Brian J. Abraham
YOU?
Author Swipe
View article: Specific oncogene activation of the cell of origin in mucosal melanoma
Specific oncogene activation of the cell of origin in mucosal melanoma Open
Mucosal melanoma (MM) is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics, we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly, …
View article: KAT6A/B inhibition synergizes with retinoic acid and enhances the efficacy of GD2-targeted immunotherapy in neuroblastoma
KAT6A/B inhibition synergizes with retinoic acid and enhances the efficacy of GD2-targeted immunotherapy in neuroblastoma Open
High-risk neuroblastoma accounts for about 15% of childhood cancer deaths and arises from precursors of the peripheral sympathetic nervous system. Retinoids are clinically used to inhibit growth of neuroblastoma cells through reconfigurati…
View article: Multitargeted Reduction of Inflammation and Atherosclerosis in <i>Tet2</i> -deficient CHIP via XPO1 Inhibition and Atf3 restoration
Multitargeted Reduction of Inflammation and Atherosclerosis in <i>Tet2</i> -deficient CHIP via XPO1 Inhibition and Atf3 restoration Open
TET2 is the second most frequently mutated gene in clonal hematopoiesis of indeterminate potential (CHIP), driving hematopoietic stem cell clonal expansion and increasing the risk of myeloid malignancies. Affected individuals often develop…
View article: Bone morphogenetic protein (BMP) signaling determines neuroblastoma cell fate and sensitivity to retinoic acid
Bone morphogenetic protein (BMP) signaling determines neuroblastoma cell fate and sensitivity to retinoic acid Open
View article: Bone morphogenetic protein (BMP) signaling determines neuroblastoma cell fate and sensitivity to retinoic acid
Bone morphogenetic protein (BMP) signaling determines neuroblastoma cell fate and sensitivity to retinoic acid Open
SUMMARY Retinoic acid (RA) is a standard-of-care neuroblastoma drug thought to be effective by inducing differentiation. Curiously, RA has little effect on primary human tumors during upfront treatment but can eliminate neuroblastoma cells…
View article: Specific oncogene activation of the cell of origin in mucosal melanoma
Specific oncogene activation of the cell of origin in mucosal melanoma Open
Mucosal melanoma (MM) is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics, we developed a zebrafish model in which all melanocytes experienced CCND1 expression and loss of PTEN and TP53. Surprisingl…
View article: Group 3 medulloblastoma transcriptional networks collapse under domain specific EP300/CBP inhibition
Group 3 medulloblastoma transcriptional networks collapse under domain specific EP300/CBP inhibition Open
View article: STAT3 couples activated tyrosine kinase signaling to the oncogenic core transcriptional regulatory circuitry of anaplastic large cell lymphoma
STAT3 couples activated tyrosine kinase signaling to the oncogenic core transcriptional regulatory circuitry of anaplastic large cell lymphoma Open
Anaplastic large cell lymphoma (ALCL) is an aggressive, CD30+ T cell lymphoma of children and adults. ALK fusion transcripts or mutations in the JAK-STAT pathway are observed in most ALCL tumors, but the mechanisms underlying tumorigenesis…
View article: 3D-super-enhancers are condensate-associated cis-regulatory communities
3D-super-enhancers are condensate-associated cis-regulatory communities Open
Transcription proteins are concentrated at nuclear transcriptional condensates. These condensates contain cis-regulatory elements (CREs), including enhancers and promoters, that are thought to regulate genes in the same condensate. The rol…
View article: Accurate Measurement of Cell Number–Normalized Differential Gene Expression in Cells Treated With Retinoic Acid
Accurate Measurement of Cell Number–Normalized Differential Gene Expression in Cells Treated With Retinoic Acid Open
Genome-wide gene expression analysis is a commonly used method to quantitatively examine the transcriptional signature of any tissue or cell state. Standard bulk cell RNA sequencing (RNA-seq) quantifies RNAs in the cells of the tissue type…
View article: PAX3-FOXO1 dictates myogenic reprogramming and rhabdomyosarcoma identity in endothelial progenitors
PAX3-FOXO1 dictates myogenic reprogramming and rhabdomyosarcoma identity in endothelial progenitors Open
Fusion-positive rhabdomyosarcoma (FP-RMS) driven by the expression of the PAX3-FOXO1 (P3F) fusion oncoprotein is an aggressive subtype of pediatric rhabdomyosarcoma. FP-RMS histologically resembles developing muscle yet occurs throughout t…
View article: Genetic predisposition to neuroblastoma results from a regulatory polymorphism that promotes the adrenergic cell state
Genetic predisposition to neuroblastoma results from a regulatory polymorphism that promotes the adrenergic cell state Open
Childhood neuroblastomas exhibit plasticity between an undifferentiated neural crest-like mesenchymal cell state and a more differentiated sympathetic adrenergic cell state. These cell states are governed by autoregulatory transcriptional …
View article: Regulatory architecture of housekeeping genes is driven by promoter assemblies
Regulatory architecture of housekeeping genes is driven by promoter assemblies Open
View article: Oncogenic <i>CDK13</i> mutations impede nuclear RNA surveillance
Oncogenic <i>CDK13</i> mutations impede nuclear RNA surveillance Open
RNA surveillance pathways detect and degrade defective transcripts to ensure RNA fidelity. We found that disrupted nuclear RNA surveillance is oncogenic. Cyclin-dependent kinase 13 ( CDK13 ) is mutated in melanoma, and patient-mutated CDK1…
View article: Supplementary Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma
Supplementary Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma Open
Supplementary Data from EP300 Selectively Controls the Enhancer Landscape of MYCN-Amplified Neuroblastoma
View article: Supplementary Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma
Supplementary Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma Open
Supplementary Data from EP300 Selectively Controls the Enhancer Landscape of MYCN-Amplified Neuroblastoma
View article: Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma
Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma Open
Gene expression is regulated by promoters and enhancers marked by histone H3 lysine 27 acetylation (H3K27ac), which is established by the paralogous histone acetyltransferases (HAT) EP300 and CBP. These enzymes display overlapping regulato…
View article: Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma
Data from EP300 Selectively Controls the Enhancer Landscape of <i>MYCN</i>-Amplified Neuroblastoma Open
Gene expression is regulated by promoters and enhancers marked by histone H3 lysine 27 acetylation (H3K27ac), which is established by the paralogous histone acetyltransferases (HAT) EP300 and CBP. These enzymes display overlapping regulato…
View article: Table S3 from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia
Table S3 from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia Open
Table S3
View article: Data from Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression
Data from Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression Open
Acquired drug resistance is a major factor limiting the effectiveness of targeted cancer therapies. Targeting tumors with kinase inhibitors induces complex adaptive programs that promote the persistence of a fraction of the original cell p…
View article: Table S2 from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia
Table S2 from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia Open
Table S2
View article: Table S6 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma
Table S6 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma Open
TEAD4 ChIP-seq results
View article: Table S2 from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia
Table S2 from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia Open
Table S2
View article: Table S1 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma
Table S1 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma Open
Neuroblastoma Molecular subtypes and clinical information.
View article: Supplementary Data from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia
Supplementary Data from TOX Regulates Growth, DNA Repair, and Genomic Instability in T-cell Acute Lymphoblastic Leukemia Open
Supplementary Data
View article: Table S3 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma
Table S3 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma Open
ARACNe-AP transcriptional network from gene expression profiles
View article: Table S3 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma
Table S3 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma Open
ARACNe-AP transcriptional network from gene expression profiles
View article: Supplementary Materials from <i>MYC</i> Drives a Subset of High-Risk Pediatric Neuroblastomas and Is Activated through Mechanisms Including Enhancer Hijacking and Focal Enhancer Amplification
Supplementary Materials from <i>MYC</i> Drives a Subset of High-Risk Pediatric Neuroblastomas and Is Activated through Mechanisms Including Enhancer Hijacking and Focal Enhancer Amplification Open
All supplemental methods, tables, figures and references
View article: Supplementary Materials from <i>MYC</i> Drives a Subset of High-Risk Pediatric Neuroblastomas and Is Activated through Mechanisms Including Enhancer Hijacking and Focal Enhancer Amplification
Supplementary Materials from <i>MYC</i> Drives a Subset of High-Risk Pediatric Neuroblastomas and Is Activated through Mechanisms Including Enhancer Hijacking and Focal Enhancer Amplification Open
All supplemental methods, tables, figures and references
View article: Supplementary Data from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma
Supplementary Data from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma Open
Supplementary Experimental Procedures; Supplementary Figures S1-S10; Supplementary Table Legends S1-S9; Supplementary Tables S8-S9; Additional References