Stephen E. Kurtz
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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: Supplemental FIgure 5 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental FIgure 5 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival within the US cohort (n = 279) based on the presence of signaling pathway mutations including (A) NRAS, (B) KRAS, (C) PTPN11, (D) BRAF, (E) NF1, and (F) WT1. Reported p-values utilized the cox model Wald test.
View article: Supplemental Figure 3 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 3 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival in patients classified as monocytic vs. non-monocytic in (A) patients classified as mPRS higher-benefit (wild-type for FLT3, N/KRAS and TP53), (B) with mutated IDH1/2 and wild-type for N/KRAS, PTPN11, FLT3-ITD, and TP53, a…
View article: Supplemental Table S1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Table S1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Patient and disease characteristics for Beat AML RNAseq cohort (N = 228)
View article: Supplemental Figure 4 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 4 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival in the subgroup of patients not receiving allogeneic cell transplantation (HCT) based on (A) monocytic vs. non-monocytic differentiation, (B) monocytic differentiation and NPM1 mutation status, (C) in the subgroup of patie…
View article: Supplemental Figure 6 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 6 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Surface expression of CD14, CD64, and CD11b in cases by genetic mutation compared to a wild-type reference cohort within the subset of patients with centralized quantitative MFC performed (n = 144). * indicates p < 0.05, ** indicates p < 0…
View article: Supplemental Figure 2 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 2 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival based on monocytic differentiation status censored at HCT for patients within specific mutation subgroups including (A) combined RAS pathway mutations (N/KRAS and PTPN11), and isolated mutations in (B) FLT3-ITD, (C) NRAS, …
View article: Supplemental Figure 8 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 8 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
RNA expression of alternative anti-apoptotic proteins based on RNA-seq defined cell differentiation state. Samples from the top quartile of each state are displayed below.
View article: Supplemental Figure 7 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 7 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
(A) mutation frequency within the Beat AML cohort (n = 228). (B) Heatmap depicting the point-biserial correlation values for RNAseq defined cell state scores in relationship to specific genetic mutations. (C) Heatmap depicting the point-bi…
View article: Supplemental Figure 1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival based on (A) NPM1 mutation status, (B) FLT3-ITD mutation status within NPM1 mutated cases only, (C) IDH1 mutation status, and (D) IDH2 mutation status. Reported p-values utilized the cox model Wald test.
View article: Supplemental Figure 9 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 9 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overview of immunophenotypic expression profiling. (A) Flow cytometry was performed on diagnostic bone marrow specimens and fluorescence measurements, forward light scatter (FSC) and right-angle light scatter (SSC) characteristics were col…
View article: Supplemental Figure 6 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 6 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Surface expression of CD14, CD64, and CD11b in cases by genetic mutation compared to a wild-type reference cohort within the subset of patients with centralized quantitative MFC performed (n = 144). * indicates p < 0.05, ** indicates p < 0…
View article: Supplemental Figure 2 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 2 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival based on monocytic differentiation status censored at HCT for patients within specific mutation subgroups including (A) combined RAS pathway mutations (N/KRAS and PTPN11), and isolated mutations in (B) FLT3-ITD, (C) NRAS, …
View article: Supplemental Figure 1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival based on (A) NPM1 mutation status, (B) FLT3-ITD mutation status within NPM1 mutated cases only, (C) IDH1 mutation status, and (D) IDH2 mutation status. Reported p-values utilized the cox model Wald test.
View article: Supplemental Figure 3 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 3 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival in patients classified as monocytic vs. non-monocytic in (A) patients classified as mPRS higher-benefit (wild-type for FLT3, N/KRAS and TP53), (B) with mutated IDH1/2 and wild-type for N/KRAS, PTPN11, FLT3-ITD, and TP53, a…
View article: Supplemental Figure 4 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 4 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival in the subgroup of patients not receiving allogeneic cell transplantation (HCT) based on (A) monocytic vs. non-monocytic differentiation, (B) monocytic differentiation and NPM1 mutation status, (C) in the subgroup of patie…
View article: Data from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Data from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Resistance to venetoclax (VEN)-based therapy in acute myeloid leukemia (AML) includes genetic (i.e., mutations in N/KRAS, FLT3-ITD, TP53) and phenotypic (i.e., monocytic differentiation) features. Whether monocytic dif…
View article: Supplemental Figure 8 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 8 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
RNA expression of alternative anti-apoptotic proteins based on RNA-seq defined cell differentiation state. Samples from the top quartile of each state are displayed below.
View article: Supplemental FIgure 5 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental FIgure 5 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overall survival within the US cohort (n = 279) based on the presence of signaling pathway mutations including (A) NRAS, (B) KRAS, (C) PTPN11, (D) BRAF, (E) NF1, and (F) WT1. Reported p-values utilized the cox model Wald test.
View article: Supplemental Figure 9 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 9 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Overview of immunophenotypic expression profiling. (A) Flow cytometry was performed on diagnostic bone marrow specimens and fluorescence measurements, forward light scatter (FSC) and right-angle light scatter (SSC) characteristics were col…
View article: Supplemental Table S1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Table S1 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
Patient and disease characteristics for Beat AML RNAseq cohort (N = 228)
View article: Supplemental Figure 7 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study
Supplemental Figure 7 from Genetic and Phenotypic Correlates of Clinical Outcomes with Venetoclax in Acute Myeloid Leukemia: The GEN-PHEN-VEN Study Open
(A) mutation frequency within the Beat AML cohort (n = 228). (B) Heatmap depicting the point-biserial correlation values for RNAseq defined cell state scores in relationship to specific genetic mutations. (C) Heatmap depicting the point-bi…
View article: Suppl Table S8 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia
Suppl Table S8 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia Open
GSEA analysis from trametinib-sensitive and resistant cells
View article: Supp Table S1 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia
Supp Table S1 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia Open
Cytokine levels in patient samples
View article: Suppl Table S5 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia
Suppl Table S5 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia Open
AML feature annotations
View article: Star Table 1 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia
Star Table 1 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia Open
Resource Table
View article: Suppl Table S7 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia
Suppl Table S7 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia Open
Phosphopeptides identified by trametinib and CCL2 treatments using a KSEA analysis
View article: Supp Table S3 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia
Supp Table S3 from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia Open
RNA-seq gene list and pathway correlation with drug resistance
View article: Data from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia
Data from Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia Open
Purpose:Emerging evidence underscores the critical role of extrinsic factors within the microenvironment in protecting leukemia cells from therapeutic interventions, driving disease progression, and promoting drug resistance in acute myelo…