A5009726120- PARP inhibition in cancer therapy
- Neuroblastoma Research and Treatments
- Microtubule and mitosis dynamics
- Lung Cancer Treatments and Mutations
- Genomics and Chromatin Dynamics
- Ubiquitin and proteasome pathways
- DNA Repair Mechanisms
- Protein Degradation and Inhibitors
- Sarcoma Diagnosis and Treatment
- CAR-T cell therapy research
- Cancer Genomics and Diagnostics
- RNA Research and Splicing
Memorial Sloan Kettering Cancer Center
2023-2024
University of California System
2023
University of California, San Francisco
2023
Boston Children's Hospital
2023
Harvard University
2023
Massachusetts Institute of Technology
2023
While oncogenes promote cancer cell growth, unrestrained proliferation represents a significant stressor to cellular homeostasis networks such as the DNA damage response (DDR). To enable oncogene tolerance, many cancers disable tumor suppressive DDR signaling through genetic loss of pathways and downstream effectors (e.g., ATM or p53 suppressor mutations). Whether how can help "self-tolerize" by creating analogous functional deficiencies in physiologic is not known. Here we focus on Ewing...
ALL cures require many MRD therapies. This strategy should drive experiments and trials in metastatic bone sarcomas.
Abstract Drug resistance remains a challenge for targeted therapy of cancers driven by EML4-ALK and related fusion oncogenes. forms cytoplasmic protein condensates, which result from networks interactions between oncogene adapter multimers. While these assemblies are associated with oncogenic signaling, their role in drug response is unclear. Here, we use optogenetics live-cell imaging to find that suppress transmembrane receptor tyrosine kinase (RTK) signaling sequestering RTK proteins...
Abstract The genetic principle of synthetic lethality is clinically validated in cancers with loss specific DNA damage response (DDR) pathway genes (i.e. BRCA1/2 tumor suppressor mutations). broader question whether and how oncogenes create tumor-specific vulnerabilities within DDR networks remains unanswered. Native FET protein family members are among the earliest proteins recruited to double-strand breaks (DSBs) during DDR, though function both native fusion oncoproteins DSB repair poorly...