A5012236767- Acute Myeloid Leukemia Research
- Hematopoietic Stem Cell Transplantation
- High-Energy Particle Collisions Research
- Particle physics theoretical and experimental studies
- Hematological disorders and diagnostics
- Quantum Chromodynamics and Particle Interactions
- Bone and Joint Diseases
- Bone health and treatments
- Mesenchymal stem cell research
- Immune cells in cancer
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Prostate Cancer Treatment and Research
- Bone Metabolism and Diseases
- Fibroblast Growth Factor Research
- Cytokine Signaling Pathways and Interactions
- Radiopharmaceutical Chemistry and Applications
- Cancer Cells and Metastasis
- Erythrocyte Function and Pathophysiology
- Effects of Radiation Exposure
- Histone Deacetylase Inhibitors Research
- Multiple Myeloma Research and Treatments
- Blood disorders and treatments
- Single-cell and spatial transcriptomics
- Medical Imaging and Pathology Studies
- Chemokine receptors and signaling
University of Rochester Medical Center
2014-2024
University of Rochester
2012-2024
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute
2019
Cancer Institute (WIA)
2019
München Klinik
2015
Technical University of Munich
2015
Klinikum rechts der Isar
2015
European Organization for Nuclear Research
2011-2013
Endocrine Society
2009
Tel Aviv Sourasky Medical Center
1992
The bone marrow microenvironment contributes to the regulation of hematopoietic stem cell (HSC) function, though its role in age-associated lineage skewing is poorly understood. Here we show that dysfunction aged macrophages (Mφs) directs HSC platelet bias. Mφs from mice and humans exhibited an activated phenotype, with increased expression inflammatory signals. Aged also displayed decreased phagocytic function. Senescent neutrophils, typically cleared by Mφs, were markedly mice, consistent...
Abstract Hematopoietic stem and progenitor cells (HSPCs), which continuously maintain all mature blood cells, are regulated within the marrow microenvironment. We previously reported that pharmacologic treatment of naïve mice with prostaglandin E2 (PGE2) expands HSPCs. However, cellular mechanisms mediating this expansion remain unknown. Here, we demonstrate PGE2 in inhibits apoptosis HSPCs without changing their proliferation rate. In a murine model sublethal total body irradiation (TBI),...
Inv(3q26) and t(3:3)(q21;q26) are specific to poor-prognosis myeloid malignancies, result in marked overexpression of EVI1, a zinc-finger transcription factor myeloid-specific oncoprotein. Despite extensive study, the mechanism by which EVI1 contributes malignancy remains unclear. Here we describe new mouse model that mimics transcriptional effects 3q26 rearrangement. We show causes global distortion hematopoiesis, with suppression erythropoiesis lymphopoiesis, premalignant expansion...
ABSTRACT Notch signaling is critical for osteoblastic differentiation; however, the specific contribution of individual ligands unknown. Parathyroid hormone (PTH) regulates ligand Jagged1 in cells. To determine if osteolineage contributes to bone homeostasis, selective deletion cells was achieved through presence Prx1 promoter‐driven Cre recombinase expression, targeting mesenchymal stem (MSCs) and their progeny (PJag1 mice). PJag1 mice were viable fertile did not exhibit any skeletal...
Abstract The chemokine CCL3 is frequently overexpressed in malignancies and overexpression leads to microenvironmental dysfunction. In murine models of chronic myelogenous leukemia (CML), critical for the maintenance a stem cell population, progression. With implicated as potentially viable therapeutic target, it important carefully characterize its role normal hematopoietic homeostasis. −/− mice were used evaluate regulating progenitor (HSPC) populations. had loss mature myeloid...
Hematopoiesis takes place in the bone marrow and is supported by a complex cellular molecular network microenvironment. Commonly used models of human microenvironment include murine two-dimensional three-dimensional tissue cultures. While these model systems have led to critical advances field, they fail recapitulate many aspects marrow. This has limited our understanding pathophysiology deficiencies therapy for pathologies such as failure syndromes leukemias. Therefore, we developed modular...
The pathogenesis of adhesions following primary tendon repair is poorly understood, but thought to involve dysregulation matrix metalloproteinases (Mmps). We have previously demonstrated that Mmp9 gene expression increased during the inflammatory phase murine flexor digitorum (FDL) in association with adhesions. To further investigate role Mmp9, cellular, molecular, and biomechanical features healing were examined WT Mmp9−/− mice using FDL model. Adhesions persisted WT, reduced by 21 days...
Abstract Leukemias are challenging diseases to treat due, in part, interactions between leukemia cells and the bone marrow microenvironment (BMME) that contribute significantly disease progression. Studies have shown leukemic secrete C‐chemokine (C‐C motif) ligand 3 (CCL3), disrupt BMME resulting loss of hematopoiesis support cell survival proliferation. In this study, a murine model blast crisis chronic myelogenous (bcCML) expresses translocation products BCR/ABL Nup98/HoxA9 was used...
Purpose: Incidents, such as nuclear facility accidents and the release of a 'dirty bomb', might result in not only external irradiation personnel, but additional internal exposures through concomitant inhalation and/or ingestion radioactive particulates. The purpose this study was to define impact combination radiation injuries on hematopoietic niche.Material methods: To assess changes murine system, we used combined exposure total body (TBI, 6 Gy) followed immediately by an...
Acute myeloid leukemia (AML) is the most aggressive adult and results in a dismal 5-year survival rate of less than 30%. While research has primarily focused on identifying intrinsic mutations driving leukemogenesis, role bone marrow microenvironment (BMME) disease progression remains poorly understood. For this purpose, conventional 2D cultures inadequately replicate complex BMME interactions crucial for maintenance normal hematopoiesis pathogenesis. In recent years, 3D or...