Tamara Codilupi
A5035851550- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Histone Deacetylase Inhibitors Research
- Multiple Myeloma Research and Treatments
- Chronic Myeloid Leukemia Treatments
- Phagocytosis and Immune Regulation
- Chronic Lymphocytic Leukemia Research
- DNA Repair Mechanisms
- Acute Myeloid Leukemia Research
- Cancer Research and Treatments
- Cancer-related Molecular Pathways
- Epigenetics and DNA Methylation
- Eosinophilic Disorders and Syndromes
- Genomics and Chromatin Dynamics
- Plant tissue culture and regeneration
- CRISPR and Genetic Engineering
- Carcinogens and Genotoxicity Assessment
- Microtubule and mitosis dynamics
- Mitochondrial Function and Pathology
University Hospital of Basel
2019-2024
University of Basel
2019-2024
University of Zurich
2017-2019
Constitutive JAK2 signaling is central to myeloproliferative neoplasm (MPN) pathogenesis and results in activation of STAT, PI3K/AKT, MEK/ERK signaling. However, the therapeutic efficacy current inhibitors limited. We investigated role MPN cell survival setting JAK inhibition. Type I II inhibition suppressed lines vitro, but not Jak2V617F MPLW515L mouse models vivo. ex vivo inhibited signaling, suggesting that cell-extrinsic factors maintain ERK identified PDGFRα as an activated kinase...
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...
DNA-crosslinking agents like cisplatin and mitomycin C (MMC) are indispensible for the treatment of many solid malignancies. These anticancer drugs generate DNA interstrand crosslinks (ICLs) that cause cell death by blocking replication forks. Many factors counteracting ICL-induced stress, including Fanconi anemia (FA) pathway, regulated ubiquitination and, therefore, ubiquitin ligases potential targets sensitization cancer cells to crosslinking agents. In this study, we investigated...
Abstract Purpose: Myeloproliferative neoplasms (MPN) dysregulate JAK2 signaling. Because clinical inhibitors have limited disease-modifying effects, type II such as CHZ868 stabilizing inactive and reducing MPN clones, gain interest. We studied whether cells escape from ll inhibition. Experimental Design: were continuously exposed to CHZ868. used phosphoproteomic analyses ATAC/RNA sequencing characterize acquired resistance inhibition, targeted candidate mediators in mice. Results: showed...
<div>AbstractPurpose:<p>Myeloproliferative neoplasms (MPN) dysregulate JAK2 signaling. Because clinical inhibitors have limited disease-modifying effects, type II such as CHZ868 stabilizing inactive and reducing MPN clones, gain interest. We studied whether cells escape from ll inhibition.</p>Experimental Design:<p>MPN were continuously exposed to CHZ868. used phosphoproteomic analyses ATAC/RNA sequencing characterize acquired resistance inhibition, targeted candidate...
<p>Codilupi et al, Supplementary figures and methods</p>
<p>Codilupi et al, Supplementary figures and methods</p>
<div>AbstractPurpose:<p>Myeloproliferative neoplasms (MPN) dysregulate JAK2 signaling. Because clinical inhibitors have limited disease-modifying effects, type II such as CHZ868 stabilizing inactive and reducing MPN clones, gain interest. We studied whether cells escape from ll inhibition.</p>Experimental Design:<p>MPN were continuously exposed to CHZ868. used phosphoproteomic analyses ATAC/RNA sequencing characterize acquired resistance inhibition, targeted candidate...
<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>