Shira Glushakow-Smith

ORCID: 0000-0002-6012-7236
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About
Contact & Profiles
Research Areas
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Chronic Myeloid Leukemia Treatments
  • Eosinophilic Disorders and Syndromes
  • Acute Myeloid Leukemia Research
  • Histone Deacetylase Inhibitors Research
  • Macrophage Migration Inhibitory Factor
  • Virus-based gene therapy research
  • Protein Degradation and Inhibitors
  • Poxvirus research and outbreaks
  • Autophagy in Disease and Therapy
  • Hematopoietic Stem Cell Transplantation
  • Immunodeficiency and Autoimmune Disorders
  • Lymphoma Diagnosis and Treatment
  • RNA Interference and Gene Delivery
  • Chronic Lymphocytic Leukemia Research
  • Animal Virus Infections Studies
  • PI3K/AKT/mTOR signaling in cancer
  • Kruppel-like factors research
  • Calcium signaling and nucleotide metabolism
  • Herpesvirus Infections and Treatments

Albert Einstein College of Medicine
2019-2025

National Institute of Allergy and Infectious Diseases
2018-2020

National Institutes of Health
2018-2020

Familial platelet disorder (FPD) is associated with germline RUNX1 mutations, establishing a preleukemic state and increasing the risk of developing leukemia. Currently, there are no intervention strategies to prevent leukemia progression. Single-cell RNA sequencing (n = 10) combined functional analysis samples from patients RUNX1-FPD > 75) revealed that FPD hematopoietic stem progenitor cells (HSPCs) displayed increased myeloid differentiation suppressed megakaryopoiesis because activation...

10.1126/scitranslmed.adn9832 article EN Science Translational Medicine 2025-01-08

Modified vaccinia virus Ankara (MVA) is an approved smallpox vaccine and a promising vector for other pathogens as well cancer therapeutics with more than 200 current or completed clinical trials. MVA was derived by passaging the parental hundreds of times in chick embryo fibroblasts during which it lost ability to replicate human most mammalian cells. Although this replication deficiency important safety feature, genetic basis host restriction not understood. Here, unbiased genome-wide RNAi...

10.1371/journal.ppat.1008845 article EN public-domain PLoS Pathogens 2020-08-31

Abstract Preexisting autoimmune disease affects between 10% and 30% of patients with myelodysplastic syndromes (MDS). Studies comparing outcomes in MDS without show discordant results. Using the Surveillance, Epidemiology, End Results Medicare database, we conducted a population analysis to define impact autoimmunity on outcomes. Cases were ascertained 2007 2017 claim algorithms used identify disease, demographic characteristics, comorbidity scores, histology, transfusion burden, treatment...

10.1182/bloodadvances.2023011050 article EN cc-by-nc-nd Blood Advances 2023-09-20

Myelodysplastic syndrome (MDS) is a clonal malignancy arising in hematopoietic stem cells (HSCs). The mechanisms of MDS initiation HSCs are still poorly understood. phosphatidylinositol 3-kinase (PI3K)/AKT pathway frequently activated acute myeloid leukemia, but MDS, PI3K/AKT often down-regulated. To determine whether PI3K down-regulation can perturb HSC function, we generated triple knockout (TKO) mouse model with

10.1126/sciadv.ade8222 article EN cc-by-nc Science Advances 2023-02-22

Replication of vaccinia virus in human cells depends on the viral C7 or K1 protein. A previous genome-wide short interfering RNA (siRNA) screen with a C7/K1 double deletion mutant revealed SAMD9 as principal host range restriction factor along additional candidates, including WDR6 and FTSJ1. To compare their abilities to restrict replication, cellular genes were individually inactivated by CRISPR/Cas9 mutagenesis. The exhibited enhanced replication each knockout (KO) cell line but reached...

10.1128/jvi.01329-18 article EN Journal of Virology 2018-09-13

Abstract Purpose: The Philadelphia chromosome–negative myeloproliferative neoplasms (MPN) polycythemia vera, essential thrombocythemia, and primary myelofibrosis are characterized by JAK/STAT pathway activation. JAK inhibitors approved for MPN treatment, but persistence has been observed, due to reactivation. Experimental Design: Using patient samples, JAK2-mutated cell lines, mouse models, we examined both the efficacy mechanism which crizotinib, ALK/MET/RON/ROS1 inhibitor treatment of...

10.1158/1078-0432.ccr-22-1763 article EN Clinical Cancer Research 2022-12-20

<div>AbstractPurpose:<p>The Philadelphia chromosome–negative myeloproliferative neoplasms (MPN) polycythemia vera, essential thrombocythemia, and primary myelofibrosis are characterized by JAK/STAT pathway activation. JAK inhibitors approved for MPN treatment, but persistence has been observed, due to reactivation.</p>Experimental Design:<p>Using patient samples, JAK2-mutated cell lines, mouse models, we examined both the efficacy mechanism which crizotinib,...

10.1158/1078-0432.c.6533203 preprint EN 2023-04-01

<div>AbstractPurpose:<p>The Philadelphia chromosome–negative myeloproliferative neoplasms (MPN) polycythemia vera, essential thrombocythemia, and primary myelofibrosis are characterized by JAK/STAT pathway activation. JAK inhibitors approved for MPN treatment, but persistence has been observed, due to reactivation.</p>Experimental Design:<p>Using patient samples, JAK2-mutated cell lines, mouse models, we examined both the efficacy mechanism which crizotinib,...

10.1158/1078-0432.c.6533203.v1 preprint EN 2023-04-01

Abstract Hematopoietic stem cells (HSCs) maintain the blood system through a delicate equilibrium between self-renewal and differentiation. Most hematopoietic growth factors cytokines signal phosphoinositide 3-kinase (PI3K) via three Class IA catalytic PI3K isoforms (P110α, β, δ), encoded by Pik3ca, Pik3cb , Pik3cd respectively. The PI3K/AKT pathway is commonly activated in acute myeloid leukemia (AML), common therapeutic target cancer. However, it not known whether required for HSC...

10.1101/2020.12.04.412593 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-12-06
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