A5009957668- Acute Myeloid Leukemia Research
- Epigenetics and DNA Methylation
- Single-cell and spatial transcriptomics
- Chronic Myeloid Leukemia Treatments
- Blood disorders and treatments
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Hematopoietic Stem Cell Transplantation
- Genomics and Chromatin Dynamics
- Cancer Genomics and Diagnostics
- SARS-CoV-2 and COVID-19 Research
- RNA modifications and cancer
- Cancer-related molecular mechanisms research
- Immune Cell Function and Interaction
- Immune cells in cancer
- Cytokine Signaling Pathways and Interactions
- Protein Degradation and Inhibitors
- Animal Virus Infections Studies
- interferon and immune responses
- COVID-19 epidemiological studies
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Jackson Laboratory
2019-2025
Clonal hematopoiesis resulting from the enhanced fitness of mutant hematopoietic stem cells (HSC) associates with both favorable and unfavorable health outcomes related to types mature blood produced, but how this lineage output is regulated unclear. Using a mouse model clonal hematopoiesis-associated mutation, DNMT3AR882/+ (Dnmt3aR878H/+), we found that aging-induced TNFα signaling promoted selective advantage HSCs stimulated production B lymphoid cells. The genetic loss receptor TNFR1...
Abstract Aging is a process of systemic deterioration and the most significant risk factor for cancers. Clonal hematopoiesis (CH) commonly occurs with aging links to higher mortality, leukemia risk, cardiovascular diseases. Age-related CH involves abnormal clonal expansion hematopoietic stem cells (HSCs) bearing somatic mutations in genes frequently mutated leukemia, including encoding epigenetic regulators, e.g., DNA demethylase TET2. While such are known alter HSC epigenome, mechanisms...
Abstract Aging is a process of systemic deterioration and the most significant risk factor for cancers. Clonal hematopoiesis (CH) commonly occurs with aging links to higher mortality, leukemia risk, cardiovascular diseases. Age-related CH involves abnormal clonal expansion hematopoietic stem cells (HSCs) bearing somatic mutations in genes frequently mutated leukemia, including encoding epigenetic regulators, e.g., DNA demethylase TET2. While such are known alter HSC epigenome, mechanisms...
Age-associated clonal hematopoiesis (CH) occurs due to somatic mutations accrued in hematopoietic stem cells (HSCs) that confer a selective growth advantage the context of aging. The mechanisms by which CH-mutant HSCs gain this with aging are not comprehensively understood. Using unbiased transcriptomic approaches, we identified Oncostatin M (OSM) signaling as candidate contributor age-related Dnmt3a-mutant CH. We found from young adult mice (3-6 months old) subjected acute OSM stimulation...
Abstract Aging is a process of systemic deterioration and the most significant risk factor for cancers. Clonal hematopoiesis (CH) commonly occurs with aging links to higher mortality, leukemia risk, cardiovascular diseases. Age-related CH involves abnormal clonal expansion hematopoietic stem cells (HSCs) bearing somatic mutations in genes frequently mutated leukemia, including encoding epigenetic regulators, such as DNA demethylase TET2. While are known alter HSC epigenome, mechanisms...
ABSTRACT Age-associated clonal hematopoiesis (CH) occurs due to somatic mutations accrued in hematopoietic stem cells (HSCs) that confer a selective advantage the context of aging. The mechanisms by which CH-mutant HSCs gain this with aging are not comprehensively understood. Using unbiased transcriptomic approaches, we identify Oncostatin M (OSM) signaling as candidate contributor aging-driven Dnmt3a -mutant CH. We find from young mice do functionally respond acute OSM stimulation respect...
Abstract The MLL-AF9 fusion protein occurring as a result of t(9;11) translocation gives rise to pediatric and adult acute leukemias distinct lineages, including lymphoblastic leukemia (ALL), myeloid (AML), mixed phenotype (MPAL). mechanisms underlying how this same results in diverse phenotypes among different individuals is not well understood. Given emerging evidence from genome-wide association studies (GWAS) that genetic risk factors contribute MLL -rearranged leukemogenesis, here we...
<div>Abstract<p>Clonal hematopoiesis resulting from the enhanced fitness of mutant hematopoietic stem cells (HSC) associates with both favorable and unfavorable health outcomes related to types mature blood produced, but how this lineage output is regulated unclear. Using a mouse model clonal hematopoiesis–associated mutation, <i>DNMT3A</i><sup>R882/+</sup> (<i>Dnmt3a</i><sup>R878H/+</sup>), we found that aging-induced TNFα...
<div>Abstract<p>Clonal hematopoiesis resulting from the enhanced fitness of mutant hematopoietic stem cells (HSC) associates with both favorable and unfavorable health outcomes related to types mature blood produced, but how this lineage output is regulated unclear. Using a mouse model clonal hematopoiesis–associated mutation, <i>DNMT3A</i><sup>R882/+</sup> (<i>Dnmt3a</i><sup>R878H/+</sup>), we found that aging-induced TNFα...
Supplementary Figure from Distinct Tumor Necrosis Factor Alpha Receptors Dictate Stem Cell Fitness versus Lineage Output in <i>Dnmt3a</i>-Mutant Clonal Hematopoiesis
Supplementary Figure from Distinct Tumor Necrosis Factor Alpha Receptors Dictate Stem Cell Fitness versus Lineage Output in <i>Dnmt3a</i>-Mutant Clonal Hematopoiesis