Daniel Bottomly
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View article: m6a and NuRD complexes regulate monocytic differentiation and resistance to BCL2/BCL2L1 inhibitors in acute myeloid leukemia
m6a and NuRD complexes regulate monocytic differentiation and resistance to BCL2/BCL2L1 inhibitors in acute myeloid leukemia Open
Frontline use of the BCL2 inhibitor, venetoclax, for acute myeloid leukemia (AML) has resulted in broad improvements in patient outcome. A major remaining challenge is the development of venetoclax resistance, frequently driven by compensa…
View article: A Rapid Gene Expression Profiler Classifies AML Tumor Responsiveness to Standard Therapies
A Rapid Gene Expression Profiler Classifies AML Tumor Responsiveness to Standard Therapies Open
The emergence of transcriptional signatures that define cell types and pathways has made it possible to guide cancer therapy selection through gene expression profiling. We developed a rapid qPCR-based platform to profile cell state, stemn…
View article: Utilizing cohort-level and individual networks to predict best response in patients with metastatic triple negative breast cancer
Utilizing cohort-level and individual networks to predict best response in patients with metastatic triple negative breast cancer Open
View article: Assessing individual head and neck squamous cell carcinoma patient response to therapy through integration of functional and genomic data
Assessing individual head and neck squamous cell carcinoma patient response to therapy through integration of functional and genomic data Open
Even though head and neck squamous cell carcinoma (HNSCC) is the seventh most common cancer worldwide, there are only two PD-1 targeted immunotherapies (pembrolizumab and nivolumab) and one tumor intrinsic EGFR targeted therapy (cetuximab)…
View article: Multiomic profiling identifies predictors of survival in African American patients with acute myeloid leukemia
Multiomic profiling identifies predictors of survival in African American patients with acute myeloid leukemia Open
View article: Supplementary Table 15 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 15 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Log2 Normalized Counts of Differentially Expressed Genes from Primary AML Blast Bulk RNA-seq (24 Hours After Drug Treatment)
View article: Supplementary Fig. 10 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 10 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Efficacy of dual FLT3/LSD1 inhibition in primary AML samples.
View article: Supplementary Table 4 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 4 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Transcription Factor Enrichment Analysis of Differentially Downregulated Genes by The Drug Combination Previously Identified as Depleting Genes in a Genome-Wide CRISPR Dropout Screen
View article: Supplementary Fig. 5 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 5 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
STAT5 and MYC play a key role in the response to FLT3/LSD1 inhibition.
View article: Supplementary Table 5 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 5 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Normalized Read Pileup and Differential Enrichment Clusters of MOLM13 H3K27Ac CUT&Tag (2 Hours After Drug Treatment)
View article: Supplementary Table 14 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 14 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Regulon Enrichment Analysis of Primary AML Blast Bulk RNA-seq from 681 Patient Samples
View article: Supplementary Table 3 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 3 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Transcription Factor Enrichment Analysis of Differentially Downregulated Genes by The Drug Combination Previously Identified as Depleting Genes in a Genome-Wide CRISPR Dropout Screen
View article: Supplementary Fig. 6 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 6 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Stat5 over-expression diminishes the efficacy of combined FLT3/LSD1 inhibition.
View article: Supplementary Table 8 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 8 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
RNA PolII Pause Index Analysis from MOLM13 RBP1 CUT&Tag (6 Hours After Drug Treatment)
View article: Supplementary Table 18 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 18 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Single Cell ATAC Cell Type Populations
View article: Supplementary Table 6 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 6 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Normalized Read Pileup and Differential Enrichment Clusters of MOLM13 H3K27Ac CUT&Tag (6 Hours After Drug Treatment) at Enhancers and Promoters
View article: Supplementary Table 9 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 9 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Differential Phosphoprotein Network Enrichment in MOLM13 Cells (24 Hours After Drug Treatment)
View article: Supplementary Table 2 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 2 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Transcription Factor Enrichment Analysis of MOLM13 Bulk RNA-Seq (24 Hours After Drug Treatment)
View article: Data from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Data from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Mutations in Fms-like tyrosine kinase 3 (FLT3) are common drivers in acute myeloid leukemia (AML) yet FLT3 inhibitors only provide modest clinical benefit. Prior work has shown that inhibitors of lysine-specific demethylase 1 (LSD1) enhanc…
View article: Supplementary Fig. 8 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 8 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Combined FLT3/LSD1 inhibition does not substantially alter myeloid differentiation.
View article: Supplementary Table 1 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 1 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Log2 Normalized Counts of Differentially Expressed Genes from MOLM13 Bulk RNA-seq (24 Hours After Drug Treatment)
View article: Supplementary Fig. 7 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 7 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
GFI1 knockdown weakens the effects of dual FLT3/LSD1 inhibition.
View article: Supplementary Fig. 12 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 12 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Dual FLT3/LSD1 inhibition disrupts LSC clonogenicity.
View article: Supplementary Fig. 9 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 9 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
SPI1 knockdown does not disrupt dual FLT3/LSD1 inhibition synergy.
View article: Supplementary Table 10 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 10 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Correlation of Regulon Enrichment Signatures with MYC Gene Expression in Primary AML
View article: Supplementary Table 7 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 7 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
GO Analysis from Regions of Differential MOLM13 H3K27Ac CUT&Tag (6 Hours After Drug Treatment) Pileup at Enhancers and Promoters
View article: Supplementary Materials and Methods from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Materials and Methods from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Supplementary Materials and Methods
View article: Supplementary Table 15 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Table 15 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Log2 Normalized Counts of Differentially Expressed Genes from Primary AML Blast Bulk RNA-seq (24 Hours After Drug Treatment)
View article: Supplementary Materials and Methods from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Materials and Methods from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Supplementary Materials and Methods
View article: Supplementary Fig. 1 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia
Supplementary Fig. 1 from Disruption of the MYC Super-Enhancer Complex by Dual Targeting of FLT3 and LSD1 in Acute Myeloid Leukemia Open
Drug synergy between FLT3 and LSD1 inhibitors in FLT3-ITD and FLT3-wildtype cell lines.