the transcriptional and chromatin landscape in t(8;21) AML (ChIP-Seq)

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