Supplementary Figure 1 from H2AX phosphorylation marks gemcitabine-induced stalled replication forks and their collapse upon S-phase checkpoint abrogation

Supplementary Figure 1 from H2AX phosphorylation marks gemcitabine-induced stalled replication forks and their collapse upon S-phase checkpoint abrogatio

Supplementary Table 1 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonuclease

Supplementary Table 1 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonucleas

Supplementary Figure 1 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonuclease

Supplementary Figure 1 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonucleas

Supplementary Figure 2 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonuclease

Supplementary Figure 2 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonucleas

Supplementary Table 2 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonuclease

Supplementary Table 2 from Killing of Chronic Lymphocytic Leukemia by the Combination of Fludarabine and Oxaliplatin Is Dependent on the Activity of XPF Endonucleas

Supplemental figures from HDAC Inhibition Induces MicroRNA-182, which Targets RAD51 and Impairs HR Repair to Sensitize Cells to Sapacitabine in Acute Myelogenous Leukemia

Supplemental Figure 1. HDAC inhibitors sensitize MV4-11 AML cells to CNDAC. Supplemental Figure 2. Action of CNDAC alone or in combination with 0.5 nM PS over time on Rad51 in MV4-11 cells. Supplemental Figure 3. Action of PS on Rad51 mRNA, Rad50 and Rad51 protein and lack of dependence on caspase-3 cleavage in the HDAC-mediated loss of Rad51 protein Supplemental Figure 4. HDAC inhibition does not decrease levels of the DNA repair proteins ATM or NBS1. Figure 5. HDAC inhibition does not increase levels of miR-182 in response to decitabine (DAC) alone. Figure 6. Recruitment of HDAC1 and HDAC2 at the miR-182 promoter in OCI-AML3 cells before and after exposure to 0.5 nM PS. Figure 7. OCI-.AML3 cells were left untreated, transfected with 100nM of scrambled oligonucleotides (Scr), miR-182 or anti-miR-182 for 48h (n=3) before a portion from each treatment was challenged with 0.5nM PS in combination with 2 μM CNDAC for 48h (n=2), following which the levels of cell death were assayed.</p

Supplemental figure legends and methods from HDAC Inhibition Induces MicroRNA-182, which Targets RAD51 and Impairs HR Repair to Sensitize Cells to Sapacitabine in Acute Myelogenous Leukemia

Supplemental figure legends and methods Table 1. Combination of sapacitabine (CNDAC) and panobinostat (PS) or vorinostat (SAHA) in leukemia cell lines. Table 2. Expression levels of the miRNA induced after HDAC inhibition in OCIAML3 cells and their predicted targets within the HR repair pathway. Table 3 Characteristics of AML blasts</p

Additional file 1 of Preclinical evaluation of combination nemtabrutinib and venetoclax in chronic lymphocytic leukemia

Additional file 1: Fig. S1. Kaplan–Meier estimated survival of all recipient mice (n=93) treated with vehicle, venetoclax (100 mg/kg), nemtabrutinib (75 mg/kg), ibrutinib (25 mg/kg), venetoclax (100 mg/kg) and nemtabrutinib (75 mg/kg), or venetoclax (100 mg/kg) and ibrutinib (25 mg/kg)

Supplemental Data from XPO1 Inhibition using Selinexor Synergizes with Chemotherapy in Acute Myeloid Leukemia by Targeting DNA Repair and Restoring Topoisomerase IIα to the Nucleus

Table S1: IC50 values of Topo IIa inhibitors (idarubicin, etoposide, mitoxantrone, daunorubicin) and selinexor at 48hrs as measured by WST-1 assay for AML cell lines MV4-11 and MOLM-13. Table S2: Combinatorial Index (CI) values of concomitant treatment of selinexor with Topo IIa inhibitors (idarubicin and daunorubicin) in AML cell lines MV4-11 and MOLM-13. Table S3: Combinatorial Index (CI) values of concomitant treatment of selinexor with Topo IIa inhibitors (idarubicin and daunorbicin) in AML patient blasts. Table S4: Combinatorial Index (CI) values of concomitant treatment of selinexor with individual Topo IIa inhibitors (etoposide, mitoxantrone) in AML cell lines MV4-11 and MOLM-13. Table S1: IC50 values of Topo IIα inhibitors and selinexor in AML cell lines Table S2: Combinatorial Index (CI) values of selinexor with idarubicin and daunorubicin in AML cell lines Table S3: Combinatorial Index (CI) values of selinexor with idarubicin/daunorubicin in AML patient cells Table S4: Combinatorial Index (CI) values of selinexor with Topo IIα inhibitors (etoposide and mitoxantrone) with selinexor in AML cell lines</p

Supplementary Data from Disruption of DNA Repair and Survival Pathways through Heat Shock Protein Inhibition by Onalespib to Sensitize Malignant Gliomas to Chemoradiation Therapy

Supplementary Data from Disruption of DNA Repair and Survival Pathways through Heat Shock Protein Inhibition by Onalespib to Sensitize Malignant Gliomas to Chemoradiation Therap