Sharon Shacham
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View article: SINE compounds activate exportin-1 degradation via an allosteric mechanism
SINE compounds activate exportin-1 degradation via an allosteric mechanism Open
The nuclear export receptor exportin 1 (XPO1/CRM1) is often overexpressed in cancer cells, leading to the mislocalization of numerous cancer-related protein cargoes 1,2 . Selinexor, a covalent XPO1 inhibitor, and other Selective Inhibitor …
View article: Oral Selinexor as Maintenance Therapy After First-Line Chemotherapy for Advanced or Recurrent Endometrial Cancer
Oral Selinexor as Maintenance Therapy After First-Line Chemotherapy for Advanced or Recurrent Endometrial Cancer Open
PURPOSE Selinexor inhibits exportin-1 (XPO1) resulting in nuclear accumulation of tumor suppressor proteins including p53 and has clinical activity in endometrial cancer (EC). The primary end point was to assess progression-free survival (…
View article: Supplementary Figure 2 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Supplementary Figure 2 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
PDF file - 53K, Serum levels of KPT-330 in mice.
View article: Supplementary Figure Legends from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Supplementary Figure Legends from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
PDF file - 84K
View article: Supplementary Figure 3. Western blot analysis of myeloma PC derived from three relapsed/refractory patients treated with selinexor and carfilzomib, alone and in combination. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Figure 3. Western blot analysis of myeloma PC derived from three relapsed/refractory patients treated with selinexor and carfilzomib, alone and in combination. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Plasma cells from patients that have failed on treatment regimens that have included proteasome inhibitors, immunomodulatory drugs, and DNA damaging agents were purified from fresh bone marrow aspirates and treated with selinexor and carfi…
View article: Supplementary Figure 4 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma
Supplementary Figure 4 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 4 - PDF file 44K, CRM1 inhibition induces a statistically significant increase in caspase-3/7 activity as single therapy or in combination with BRAF inhibition
View article: Supplementary Figure 1 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma
Supplementary Figure 1 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 1 - PDF file 29K, CRM1 and BRAF inhibition decrease melanoma cell proliferation and are synergistic in vitro
View article: Supplementary Methods and Figure Legends from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma
Supplementary Methods and Figure Legends from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Methods and Figure Legends - PDF 133K, Supplementary methods and figure legends
View article: Supplementary Figure 3 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Supplementary Figure 3 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
PDF file - 87K, Survivin protein levels normalized to tubulin.
View article: Supplementary Figure 4 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Supplementary Figure 4 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
PDF file - 51K, Knockdown of XIAP has no effect on survivin degradation.
View article: Supplementary Figure 4. Changes in body weight of mice receiving single agent or combination treatment with selinexor or carfilzomib. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Figure 4. Changes in body weight of mice receiving single agent or combination treatment with selinexor or carfilzomib. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Body weights of all xenografted mice treated with selinexor and carfilzomib, alone and in combination.
View article: Supplementary Figure 1 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Supplementary Figure 1 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
PDF file - 66K, Molecular structures of the KPT-SINES.
View article: Supplementary Figure 1. Effects of long term pan-caspase inhibition on autophagy in myeloma cells. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Figure 1. Effects of long term pan-caspase inhibition on autophagy in myeloma cells. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Western blot analysis of markers for autophagy and apoptosis in MM1.S cells treated for the indicated time with pan-caspase inhibitor.
View article: Supplementary Figure Legends from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Supplementary Figure Legends from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
PDF file - 84K
View article: Supplementary Figure 2. Representative images used in aggresome analysis. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Figure 2. Representative images used in aggresome analysis. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Representative images of RPMI 8226 cells used for calculation of aggresome formation in response to selinexor and carfilzomib treatment.
View article: Supplementary Figure 1 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma
Supplementary Figure 1 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 1 - PDF file 29K, CRM1 and BRAF inhibition decrease melanoma cell proliferation and are synergistic in vitro
View article: Supplementary Figures 1-9 from Novel p21-Activated Kinase 4 (PAK4) Allosteric Modulators Overcome Drug Resistance and Stemness in Pancreatic Ductal Adenocarcinoma
Supplementary Figures 1-9 from Novel p21-Activated Kinase 4 (PAK4) Allosteric Modulators Overcome Drug Resistance and Stemness in Pancreatic Ductal Adenocarcinoma Open
Supplementary Figure1. IC50 analysis for PAM activity across a panel of cell lines. MTT assay was performed at 72 hrs; Supplementary Figure 2. PDAC cell lines were grown at a density of 50,000 cells per well overnight and exposed to PAMs (…
View article: Data from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Data from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
Inhibition of XPO1 (CRM1)-mediated nuclear export of multiple tumor suppressor proteins has been proposed as a novel cancer therapeutic strategy to turn off oncogenic signals and enhance tumor suppression. Survivin is a multifunctional pro…
View article: Supplementary Figure 6 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma
Supplementary Figure 6 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 6 - PDF file 57K, CRM1/BRAF inhibition in PTEN null/BRAF mutant melanoma Xenograft model
View article: Supplementary Figure 4. Changes in body weight of mice receiving single agent or combination treatment with selinexor or carfilzomib. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Figure 4. Changes in body weight of mice receiving single agent or combination treatment with selinexor or carfilzomib. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Body weights of all xenografted mice treated with selinexor and carfilzomib, alone and in combination.
View article: Data from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Data from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Exportin1 (XPO1; also known as chromosome maintenance region 1, or CRM1) controls nucleo-cytoplasmic transport of most tumor suppressors and is overexpressed in many cancers, including multiple myeloma, functionally impairing tumor suppres…
View article: Supplementary Materials and Methods from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Materials and Methods from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Additional details of antibodies, reagents, and methods used in this manuscript.
View article: Data from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma
Data from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Resistance to BRAF inhibitor therapy places priority on developing BRAF inhibitor-based combinations that will overcome de novo resistance and prevent the emergence of acquired mechanisms of resistance. The CRM1 receptor mediates th…
View article: Supplementary Figure 2 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer
Supplementary Figure 2 from XPO1 (CRM1) Inhibition Represses STAT3 Activation to Drive a Survivin-Dependent Oncogenic Switch in Triple-Negative Breast Cancer Open
PDF file - 53K, Serum levels of KPT-330 in mice.
View article: Supplementary Figure 7. Immunofluorescent localization of Fas and p62. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Figure 7. Immunofluorescent localization of Fas and p62. from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
MM1.S cells were left untreated or treated with Selinexor and Carfilzomib (CFZ; 50 nm each) overnight. Cells were then processed as described for immunofluorescence microscopy using anti-Fas mouse monoclonal antibody and anti-p62 rabbit po…
View article: Supplementary Materials and Methods from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Supplementary Materials and Methods from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Additional details of antibodies, reagents, and methods used in this manuscript.
View article: Data from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor
Data from Synergistic Myeloma Cell Death via Novel Intracellular Activation of Caspase-10–Dependent Apoptosis by Carfilzomib and Selinexor Open
Exportin1 (XPO1; also known as chromosome maintenance region 1, or CRM1) controls nucleo-cytoplasmic transport of most tumor suppressors and is overexpressed in many cancers, including multiple myeloma, functionally impairing tumor suppres…
View article: Supplementary figures 1-3 from XPO1 Inhibitor Selinexor Overcomes Intrinsic Ibrutinib Resistance in Mantle Cell Lymphoma via Nuclear Retention of IκB
Supplementary figures 1-3 from XPO1 Inhibitor Selinexor Overcomes Intrinsic Ibrutinib Resistance in Mantle Cell Lymphoma via Nuclear Retention of IκB Open
Suppl. Fig.1. Selinexor changes cell cycle progression in both ibrutinib-sensitive and -resistant MCL cells. Suppl. Fig.2. Selinexor retains IκBα and NF-κB subunits P65/P50 in the nuclei of Granta-519 cells. Suppl. Fig. 3. Selinexor retain…
View article: Data from Novel p21-Activated Kinase 4 (PAK4) Allosteric Modulators Overcome Drug Resistance and Stemness in Pancreatic Ductal Adenocarcinoma
Data from Novel p21-Activated Kinase 4 (PAK4) Allosteric Modulators Overcome Drug Resistance and Stemness in Pancreatic Ductal Adenocarcinoma Open
The p21-activated kinase 4 (PAK4) is a key downstream effector of the Rho family GTPases and is found to be overexpressed in pancreatic ductal adenocarcinoma (PDAC) cells but not in normal human pancreatic ductal epithelia (HPDE). Gene cop…
View article: Supplementary Figure 7 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma
Supplementary Figure 7 from CRM1 and BRAF Inhibition Synergize and Induce Tumor Regression in BRAF-Mutant Melanoma Open
Supplementary Figure 7 - PDF file, TP53 knockdown in A375 reduces the effect of CRM1 inhibition on A375 proliferation but not on caspase-3/7 activity