Robert J. Wechsler‐Reya
A5066651467- Glioma Diagnosis and Treatment
- Hedgehog Signaling Pathway Studies
- Epigenetics and DNA Methylation
- Cancer Cells and Metastasis
- Microtubule and mitosis dynamics
- Protein Degradation and Inhibitors
- Neuroblastoma Research and Treatments
- Cancer Genomics and Diagnostics
- Chromatin Remodeling and Cancer
- CAR-T cell therapy research
- Cancer Immunotherapy and Biomarkers
- RNA modifications and cancer
- Cancer-related molecular mechanisms research
- Virus-based gene therapy research
- Genomics and Chromatin Dynamics
- Immune cells in cancer
- Immunotherapy and Immune Responses
- Cancer-related Molecular Pathways
- Nanoplatforms for cancer theranostics
- RNA Research and Splicing
- Cancer, Hypoxia, and Metabolism
- Histone Deacetylase Inhibitors Research
- Single-cell and spatial transcriptomics
- Cancer Research and Treatments
- Multiple Myeloma Research and Treatments
Discovery Institute
2016-2025
Sanford Burnham Prebys Medical Discovery Institute
2016-2025
Columbia University Irving Medical Center
2022-2024
Columbia University
2024
University of Minnesota
2023
University of Massachusetts Chan Medical School
2023
University of California, San Diego
2013-2023
Sanford Consortium for Regenerative Medicine
2012-2023
National Cancer Institute
2013-2023
Children’s Institute
2018-2023
Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique...
Internal N
Abstract Purpose: MYC-amplified medulloblastomas are highly lethal tumors. Bromodomain and extraterminal (BET) bromodomain inhibition has recently been shown to suppress MYC-associated transcriptional activity in other cancers. The compound JQ1 inhibits BET bromodomain-containing proteins, including BRD4. Here, we investigate targeting for the treatment of medulloblastoma. Experimental Design: We evaluated effects genetic pharmacologic bromodomains on proliferation, cell cycle, apoptosis...
Medulloblastoma comprises four distinct molecular subgroups: WNT, SHH, Group 3, and 4. Current medulloblastoma protocols stratify patients based on clinical features: patient age, metastatic stage, extent of resection, histologic variant. Stark prognostic genetic differences among the subgroups suggest that subgroup-specific biomarkers could improve prognostication.Molecular were identified from a discovery set 673 medulloblastomas 43 cities around world. Combined risk stratification models...
Cerebellar granule cells are the most abundant neurons in brain, and cell precursors (GCPs) a common target of transformation pediatric brain tumor medulloblastoma. Proliferation GCPs is regulated by secreted signaling molecule Sonic hedgehog (Shh), but mechanisms which Shh controls proliferation remain inadequately understood. We used DNA microarrays to identify targets these found that activates program transcription promotes cycle entry replication. Among genes robustly induced cyclin D1...
Medulloblastoma is the most common malignant brain tumor in children. It thought to result from transformation of granule cell precursors (GCPs) developing cerebellum, but little known about early stages disease. Here, we identify a pre-neoplastic stage medulloblastoma patched heterozygous mice, model human We show that cells are present majority mutants, although only 16% these mice develop tumors. Pre-neoplastic cells, like exhibit activation Sonic hedgehog pathway and constitutive...
Telomerase reverse transcriptase (TERT) promoter mutations were recently shown to drive telomerase activity in various cancer types, including medulloblastoma. However, the clinical and biological implications of TERT medulloblastoma have not been described. Hence, we sought describe these their impact a subgroup-specific manner. We analyzed by direct sequencing genotyping 466 medulloblastomas. The mutational distributions determined according subgroup affiliation, demographics, clinical,...