A5014589353- Glioma Diagnosis and Treatment
- Neuroblastoma Research and Treatments
- Chromatin Remodeling and Cancer
- Pharmacological Effects and Toxicity Studies
- Cancer Research and Treatments
- Cancer, Hypoxia, and Metabolism
- Protein Degradation and Inhibitors
- Microtubule and mitosis dynamics
- Renal and related cancers
- Parathyroid Disorders and Treatments
- ATP Synthase and ATPases Research
- PARP inhibition in cancer therapy
- CRISPR and Genetic Engineering
- Liver Disease Diagnosis and Treatment
- Cellular Mechanics and Interactions
- Urinary Bladder and Prostate Research
- Telomeres, Telomerase, and Senescence
- Ferroptosis and cancer prognosis
- Venous Thromboembolism Diagnosis and Management
- Cancer Cells and Metastasis
- Urologic and reproductive health conditions
- Caveolin-1 and cellular processes
- 3D Printing in Biomedical Research
- Diabetes and associated disorders
- Immunotherapy and Immune Responses
University of Cambridge
2023-2024
National Cancer Institute
2021-2023
National Institutes of Health
2023
Center for Cancer Research
2021-2023
Cancer Research UK Cambridge Center
2023
Cancer Institute (WIA)
2023
Brain Tumour Research
2023
Heidelberg University
2019-2021
University Hospital Heidelberg
2021
Medizinische Fakultät Mannheim
2019
Abstract Pediatric high-grade gliomas (pHGG) are lethal, incurable brain tumors frequently driven by clonal mutations in histone genes. They often harbor a range of additional genetic alterations that correlate with different ages, anatomic locations, and tumor subtypes. We developed models representing 16 pHGG subtypes combinations targeted to specific regions. Tumors varying latencies cell lines derived from these engrafted syngeneic, immunocompetent mice high penetrance. Targeted drug...
Abstract Expression of the immediate-early response gene IER2 has been associated with progression several types cancer, but its functional role is poorly understood. We found that increased expression in human melanoma shorter overall survival, and subsequently investigated mechanisms through which exerts this effect. In experimental models, sustained induced senescence a subset cells p53/MAPK/AKT-dependent manner. The senescent produced characteristic secretome included high levels...
ABSTRACT Glioblastoma multiforme (GBM) is the most commonly diagnosed brain cancer in adults, characterized by rapid proliferation and aggressive invasion into stroma. Advances our understanding of molecular subtypes GBM have provided attractive druggable targets. However, high degree heterogeneity both among patients within individual tumors has proven a significant challenge for development effective therapies. We hypothesized that this also represented mechanical phenotypes GBM, as...
Pediatric brain tumors comprise a diverse set of diseases. (Epi)genomic analyses have provided insights into the biology these tumors, stratifying them distinct subtypes with different oncogenic driver mechanisms and developmental origins. A feature shared by is their initiation within neural stem or progenitor cells that undergo stalled differentiation in unique, niche-dependent ways. In this review, we provide an overview how (epi)genomic characterization has revealed pediatric tumor...
<p>Figures describing hindbrain vs ganglionic eminence targeting strategies, each of the 16 models generated and validation that they expressed introduced mutations, survival GE CTX-electroporated embryos, cell viability data shown in bar graph format.</p>
<p>Figures describing hindbrain vs ganglionic eminence targeting strategies, each of the 16 models generated and validation that they expressed introduced mutations, survival GE CTX-electroporated embryos, cell viability data shown in bar graph format.</p>
<p><b>A</b>, Left: acid-extracted histone and protein lysates prepared from <i>ex vivo</i> GS lines derived the two-hit <i>de novo</i> models (KP, H3.1KP, KF, KN) were probed for K27M, K27me3, HA, total H3.3 levels. NSCs LRL (LRL NSC) used as controls. Middle: validation of FGFR1 overexpression in KF cells; GAPDH was a loading control. Right: p53 NF1 downregulation cells by qRT-PCR. Data are presented means ± SD at least <i>n</i> = 3...
Abstract Pediatric high-grade gliomas (pHGGs) are lethal, incurable brain tumors frequently driven by clonal mutations in histone genes. They often harbor a range of additional genetic alterations that correlate with different ages, anatomical locations, and tumor subtypes. We developed models representing 16 pHGG subtypes combinations targeted to specific regions. Tumors varying latencies cell lines derived from these engrafted syngeneic, immunocompetent mice high penetrance. Targeted drug...
<div>Abstract<p>Pediatric high-grade gliomas (pHGG) are lethal, incurable brain tumors frequently driven by clonal mutations in histone genes. They often harbor a range of additional genetic alterations that correlate with different ages, anatomic locations, and tumor subtypes. We developed models representing 16 pHGG subtypes combinations targeted to specific regions. Tumors varying latencies cell lines derived from these engrafted syngeneic, immunocompetent mice high...
<div>Abstract<p>Pediatric high-grade gliomas (pHGGs) are lethal, incurable brain tumors frequently driven by clonal mutations in histone genes. They often harbor a range of additional genetic alterations that correlate with different ages, anatomical locations, and tumor subtypes. We developed models representing 16 pHGG subtypes combinations targeted to specific regions. Tumors varying latencies cell lines derived from these engrafted syngeneic, immunocompetent mice high...
<div>Abstract<p>Pediatric high-grade gliomas (pHGGs) are lethal, incurable brain tumors frequently driven by clonal mutations in histone genes. They often harbor a range of additional genetic alterations that correlate with different ages, anatomical locations, and tumor subtypes. We developed models representing 16 pHGG subtypes combinations targeted to specific regions. Tumors varying latencies cell lines derived from these engrafted syngeneic, immunocompetent mice high...
<p>Figures describing hindbrain vs ganglionic eminence targeting strategies, each of the 16 models generated and validation that they expressed introduced mutations, survival GE CTX-electroporated embryos, cell viability data shown in bar graph format.</p>
<p>Figures describing hindbrain vs ganglionic eminence targeting strategies, each of the 16 models generated and validation that they expressed introduced mutations, survival GE CTX-electroporated embryos, cell viability data shown in bar graph format.</p>
<p>Figures describing hindbrain vs ganglionic eminence targeting strategies, each of the 16 models generated and validation that they expressed introduced mutations, survival GE CTX-electroporated embryos, cell viability data shown in bar graph format.</p>