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ChIP-seq of EGR1 in human primary unstimulated monocytes and in unstimulated human monocytes from three CMML patients

ABSTRACT: Identification of EGR1 chromatin localization in human primary monocytes (2 donors), in human primary monocytes from 2 CMML patients with TET2 truncating mutations (high VAF) and in human primary monocytes from 1 CMML patients with TET2 truncating mutations with low VAF.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER: Nathalie Droin

PROVIDER: E-MTAB-11132 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ChIP-seq of CSF-1R, H3K4me1, H3K4me3 in human primary unstimulated monocytes and monocytes differentiated 72h with CSF-1 (3 healthy donors buffy coat) and in monocytes from two CMML patients and one healthy donor, EGR1 ChIP-seq in unstimulated monocytes (3 healthy donors buffy coat)

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ChIP-seq of EGR1 in human primary unstimulated monocytes and in unstimulated human monocytes from three CMML patients

Project description:ChIP-seq of EGR1 in human primary unstimulated monocytes and in unstimulated human monocytes from three CMML patients

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The Transcriptome Of Cmml Monocytes Is Highly Inflammatory And Reflects Leukemia-Specific And Age-Related Alterations

Project description:Chronic myelomonocytic leukemia (CMML) is an aggressive myeloid neoplasm of older individuals characterized by persistent monocytosis. Somatic mutations in CMML are heterogeneous and only partially explain the variability in clinical outcomes. Recent data suggest that cardiovascular morbidity is increased in CMML and contributes to reduced survival. Clonal hematopoiesis of indeterminate potential (CHIP), the presence of mutated blood cells in hematologically normal individuals, is a precursor of age-related myeloid neoplasms and associated with increased cardiovascular risk. To isolate CMML-specific alterations from those related to aging, we performed RNA sequencing and DNA methylation profiling on purified monocytes from CMML patients and from age-matched (old) and young healthy controls. We found that the transcriptional signature of CMML monocytes is highly pro-inflammatory, with upregulation of multiple inflammatory pathways, including tumor necrosis factor, IL-6 and IL-17 signaling, while age per se does not significantly contribute to this pattern. We observed no consistent correlations between aberrant gene expression and CpG island methylation, suggesting that pro-inflammatory signaling in CMML monocytes is governed by multiple and complex regulatory mechanisms. We propose that pro-inflammatory monocytes may contribute to cardiovascular morbidity in CMML patients, and promote progression by selection of mutated cell clones. Our data raise questions whether asymptomatic CMML patients may benefit from monocyte-depleting or anti-inflammatory therapies.

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