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ABSTRACT: Clonal hematopoiesis of indeterminate potential patients with multiple myeloma

PROVIDER: PRJNA1089797 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28392758_1.fastq.gz	Fastqsanger.gz
	SRR28392758_2.fastq.gz	Fastqsanger.gz
	SRR28392759_1.fastq.gz	Fastqsanger.gz
	SRR28392759_2.fastq.gz	Fastqsanger.gz
	SRR28392760_1.fastq.gz	Fastqsanger.gz

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Project description:Mechanisms and Dynamics of Clonal Hematopoiesis of Indeterminate Potential

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Tet2-mediated clonal hematopoiesis in nonconditioned mice accelerates age-associated cardiac dysfunction

Project description:Clonal hematopoiesis of indeterminate potential is prevalent in elderly individuals and associated with increased risks of all-cause mortality and cardiovascular disease. However, mouse models to study the dynamics of clonal hematopoiesis and its consequences on the cardiovascular system under homeostatic conditions are lacking. We used a model of clonal hematopoiesis using adoptive transfer of unfractionated ten-eleven translocation 2-mutant (Tet2-mutant) bone marrow cells into nonirradiated mice. Consistent with age-related clonal hematopoiesis observed in humans, these mice displayed a progressive expansion of Tet2-deficient cells in multiple hematopoietic stem and progenitor cell fractions and blood cell lineages. The expansion of the Tet2-mutant fraction was also observed in bone marrow-derived CCR+ myeloid cell populations within the heart, but there was a negligible impact on the yolk sac-derived CCR2- cardiac resident macrophage population. Transcriptome profiling revealed an enhanced inflammatory signature in the donor-derived macrophages isolated from the heart. Mice receiving Tet2-deficient bone marrow cells spontaneously developed age-related cardiac dysfunction characterized by greater hypertrophy and fibrosis. Altogether, we show that Tet2- mediated hematopoiesis contributes to cardiac dysfunction in a nonconditioned setting that faithfully models the human clonal hematopoiesis in unperturbed bone marrow. Our data support clinical findings that clonal hematopoiesis per se may contribute to diminished health span.

2020-03-12 | GSE146812 | GEO

Nanostring immune profiling of air and cigarette smoke exposed wildtype bone marrow hematopoietic cells and Nanostring immune profiling of air and cigarette smoke exposed bone marrow hematopoietic cells from mice containing Jak2V617F mutant cells

Project description:Extrinsic stressors must have a role in driving clonal hematopoiesis since only a fraction of individuals with clonal hematopoiesis of indeterminate potential (CHIP) develop hematologic malignancy. Smoking behavior is associated with CHIP, but the effects of cigarette smoke on hematopoietic stem cells (HSCs) are unknown. The exploding use of electronic (E)-cigarettes has led to significant concern on their health effects. In this project, we aimed to determine the impact of cigarette smoke on the frequency and numbers of HSCs and inflammatory gene expression changes in bone marrow hematopoietic cells using wildtype mice. We also determined if cigarette smoke drives clonal expansion in mosaic mice containing both wildtype and Jak2V617F mutant cells. We also performed gene expression profiling on the wildtype fraction of bone marrow hematopoietic cells from mosaic mice exposed to cigarette smoke or air to determine if the presence of mutant cells alters the signature of wildtype cells.

2023-12-01 | E-MTAB-13133 | biostudies-arrayexpress

Serum protein N-glycosylation changes in multiple myeloma

Project description:<h4><strong>BACKGROUND:</strong> Multiple myeloma is characterized by clonal proliferation of malignant plasma cells in the bone marrow that produce monoclonal immunoglobulins. N-glycosylation changes of these monoclonal immunoglobulins have been reported in multiple myeloma, but previous studies only detected limited serum N-glycan features.</h4><h4><strong>METHODS:</strong> Here, a more detailed study of the human serum N-glycome of 91 multiple myeloma patients and 51 controls was performed. We additionally analyzed sequential samples from patients (n = 7) which were obtained at different time points during disease development as well as 16 paired blood serum and bone marrow plasma samples. N-glycans were enzymatically released and measured by mass spectrometry after linkage specific derivatization of sialic acids.</h4><h4><strong>RESULTS:</strong> A decrease in both α2,3- and α2,6-sialylation, galactosylation and an increase in fucosylation within complex-type N-glycans were found in multiple myeloma patients compared to controls, as well as a decrease in difucosylation of diantennary glycans. The observed glycosylation changes were present in all ISS stages, including the 'low-risk' ISS I. In individual patients, difucosylation of diantennary glycans decreased with development of the disease. Protein N-glycosylation features from blood and bone marrow showed strong correlation. Moreover, associations of monoclonal immunoglobulin (M-protein) and albumin levels with glycan traits were discovered in multiple myeloma patients.</h4><h4><strong>CONCLUSIONS & GENERAL SIGNIFICANCE: </strong>In conclusion, serum protein N-glycosylation analysis could successfully distinguish multiple myeloma from healthy controls. Further studies are needed to assess the potential roles of glycan trait changes and the associations of glycans with clinical parameters in multiple myeloma early detection and prognosis.</h4>

2022-04-27 | MTBLS676 | MetaboLights

Homo sapiens

Project description:CLINICAL IMPACT AND PREVALENCE OF CLONAL HEMATOPOIESIS IN MULTIPLE MYELOMA PATIENTS: RETROSPECTIVE MULTICENTRIC ANALYSIS

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DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts

Project description:Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A) drive clonal hematopoiesis of indeterminate potential (CHIP) and are associated with adverse prognosis in patients with heart failure (HF). The interactions between CHIP-mutated cells and other cardiac cell types remain unknown. Here, we identify fibroblasts as potential interaction partners of CHIP-mutated monocytes using combined transcriptomic data from peripheral blood mononuclear cells of HF patients with and without CHIP and cardiac tissue. We demonstrate that DNMT3A inactivation augments macrophage-to-cardiac fibroblasts interactions and induces cardiac fibrosis in mice and humans. Mechanistically, DNMT3A inactivation increases the release of heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) to activate cardiac fibroblasts. These findings not only identify a novel pathway of DNMT3A CHIP-driver mutation-induced instigation and progression of HF, but may also provide a rationale for the development of new anti-fibrotic strategies.

2023-10-20 | E-MTAB-13384 | biostudies-arrayexpress

DNA sequencing of human blood sample for Clonal Hematopoiesis of Indeterminate Potential (CHIP) detection.

Project description:DNA sequencing of human blood sample for Clonal Hematopoiesis of Indeterminate Potential (CHIP) detection.

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Project description:Distribution of Clonal Hematopoiesis of Indeterminate Potential (CHIP) is not associated with Race in Patients with Plasma Cell Neoplasms

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Effect of common mutations in clonal hematopoiesis of indeterminate potential (CHIP) on the transcriptome in bone marrow derived macrophages (BMDM).

Project description:Clonal hematopoiesis of indeterminate potential (CHIP) is associated with an increased risk of inflammatory conditions, including cardiovascular disease, in humans. The goal of the present data set was to examine the molecular mechanism underlying the increase in inflammation seen with the two most common CHIP mutations, namely loss-of-function mutations in Dnmt3a and Tet2, using murine bone-marrow derived macrophages (BMDM) as a model system.

2023-07-26 | GSE237599 | GEO

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