Emily Guzzardi
A5057971687- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Histone Deacetylase Inhibitors Research
- Multiple Myeloma Research and Treatments
- Chronic Myeloid Leukemia Treatments
- Cytokine Signaling Pathways and Interactions
- Chemical Synthesis and Analysis
- Eosinophilic Disorders and Syndromes
- DNA and Nucleic Acid Chemistry
- Advanced biosensing and bioanalysis techniques
- Acute Myeloid Leukemia Research
Memorial Sloan Kettering Cancer Center
2022-2024
Center for Discovery
2024
Abstract Gain-of-function mutations activating JAK/STAT signaling are seen in the majority of patients with myeloproliferative neoplasms (MPN), most commonly JAK2V617F. Although clinically approved JAK inhibitors improve symptoms and outcomes MPNs, remissions rare, mutant allele burden does not substantively change chronic therapy. We hypothesized this is due to limitations current potently specifically abrogate JAK2 signaling. therefore developed a conditionally inducible mouse model...
<p>Functional consequences of Jak2V617F reversion ex vivo</p>
<p>Functional characterization of Jak2RL knock-in/knock-out in vivo</p>
<p>Effects of Jak2V617F deletion on MPN stem cell fitness and disease transplantability</p>
<p>Differential gene expression responses of Jak2V617F deletion compared to JAK inhibitor therapy</p>
<p>Acute phenotypic and transcriptional changes following Jak2V617F reversion</p>
<p>Differential responses of Jak2V617F deletion compared to JAK inhibitor therapy in vivo</p>
<p>Assessment of tamoxifen toxicity on Jak2RL knock-in cells</p>
<p>Phenotypic characterization and validation of Jak2RL activation in vivo</p>
<p>Phenotypic characterization and Jak2V617F oncogenic dependency in the setting of concomitant Tet2 loss</p>
<p>Phenotypic characterization and Jak2V617F oncogenic dependency in the setting of concomitant Tet2 loss</p>
<p>Differential gene expression responses of Jak2V617F deletion compared to JAK inhibitor therapy</p>
<p>Phenotypic characterization and validation of Jak2RL activation in vivo</p>
<div>Abstract<p>Gain-of-function mutations activating JAK/STAT signaling are seen in the majority of patients with myeloproliferative neoplasms (MPN), most commonly <i>JAK2</i><sup>V617F</sup>. Although clinically approved JAK inhibitors improve symptoms and outcomes MPNs, remissions rare, mutant allele burden does not substantively change chronic therapy. We hypothesized this is due to limitations current potently specifically abrogate JAK2 signaling....
<div>Abstract<p>Gain-of-function mutations activating JAK/STAT signaling are seen in the majority of patients with myeloproliferative neoplasms (MPN), most commonly <i>JAK2</i><sup>V617F</sup>. Although clinically approved JAK inhibitors improve symptoms and outcomes MPNs, remissions rare, mutant allele burden does not substantively change chronic therapy. We hypothesized this is due to limitations current potently specifically abrogate JAK2 signaling....
<p>Assessment of tamoxifen toxicity on Jak2RL knock-in cells</p>