Meghan Wyatt
A5037831100- Glioma Diagnosis and Treatment
- Chromatin Remodeling and Cancer
- Cancer Mechanisms and Therapy
- CRISPR and Genetic Engineering
- Protein Degradation and Inhibitors
- Single-cell and spatial transcriptomics
- Advanced biosensing and bioanalysis techniques
- Cell Image Analysis Techniques
- Immune Cell Function and Interaction
- CAR-T cell therapy research
- Immunotherapy and Immune Responses
- Pluripotent Stem Cells Research
Broad Institute
2017-2023
Massachusetts Institute of Technology
2022
University of Connecticut
2022
The CRISPR-Cas9 system has revolutionized gene editing both on single genes and in multiplexed loss-of-function screens, enabling precise genome-scale identification of essential to proliferation survival cancer cells. However, previous studies reported that an anti-proliferative effect Cas9-mediated DNA cleavage confounds such measurement genetic dependency, particularly the setting copy number gain 1-4 . We performed essentiality screens 342 cell lines found this is common all lines,...
The solid tumor microenvironment (TME) suppresses immune responses. Three alterations in the TME converge on a pathway triggered by elevated cyclic AMP (cAMP) that T cell receptor (TCR) signaling. We developed phenotypic assay to screen for small molecules interfere with this using TALL-104 human leukemic cytotoxic lymphocytes pretreated prostaglandin E2 elevate cAMP. Beads coated anti-CD3 antibodies stimulate lytic granule exocytosis, which is detected via binding of an antibody against...
<div>Abstract<p>Diffuse midline gliomas are uniformly fatal pediatric central nervous system cancers that refractory to standard-of-care therapeutic modalities. The primary genetic drivers a set of recurrent amino acid substitutions in genes encoding histone H3 (H3K27M), which currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting an aberrant epigenetic landscape. To interrogate for dependencies, we performed CRISPR screen and show...
<div>Abstract<p>Diffuse midline gliomas are uniformly fatal pediatric central nervous system cancers that refractory to standard-of-care therapeutic modalities. The primary genetic drivers a set of recurrent amino acid substitutions in genes encoding histone H3 (H3K27M), which currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting an aberrant epigenetic landscape. To interrogate for dependencies, we performed CRISPR screen and show...
Supplementary Figure from BAF Complex Maintains Glioma Stem Cells in Pediatric H3K27M
Supplementary Figure from BAF Complex Maintains Glioma Stem Cells in Pediatric H3K27M
Abstract Epigenetic dysregulation resulting in stalled development plays a crucial role pediatric cancer tumorigenesis. Diffuse midline gliomas (DMG) are universally fatal brain cancers refractory to standard of care treatment modalities. These malignancies driven by heterozygous mutations genes encoding histone 3 (H3K27M) which create an aberrant epigenetic landscape that keeps glioma cells undifferentiated stem-like state. Consequently, targeting regulators restore the epigenome and force...