A5070382979- Acute Myeloid Leukemia Research
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Protein Degradation and Inhibitors
- Cytokine Signaling Pathways and Interactions
- Blood disorders and treatments
- Chronic Myeloid Leukemia Treatments
- Hematopoietic Stem Cell Transplantation
- Single-cell and spatial transcriptomics
- interferon and immune responses
- Chemokine receptors and signaling
- Epigenetics and DNA Methylation
- Immune cells in cancer
- Genomics and Chromatin Dynamics
- Multiple Myeloma Research and Treatments
- Ubiquitin and proteasome pathways
- Immune Cell Function and Interaction
- Physiological and biochemical adaptations
- Cellular transport and secretion
- Fish biology, ecology, and behavior
- Chronic Lymphocytic Leukemia Research
- Academic and Historical Perspectives in Psychology
- Cancer Mechanisms and Therapy
- Cancer Genomics and Diagnostics
- Gender Roles and Identity Studies
- Mitochondrial Function and Pathology
Jackson Laboratory
2019-2024
Tufts University
2022-2024
Montgomery General Hospital
2019
Massachusetts General Hospital
2018
Harvard University
2018
Dana-Farber Cancer Institute
2018
Université de Montréal
2015
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...
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 Somatic mutations in hematopoietic stem/progenitor cells (HSPCs) can lead to clonal hematopoiesis of indeterminate potential (CHIP), potentially progressing myelodysplastic syndromes (MDS). Here, we investigated how CHIP and MDS remodel the human bone marrow (BM) niche relative healthy elderly donors, using single cell anatomical analyses a large BM cohort. We found distinct inflammatory remodeling MDS. Furthermore, stromal compartment progressively lost its HSPC-supportive...
Oncostatin M (OSM) is a member of the interleukin-6 (IL-6) family cytokines and has been found to have anti-inflammatory pro-inflammatory properties in various cellular disease contexts. OSM signals through two receptor complexes, one which includes OSMRβ. Here, we investigated OSM-OSMRβ signaling adult mouse hematopoietic stem cells (HSCs) using conditional Osmr
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
Oncostatin M (OSM) is a member of the interleukin-6 (IL-6) family cytokines and has been found to have distinct anti-inflammatory pro-inflammatory properties in various cellular disease contexts. OSM signals through two receptor complexes, one which includes OSMRβ. To investigate OSM-OSMRβ signaling adult hematopoiesis, we utilized readily available conditional Osmrfl/fl mouse model B6;129-Osmrtm1.1Nat/J, poorly characterized literature. This contains loxP sites flanking exon 2 Osmr gene. We...
Abstract Clonal hematopoiesis resulting from enhanced fitness of mutant hematopoietic stem cells (HSCs) associates with both favorable and unfavorable health outcomes related to the types mature blood produced, but how this lineage output is regulated unclear. Using a mouse model clonal hematopoiesis-associated mutation, DNMT3A R882/+ ( Dnmt3a R878H/+ ), we found that aging-induced TNFα signaling promoted selective advantage HSCs as well stimulated B lymphoid cell production. Genetic loss...