William A. Weiss
A5073603294- Glioma Diagnosis and Treatment
- Cancer, Hypoxia, and Metabolism
- Neuroblastoma Research and Treatments
- Lung Cancer Treatments and Mutations
- Protein Degradation and Inhibitors
- Ubiquitin and proteasome pathways
- Microtubule and mitosis dynamics
- PI3K/AKT/mTOR signaling in cancer
- Hedgehog Signaling Pathway Studies
- ATP Synthase and ATPases Research
- Cancer Genomics and Diagnostics
- Epigenetics and DNA Methylation
- Lung Cancer Diagnosis and Treatment
- Cancer Mechanisms and Therapy
- RNA modifications and cancer
- Occupational and environmental lung diseases
- Chromatin Remodeling and Cancer
- Genomics and Chromatin Dynamics
- Cancer Research and Treatments
- CRISPR and Genetic Engineering
- Histone Deacetylase Inhibitors Research
- Cancer Cells and Metastasis
- MicroRNA in disease regulation
- Multiple Myeloma Research and Treatments
- Cancer-related Molecular Pathways
Neurological Surgery
2016-2025
University of California, San Francisco
2016-2025
UCSF Helen Diller Family Comprehensive Cancer Center
2016-2025
City College of San Francisco
2010-2025
Neurology, Inc
2005-2023
Comprehensive Blood & Cancer Center
2023
The University of Texas Medical Branch at Galveston
2023
San Francisco General Hospital
2023
University of Utah
2022
GlaxoSmithKline (United Kingdom)
2022
Back with a Vengeance After surgery, gliomas (a type of brain tumor) recur in nearly all patients and often more aggressive form. Johnson et al. (p. 189 , published online 12 December 2013) used exome sequencing to explore whether recurrent tumors harbor different mutations than the primary mutational profile recurrences is influenced by postsurgical treatment temozolomide (TMZ), chemotherapeutic drug known damage DNA. In 40% cases, at least half initial glioma were undetected recurrence....
Abstract Background Glioblastoma multiforme (GBM) is an invariably fatal central nervous system tumor despite treatment with surgery, radiation, and chemotherapy. Further insights into the molecular cellular mechanisms that drive GBM formation are required to improve patient outcome. MicroRNAs emerging as important regulators of differentiation proliferation, have been implicated in etiology a variety cancers, yet role microRNAs remains poorly understood. In this study, we investigated...
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...
Bromodomain inhibition comprises a promising therapeutic strategy in cancer, particularly for hematologic malignancies. To date, however, genomic biomarkers to direct clinical translation have been lacking. We conducted cell-based screen of genetically defined cancer cell lines using prototypical inhibitor BET bromodomains. Integration genetic features with chemosensitivity data revealed robust correlation between MYCN amplification and sensitivity bromodomain inhibition. characterized the...
Reports detailing the prognostic impact of TP53 mutations in medulloblastoma offer conflicting conclusions. We resolve this issue through inclusion molecular subgroup profiles.We determined affiliation, mutation status, and clinical outcome a discovery cohort 397 medulloblastomas. subsequently validated our results on an independent 156 medulloblastomas.TP53 are enriched wingless (WNT; 16%) sonic hedgehog (SHH; 21%) medulloblastomas virtually absent subgroups 3 4 tumors (P < .001). Patients...
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...
Combined inhibition of PI3K, mTOR, and autophagy promotes glioma cell death.