A5037360643- Protein Degradation and Inhibitors
- Ubiquitin and proteasome pathways
- Chromatin Remodeling and Cancer
- Histone Deacetylase Inhibitors Research
- Cancer-related Molecular Pathways
- interferon and immune responses
- Peptidase Inhibition and Analysis
- Dementia and Cognitive Impairment Research
University of North Carolina at Chapel Hill
2019-2023
University of California, Irvine
2023
Human papilloma virus (HPV)-negative head and neck squamous cell carcinoma (HNSCC) is a common cancer worldwide with an unmet need for more effective, less toxic treatments. Currently, both the disease treatment of HNSCC cause significant mortality morbidity. Targeted therapies hold new promise patients HPV-negative status whose tumors harbor oncogenic HRAS mutations. Recent promising clinical results have renewed interest in development farnesyltransferase inhibitors (FTIs) as therapeutic...
<div>Abstract<p>Human papilloma virus (HPV)-negative head and neck squamous cell carcinoma (HNSCC) is a common cancer worldwide with an unmet need for more effective, less toxic treatments. Currently, both the disease treatment of HNSCC cause significant mortality morbidity. Targeted therapies hold new promise patients HPV-negative status whose tumors harbor oncogenic <i>HRAS</i> mutations. Recent promising clinical results have renewed interest in development...
<div>Abstract<p>Human papilloma virus (HPV)-negative head and neck squamous cell carcinoma (HNSCC) is a common cancer worldwide with an unmet need for more effective, less toxic treatments. Currently, both the disease treatment of HNSCC cause significant mortality morbidity. Targeted therapies hold new promise patients HPV-negative status whose tumors harbor oncogenic <i>HRAS</i> mutations. Recent promising clinical results have renewed interest in development...
Abstract Head and neck squamous cell carcinoma (HNSCC) affects more than 50,000 people annually. The five-year survival rate has not improved significantly in the last decades. In addition, many treatment modalities are associated with significant morbidity that negatively impacts survivors’ quality of life. Mutations HRAS oncogene presented 5-10% cases HNSCC. Our group established its critical importance for growth protein undergoes crucial post-translational modifications prompted by...
Supplementary Figure from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth HRAS Mutant Head Neck Squamous Cell Carcinoma
Supplementary Figure from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth HRAS Mutant Head Neck Squamous Cell Carcinoma
Supplementary Data from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth HRAS Mutant Head Neck Squamous Cell Carcinoma
Supplementary Data from Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth HRAS Mutant Head Neck Squamous Cell Carcinoma
Abstract Background Neuropsychiatric symptoms (NPS) emerging after the age of 50 may be a risk factor or an early clinical expression AD dementia. Mild Behavioral Impairment (MBI) is syndrome new‐onset and persistent NPS in older adults either with without cognitive impairment. context race ethnicity have not been studied influence biology culture on unknown. Method Participants over 60 ranging from cognitively normal to mild (N = 17,491) National Alzheimer’s Coordinating Center were...
Abstract Activating mutations in the HRAS oncogene are present 5-11% of head and neck squamous cell carcinomas (HNSCC), but whether mutant drives HNSCC growth was not known. The clinical candidate FTI, tipifarnib, is currently under investigation HRAS-mutant HNSCC, patient responses to tipifarnib due blocking membrane association or action on another FTI target/s also unclear. We found that FTIs lonafarnib inhibited a target-dependent manner, farnesylation association. genetic depletion...
Activating mutations in the HRAS oncogene are present 5-11% of head and neck squamous cell carcinomas (HNSCC), but whether mutant drives HNSCC growth was not known. The clinical candidate FTI, tipifarnib, is currently under investigation HRAS-mutant HNSCC, patient responses to tipifarnib due blocking membrane association or action on another FTI target/s also unclear. We found that FTIs lonafarnib inhibited a target-dependent manner, farnesylation association. genetic depletion...
Abstract Activating mutations in the HRAS oncogene are present 5-11% of head and neck squamous cell cancers (HNSCC). We set out to determine if is a driver HNSCC growth whether pharmacologic inhibitors membrane association and/or RAS effector signaling may have therapeutic value these cancers. To importance HRAS, we depleted it genetically from HRAS-mutant lines by shRNA evaluated effects on survival. potential blocking through key effector, ERK MAPK, treated cells with farnesyltransferase...