Judith E. Karp
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View article: P18.18.B A NOVEL, POOLED, HIGH-THROUGHPUT SCREENING OF A CNS PENETRANT COMPOUND LIBRARY IDENTIFIES POTENTIAL BIOMARKER-DRIVEN THERAPEUTICS FOR GLIOBLASTOMA
P18.18.B A NOVEL, POOLED, HIGH-THROUGHPUT SCREENING OF A CNS PENETRANT COMPOUND LIBRARY IDENTIFIES POTENTIAL BIOMARKER-DRIVEN THERAPEUTICS FOR GLIOBLASTOMA Open
BACKGROUND Identifying drug sensitivities that will translate to clinical practice for patients with glioblastoma (GBM) necessitates the use of a variety of cell models that recapitulate the heterogeneity of the disease. Screening of large…
View article: Genomic testing and patient rights
Genomic testing and patient rights Open
View article: Prognostic impact of secondary versus de novo ontogeny in acute myeloid leukemia is accounted for by the European LeukemiaNet 2022 risk classification
Prognostic impact of secondary versus de novo ontogeny in acute myeloid leukemia is accounted for by the European LeukemiaNet 2022 risk classification Open
View article: Supplemental Figure 5A from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Supplemental Figure 5A from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Representative Individual Concentration versus Time Pharmacokinetic Profiles for Total or Unbound lavopiridol Using Bolus (A) or Hybrid (B) Dosing Schemes.
View article: Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia
Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia Open
Purpose: In preclinical studies, the PARP inhibitor veliparib enhanced the antileukemic action of temozolomide through potentiation of DNA damage. Accordingly, we conducted a phase 1 study of temozolomide with escalating doses of ve…
View article: Supplemental Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia
Supplemental Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia Open
Table S1. Changes in Proportion (%) of γH2AX-Positive Cells in Peripheral Blood upon Veliparib and Veliparib/Temozolomide Treatment Figure S1. FANCD2 monoubiquitination following ex vivo melphalan treatment of patient bone marrow cells Fig…
View article: Supplemental Figure Legends and Tables from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies
Supplemental Figure Legends and Tables from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies Open
7 tables and 3 figure legends
View article: Data from Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms
Data from Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms Open
Purpose: DNA repair defects have been previously reported in myeloproliferative neoplasms (MPN). Inhibitors of PARP have shown activity in solid tumors with defects in homologous recombination (HR). This study was performed to asses…
View article: Supplemental Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia
Supplemental Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia Open
Table S1. Changes in Proportion (%) of γH2AX-Positive Cells in Peripheral Blood upon Veliparib and Veliparib/Temozolomide Treatment Figure S1. FANCD2 monoubiquitination following ex vivo melphalan treatment of patient bone marrow cells Fig…
View article: Supplemental Figure 3 from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Supplemental Figure 3 from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Conditional Weighted Residuals versus Time or Predicted Concentration: Total Flavopiridol (A and C), Unbound Flavopiridol (B and D).
View article: Supplemental Figure 1B from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies
Supplemental Figure 1B from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies Open
Relationship between AUC and Cmax at steady state (B
View article: Supplemental Table and Figures from Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms
Supplemental Table and Figures from Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms Open
Table S1: Primers for Methylation Analysis. Figure S1: Sensitivity of erythroid and myeloid progenitors to veliparib. Figure S2: Reproducibility of colony forming assays. Figure S3: Veliparib IC50 as a function of BRCA1 Promotor Methylatio…
View article: Supplementary Figures S1-S2 from NF1 Inactivation in Adult Acute Myelogenous Leukemia
Supplementary Figures S1-S2 from NF1 Inactivation in Adult Acute Myelogenous Leukemia Open
Supplementary Figures S1-S2 from NF1 Inactivation in Adult Acute Myelogenous Leukemia
View article: Data from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Data from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Purpose: To elucidate any differences in the exposure–response of alvocidib (flavopiridol) given by 1-hour bolus or a hybrid schedule (30-minute bolus followed by a 4-hour infusion) using a flavopiridol/cytosine arabinoside/mitoxant…
View article: Supplemental Table and Figures from Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms
Supplemental Table and Figures from Poly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms Open
Table S1: Primers for Methylation Analysis. Figure S1: Sensitivity of erythroid and myeloid progenitors to veliparib. Figure S2: Reproducibility of colony forming assays. Figure S3: Veliparib IC50 as a function of BRCA1 Promotor Methylatio…
View article: Supplementary Tables 1 - 2, Figure 1 from Effects of Selective Checkpoint Kinase 1 Inhibition on Cytarabine Cytotoxicity in Acute Myelogenous Leukemia Cells <i>In Vitro</i>
Supplementary Tables 1 - 2, Figure 1 from Effects of Selective Checkpoint Kinase 1 Inhibition on Cytarabine Cytotoxicity in Acute Myelogenous Leukemia Cells <i>In Vitro</i> Open
PDF file, 105K, This file contains Supplemental Table 1 (Description of Patients Providing Samples for Assessment of Chk1 phosphorylation ), Supplemental Table 2 (Quantitative Effects of Cytarabine, SCH 900776 and the Combination on Sample…
View article: Data from CDK2-Mediated Upregulation of TNFα as a Mechanism of Selective Cytotoxicity in Acute Leukemia
Data from CDK2-Mediated Upregulation of TNFα as a Mechanism of Selective Cytotoxicity in Acute Leukemia Open
Although inhibitors of the kinases CHK1, ATR, and WEE1 are undergoing clinical testing, it remains unclear how these three classes of agents kill susceptible cells and whether they utilize the same cytotoxic mechanism. Here we observed tha…
View article: Supplementary Data from CDK2-Mediated Upregulation of TNFα as a Mechanism of Selective Cytotoxicity in Acute Leukemia
Supplementary Data from CDK2-Mediated Upregulation of TNFα as a Mechanism of Selective Cytotoxicity in Acute Leukemia Open
Supplementary methods, three supplementary tables and 16 supplementary figures
View article: Supplemental Figure 1A from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies
Supplemental Figure 1A from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies Open
Relationship between AUC and Cmax after single dose (A)
View article: Supplemental Figure 1A from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies
Supplemental Figure 1A from Exposure–Response of Veliparib to Inform Phase II Trial Design in Refractory or Relapsed Patients with Hematological Malignancies Open
Relationship between AUC and Cmax after single dose (A)
View article: Supplemental Data from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Supplemental Data from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Supplemental Tables 1-5 and upplemental Figure Legends
View article: Supplemental Figure 5B from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Supplemental Figure 5B from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Representative Individual Concentration versus Time Pharmacokinetic Profiles for Total or Unbound Flavopiridol Using Bolus (A) or Hybrid (B) Dosing Schemes.
View article: Supplemental Figure 5B from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Supplemental Figure 5B from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Representative Individual Concentration versus Time Pharmacokinetic Profiles for Total or Unbound Flavopiridol Using Bolus (A) or Hybrid (B) Dosing Schemes.
View article: Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia
Data from A Phase 1 Study of the PARP Inhibitor Veliparib in Combination with Temozolomide in Acute Myeloid Leukemia Open
Purpose: In preclinical studies, the PARP inhibitor veliparib enhanced the antileukemic action of temozolomide through potentiation of DNA damage. Accordingly, we conducted a phase 1 study of temozolomide with escalating doses of ve…
View article: Supplemental Figure 1 from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Supplemental Figure 1 from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Observed Total Flavopiridol Concentrations versus Time for Bolus and Hybrid Administration.
View article: Supplemental Figure 2 from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients
Supplemental Figure 2 from Exposure–Response Analysis of Alvocidib (Flavopiridol) Treatment by Bolus or Hybrid Administration in Newly Diagnosed or Relapsed/Refractory Acute Leukemia Patients Open
Observed versus Predicted Flavopiridol Concentrations: Total Individual (A), Unbound Individual (B), Total Population (C), or Unbound Population (D).
View article: Supplemental Figures and Tables from A Phase I Study of Topotecan, Carboplatin and the PARP Inhibitor Veliparib in Acute Leukemias, Aggressive Myeloproliferative Neoplasms, and Chronic Myelomonocytic Leukemia
Supplemental Figures and Tables from A Phase I Study of Topotecan, Carboplatin and the PARP Inhibitor Veliparib in Acute Leukemias, Aggressive Myeloproliferative Neoplasms, and Chronic Myelomonocytic Leukemia Open
Supplemental Figure S1. A, pretreatment bone marrow samples were treated diluent (-) with 10 μM melphalan (+) for 6 h and analyzed by immmunoblotting for FANCD2, ubiquitinated FANCD2 (Ub-FANCD2) and, as a loading control, heat shock protei…
View article: Supplementary Tables 1 - 2, Figure 1 from Effects of Selective Checkpoint Kinase 1 Inhibition on Cytarabine Cytotoxicity in Acute Myelogenous Leukemia Cells <i>In Vitro</i>
Supplementary Tables 1 - 2, Figure 1 from Effects of Selective Checkpoint Kinase 1 Inhibition on Cytarabine Cytotoxicity in Acute Myelogenous Leukemia Cells <i>In Vitro</i> Open
PDF file, 105K, This file contains Supplemental Table 1 (Description of Patients Providing Samples for Assessment of Chk1 phosphorylation ), Supplemental Table 2 (Quantitative Effects of Cytarabine, SCH 900776 and the Combination on Sample…
View article: Data from A Phase I Study of Topotecan, Carboplatin and the PARP Inhibitor Veliparib in Acute Leukemias, Aggressive Myeloproliferative Neoplasms, and Chronic Myelomonocytic Leukemia
Data from A Phase I Study of Topotecan, Carboplatin and the PARP Inhibitor Veliparib in Acute Leukemias, Aggressive Myeloproliferative Neoplasms, and Chronic Myelomonocytic Leukemia Open
Purpose: The PARP inhibitor veliparib delays DNA repair and potentiates cytotoxicity of multiple classes of chemotherapy drugs, including topoisomerase I inhibitors and platinating agents. This study evaluated veliparib incorporatio…
View article: Data from Effects of Selective Checkpoint Kinase 1 Inhibition on Cytarabine Cytotoxicity in Acute Myelogenous Leukemia Cells <i>In Vitro</i>
Data from Effects of Selective Checkpoint Kinase 1 Inhibition on Cytarabine Cytotoxicity in Acute Myelogenous Leukemia Cells <i>In Vitro</i> Open
Purpose: Previous studies have shown that the replication checkpoint, which involves the kinases ataxia telangiectasia mutated and Rad3 related (ATR) and Chk1, contributes to cytarabine resistance in cell lines. In the present study…