- Cancer Genomics and Diagnostics
- Glioma Diagnosis and Treatment
- Mathematical Biology Tumor Growth
- Ferroptosis and cancer prognosis
- RNA and protein synthesis mechanisms
- Antibiotic Resistance in Bacteria
- Single-cell and spatial transcriptomics
- Bacterial Genetics and Biotechnology
New York University
2021
Broad Institute
2020
Massachusetts General Hospital
2020
Abstract Background Tumors can evolve and adapt to therapeutic pressure by acquiring genetic epigenetic alterations that may be transient or stable. A precise understanding of how such events contribute intratumoral heterogeneity, dynamic subpopulations, overall tumor fitness will require experimental approaches prospectively label, track, characterize resistant otherwise adaptive populations at the single-cell level. In glioblastoma, poor efficacy receptor tyrosine kinase (RTK) therapies...
Abstract Therapeutic pressure can result in tumor evolution and adaptation via genetic epigenetic mechanisms, which may be transient or stable. Knowledge of how these events contribute to intratumoral heterogeneity dynamic subpopulations will require single cell-resolution experimental approaches that prospectively label, longitudinally track, functionally characterize adaptive subclonal populations. In glioblastoma, poor efficacy therapies targeting receptor tyrosine kinases (RTKs)...