Ramon Parsons
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View article: The BrainWaves study of adolescent wellbeing and mental health: methods development and pilot data
The BrainWaves study of adolescent wellbeing and mental health: methods development and pilot data Open
Adolescent mental health and wellbeing are of growing concern globally with increased incidence of mental health disorders in young people. BrainWaves provides a framework for relevant and diverse research programmes into adolescent mental…
View article: Parental and adolescent positive affect and optimism as predictors of post-surgical mood and functioning in adolescents undergoing spinal fusion surgery
Parental and adolescent positive affect and optimism as predictors of post-surgical mood and functioning in adolescents undergoing spinal fusion surgery Open
While most adolescents display a steady recovery trajectory following surgery, some develop chronic postsurgical pain (CPP), which can significantly impact their functioning. Psychosocial factors are known to play a role in the recovery fr…
View article: The BrainWaves study of adolescent wellbeing and mental health: methods development and pilot data
The BrainWaves study of adolescent wellbeing and mental health: methods development and pilot data Open
Adolescent mental health and wellbeing are of growing concern globally with increased incidence of mental health disorders in young people. BrainWaves provides a framework for relevant and diverse research programmes into adolescent mental…
View article: The BrainWaves study of adolescent wellbeing and mental health: methods development and pilot data
The BrainWaves study of adolescent wellbeing and mental health: methods development and pilot data Open
Adolescent mental health and wellbeing are of growing concern globally with increased incidence of mental health disorders in young people. BrainWaves provides a framework for relevant and diverse research programmes into adolescent mental…
View article: Harnessing the TAF1 Acetyltransferase for Targeted Acetylation of the Tumor Suppressor p53
Harnessing the TAF1 Acetyltransferase for Targeted Acetylation of the Tumor Suppressor p53 Open
Pharmacological reactivation of the tumor suppressor p53 remains a key challenge for the treatment of cancer. Ace tylation Ta rgeting C himera (AceTAC), a novel technology is previously reported that hijacks lysine acetyltransferases p300/…
View article: Design, Synthesis, and Evaluation of p53Y220C Acetylation Targeting Chimeras (AceTACs)
Design, Synthesis, and Evaluation of p53Y220C Acetylation Targeting Chimeras (AceTACs) Open
The well-known tumor suppressor p53 is mutated in approximately half of all cancers. The Y220C mutation is one of the major p53 hotspot mutations. Several small-molecule stabilizers of p53Y220C have been developed. We recently developed a …
View article: Differential histone acetylation and super-enhancer regulation underlie melanoma cell dedifferentiation
Differential histone acetylation and super-enhancer regulation underlie melanoma cell dedifferentiation Open
Dedifferentiation or phenotype switching refers to the transition from a proliferative to an invasive cellular state. We previously identified a 122-gene epigenetic gene signature that classifies primary melanomas as low versus high risk (…
View article: Molecular mechanisms in colitis-associated colorectal cancer
Molecular mechanisms in colitis-associated colorectal cancer Open
View article: Etiology of super-enhancer reprogramming and activation in cancer
Etiology of super-enhancer reprogramming and activation in cancer Open
View article: Acetylation Targeting Chimera Enables Acetylation of the Tumor Suppressor p53
Acetylation Targeting Chimera Enables Acetylation of the Tumor Suppressor p53 Open
With advances in chemically induced proximity technologies, heterobifunctional modalities such as proteolysis targeting chimeras (PROTACs) have been successfully advanced to clinics for treating cancer. However, pharmacologic activation of…
View article: AKT activation because of PTEN loss upregulates xCT via GSK3β/NRF2, leading to inhibition of ferroptosis in PTEN-mutant tumor cells
AKT activation because of PTEN loss upregulates xCT via GSK3β/NRF2, leading to inhibition of ferroptosis in PTEN-mutant tumor cells Open
View article: Author Correction: A local tumor microenvironment acquired super-enhancer induces an oncogenic driver in colorectal carcinoma
Author Correction: A local tumor microenvironment acquired super-enhancer induces an oncogenic driver in colorectal carcinoma Open
View article: Supplementary Figure S7 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition
Supplementary Figure S7 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition Open
Supplementary Figure S7. Model.
View article: Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma Open
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
View article: Supplementary Figure S3 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition
Supplementary Figure S3 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition Open
Supplementary Figure S3. PTEN loss confers sensitivity to de novo pyrimidine synthesis inhibition.
View article: Data from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
Data from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma Open
Subunits of SWI/SNF chromatin remodeling complexes are frequently mutated in human malignancies. The PBAF complex is composed of multiple subunits, including the tumor-suppressor protein PBRM1 (BAF180), as well as ARID2 (BAF200), that are …
View article: Supplementary Figure S2 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition
Supplementary Figure S2 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition Open
Supplementary Figure S2. Pyrimidine synthesis is upregulated in Pten-/- MEFs.
View article: Supplementary Figure S1 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition
Supplementary Figure S1 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition Open
Supplementary Figure S1. Loss of Pten increases proliferation.
View article: Supplementary Figures 1-4 from <i>PIK3CA</i> and <i>p53</i> Mutations Promote 4NQO-Initated Head and Neck Tumor Progression and Metastasis in Mice
Supplementary Figures 1-4 from <i>PIK3CA</i> and <i>p53</i> Mutations Promote 4NQO-Initated Head and Neck Tumor Progression and Metastasis in Mice Open
Figure S1. Experimental scheme. Figure S2. Immunohistochemical analysis of the E20/p53 mouse. Figure S3. Representative YFP (+) metastatic cells isolated from the lymph node of an E20p53(YFP) double mutant mouse. Figure S4. Combination ind…
View article: Data from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes
Data from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes Open
TP53 is the most commonly mutated tumor suppressor gene and its mutation drives tumorigenesis. Using ChIP-seq for p53 in the absence of acute cell stress, we found that wild-type but not mutant p53 binds and activates numerous tumor…
View article: Supplementary Spreadsheet S5 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes
Supplementary Spreadsheet S5 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes Open
List of genes amplified at a frequency of 0.5% or greater in all cancer types in TCGA (used in GSEA). Acronyms for cancer types are expanded in the Materials and Methods.
View article: Supplementary Data from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B
Supplementary Data from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B Open
Supplementary Data from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B
View article: Supplementary Figure S7 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition
Supplementary Figure S7 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition Open
Supplementary Figure S7. Model.
View article: Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma Open
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
View article: Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma Open
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
View article: Supplementary Data from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B
Supplementary Data from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B Open
Supplementary Data from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B
View article: Supplementary Figure S6 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition
Supplementary Figure S6 from PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition Open
Supplementary Figure S6. ATR signaling defects contribute to synthetic lethality.
View article: Supplementary Spreadsheet S1 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes
Supplementary Spreadsheet S1 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes Open
Basal p53 ChIP-seq peaks in MCF10A cells (after raw data analysis described in Materials in Methods section) ordered by significance of the peak call. Spreadsheet includes (columns left to right) peak locus (Chromosome, start, end), MACS2 …
View article: Supplementary Table from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B
Supplementary Table from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B Open
Supplementary Table from AKT Degradation Selectively Inhibits the Growth of PI3K/PTEN Pathway–Mutant Cancers with Wild-Type KRAS and BRAF by Destabilizing Aurora Kinase B
View article: Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma Open
Supplementary Figure from Loss of PBRM1 Alters Promoter Histone Modifications and Activates ALDH1A1 to Drive Renal Cell Carcinoma