A5043938379- Cancer Mechanisms and Therapy
- CRISPR and Genetic Engineering
- Chromatin Remodeling and Cancer
- Bioinformatics and Genomic Networks
- Lipid Membrane Structure and Behavior
- Cancer Genomics and Diagnostics
- Cellular transport and secretion
- Machine Learning in Bioinformatics
- Gene Regulatory Network Analysis
- Melanoma and MAPK Pathways
- Computational Drug Discovery Methods
- Hematological disorders and diagnostics
- Microtubule and mitosis dynamics
- Neuroscience and Neuropharmacology Research
- interferon and immune responses
- Genomics and Rare Diseases
- Neutropenia and Cancer Infections
- Calcium signaling and nucleotide metabolism
- Advanced Proteomics Techniques and Applications
- Acute Myeloid Leukemia Research
- Single-cell and spatial transcriptomics
Columbia University Irving Medical Center
2019-2021
Herbert Irving Comprehensive Cancer Center
2021
Columbia University
2021
Seattle Cancer Care Alliance
2020
Yale University
2013
Abstract Mutations in ARID1A rank among the most common molecular aberrations human cancer. However, oncogenic consequences of mutation cells remain poorly defined due to lack forward genetic models. Here, CRISPR/Cas9-mediated knockout (KO) primary TP53−/− gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/β-catenin activation rescued differentiation, but not hyperproliferation, suggesting alternative pathways KO-mediated...
Abstract To improve patient quality of life and reduce health care costs, many conditions formerly thought to require inpatient are now treated in the outpatient setting. Outpatient induction chemotherapy for acute myeloid leukemia (AML) may confer similar benefits. This possibility prompted a pilot study explore safety feasibility intensive initial or salvage administration adults with AML high-risk myelodysplastic syndrome (MDS). Patients no significant organ dysfunction treatment-related...
Abstract Pooled CRISPRi-mediated silencing of >1,000 transcriptional regulators expressed in single colorectal adenocarcinoma cells, followed by single-cell RNA-seq profiling at two timepoints, 1 day and 4 days, allowed reverse engineering the underlying tumor context-specific, causal regulatory network. Furthermore, availability experimentally derived, highly multiplexed gene reporter assays for each regulator, as identified this analysis, accurate assessment differential protein...
Abstract Despite considerable pan-cancer efforts, the link between genomics and transcriptomics in cancer remains relatively weak mostly based on statistical rather than mechanistic principles. By performing integrative analysis of transcriptomic mutational profiles a sample-by-sample basis, via regulatory/signaling networks, we identified repertoire 407 Master-Regulator proteins responsible for canalizing genetics 20 TCGA cohorts into 112 transcriptionally-distinct tumor subtypes. Further...
Abstract Mutations in ARID1A, encoding a subunit of the BAF chromatin remodeling complex, rank amongst most common molecular aberrations human cancer. However, oncogenic consequences ARID1A mutation cells remain poorly defined due to lack forward genetic model systems. Here, CRISPR/Cas9 knockout primary TP53-/- gastric organoids induced morphologic dysplasia, tumorigenicity and mucinous differentiation but impaired Wnt/β-catenin signaling. Genetic Wnt pathway activation rescued...
<div>Abstract<p>Mutations in <i>ARID1A</i> rank among the most common molecular aberrations human cancer. However, oncogenic consequences of mutation cells remain poorly defined due to lack forward genetic models. Here, CRISPR/Cas9-mediated knockout (KO) primary <i>TP53<sup>−/−</sup></i> gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/β-catenin activation rescued differentiation, but...
<p>Key Resources Tables</p>
<p>Key Resources Tables</p>
<p>Supplementary Figure 1</p>
<p>Supplementary Figure 1</p>
<div>Abstract<p>Mutations in <i>ARID1A</i> rank among the most common molecular aberrations human cancer. However, oncogenic consequences of mutation cells remain poorly defined due to lack forward genetic models. Here, CRISPR/Cas9-mediated knockout (KO) primary <i>TP53<sup>−/−</sup></i> gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/β-catenin activation rescued differentiation, but...
<p>Supplementary Figure 7</p>
<p>Supplementary Figure 2</p>
<p>Supplementary Figure 7</p>
<p>Supplementary Figure 5</p>
<p>Supplementary Figure 6</p>
<p>Supplementary Figure 5</p>
<p>Supplementary Figure 3</p>
<p>Supplementary Figure 3</p>
<p>Supplementary Figure 2</p>