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View article: Supplementary Figure S13 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S13 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Time course study design for imaging and OT-82 treatment for hyperpolarized pyruvate 13C-MRSI. Post treatment MRSI was performed 5 hours post OT-82 dose #2.
View article: Supplementary Figure S2. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S2. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Validation studies to evaluate inhibition of additional HLRCC cell lines by NAMPT inhibitors. A) Effects of the NAMPT inhibitor GNE-618 on cell viability in FH -/- HLRCC cells lines UOK348, UOK271, UOK350, UOK268, UOK365, FH restored UOK26…
View article: Supplementary Figure S6. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S6. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Real-time invasion analysis of UOK262 and UOK365 cells treated with OT-82. Real-time invasion analysis of UOK262 and UOK365 cells demonstrating cell line invasion over 5 days (120 hrs) was performed (A) to show that DMSO (used as the vehic…
View article: Supplementary Figure S10 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S10 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
NAMPT immunohistochemical analysis in HLRCC tumors and normal kidney. (A) In patient #1, both a primary kidney HLRCC tumor (upper panel) and an associated metastatic mass (lower panel) demonstrated strong NAMPT staining. Surrounding non-tu…
View article: Supplementary Figure S7 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S7 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
In vivo effects of NAMPT inhibitors in HLRCC xenograft models. Mean body weights are constant throughout the drug study for animals harboring UOK262 xenografts (A) and UOK365 xenografts (B; study shown in Figure 3A-B, n = 10 mice per arm, …
View article: Data from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Data from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Hereditary leiomyomatosis and renal cell cancer (HLRCC) is an inherited cancer syndrome caused by germline pathogenic variants in the fumarate hydratase (FH) gene. Affected individuals are at risk for developing cutaneous and uterine leiom…
View article: Supplementary Figure S11 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S11 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Proliferation analysis of UOK268 and RPTEC in response to OT-82 and nicotinic acid rescue of NAD+/NADH depletion. (A-B) UOK268 or RPTEC cells were grown in 96 well plates from an initial plating of 2,000 cells and cellular confluency was m…
View article: Supplementary Table S1 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Table S1 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Validation of MIPE hits in 96-well cytotoxicity screens and comparison of NAMPT inhibitor efficacy across a panel of HLRCC cell lines.
View article: Supplementary Figure S8 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S8 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Pharmacokinetic profile of OT-82 in nude and NSG mice. (A) Bioanalysis of plasma concentrations of OT-82 were made using a validated LC-MS/MS assay (n=3 nude mice, 50 mg/kg, 7 intervals; n=3 NSG mice, 75mg/kg, 7 intervals). (B) Pharmacokin…
View article: Supplementary Figure S5. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S5. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
HLRCC spheroid characterization and OT-82 effect on 3D culture. A) UOK262 and (B) UOK365 spheroids plated at different cell densities (8000, 4000, and 2000 cells/well in triplicate) after 24h, showing different degrees of cell aggregation.…
View article: Supplementary Figure S1 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S1 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Structural figures of NAMPT inhibitors.
View article: Supplementary Figure S3. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S3. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Cell proliferation rates of HLRCC cell lines treated with low and high concentrations of NAMPT inhibitors. A) Effect of OT-82 at 0.8nM or 100nM (left) and GNE-618 at 8nM or 200nM (right) on cell proliferation of UOK262 after 96 hours. B) E…
View article: Supplementary Figure S12 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S12 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
In vitro analysis of NAMPT inhibition on glycolysis in FH-deficient tumor cells. (A) Effects of the NAMPT inhibitor OT-82 (100 nM) on the extracellular acidification rate (ECAR) in the UOK262 and UOK365 HLRCC cell lines and the RPTEC norma…
View article: Supplementary Figure S4. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S4. from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
NAD+ and NADH analysis of UOK365 cells. Analysis of the relative levels of NAD+ and NADH and their ratio after 24 hour treatment of the UOK365 cell line model with a range of concentrations (0.5-100 nM) of either GNE-618 (A-B) or OT-82 (C-…
View article: Supplementary Figure S9 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Supplementary Figure S9 from Targeting NAD<sup>+</sup> Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Expression levels of NAD+ biosynthetic and salvage pathway genes in HLRCC tumors, normal kidney samples and pan-kidney data from TCGA. (A) Overview of NAD+ biosynthetic and salvage pathways. (B-E) Box plots for selected NAD+ biosynthetic g…
View article: Targeting NAD+ Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82
Targeting NAD+ Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82 Open
Hereditary leiomyomatosis and renal cell cancer (HLRCC) is an inherited cancer syndrome caused by germline pathogenic variants in the fumarate hydratase (FH) gene. Affected individuals are at risk for developing cutaneous and uterine leiom…
View article: Metastatic organotropism in small cell lung cancer
Metastatic organotropism in small cell lung cancer Open
Metastasis is the leading cause of cancer-related deaths, yet its regulatory mechanisms are not fully understood. Small-cell lung cancer (SCLC) is the most metastatic form of lung cancer, with most patients presenting with widespread disea…
View article: Toward a CRISPR-based mouse model of <i>Vhl</i> -deficient clear cell kidney cancer: Initial experience and lessons learned
Toward a CRISPR-based mouse model of <i>Vhl</i> -deficient clear cell kidney cancer: Initial experience and lessons learned Open
CRISPR is revolutionizing the ability to do somatic gene editing in mice for the purpose of creating new cancer models. Inactivation of the VHL tumor suppressor gene is the signature initiating event in the most common form of kidney cance…
View article: Preclinical Therapeutic Efficacy of RAF/MEK/ERK and IGF1R/AKT/mTOR Inhibition in Neuroblastoma
Preclinical Therapeutic Efficacy of RAF/MEK/ERK and IGF1R/AKT/mTOR Inhibition in Neuroblastoma Open
Activating mutations in the RAS/MAPK pathway are observed in relapsed neuroblastoma. Preclinical studies indicate that these tumors have an increased sensitivity to inhibitors of the RAS/MAPK pathway, such as MEK inhibitors. MEK inhibitors…
View article: Supplemental Figure legends from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease
Supplemental Figure legends from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease Open
Figure legends for Supplemental Figures
View article: Data from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease
Data from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease Open
Renal cell carcinoma (RCC) associated with Xp11.2 translocation (TFE3-RCC) has been recently defined as a distinct subset of RCC classified by characteristic morphology and clinical presentation. The Xp11 translocations involve the TFE3 tr…
View article: Supplementary Figures and Tables from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease
Supplementary Figures and Tables from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease Open
Supplemental Figure S1. Representative images of TFE3 immunohistochemistry of renal papillae and renal pelvis (a, b), ureters (c, d), and bladders (e, f) from a 10-month-old PRCC-TFE3; KSP-Cre- (a, c, e) mouse and a PRCC-TFE3; KSP-Cre+ (b,…
View article: Supplementary Figures and Tables from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease
Supplementary Figures and Tables from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease Open
Supplemental Figure S1. Representative images of TFE3 immunohistochemistry of renal papillae and renal pelvis (a, b), ureters (c, d), and bladders (e, f) from a 10-month-old PRCC-TFE3; KSP-Cre- (a, c, e) mouse and a PRCC-TFE3; KSP-Cre+ (b,…
View article: Supplemental Figure legends from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease
Supplemental Figure legends from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease Open
Figure legends for Supplemental Figures
View article: Data from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease
Data from TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease Open
Renal cell carcinoma (RCC) associated with Xp11.2 translocation (TFE3-RCC) has been recently defined as a distinct subset of RCC classified by characteristic morphology and clinical presentation. The Xp11 translocations involve the TFE3 tr…
View article: Supplementary Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis
Supplementary Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis Open
Supplementary Figures S1-S5; Supplementary Materials and Methods.
View article: Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis
Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis Open
Purpose: Brain metastases of breast cancer contribute significantly to patient morbidity and mortality. We have tested pazopanib, a recently approved antiangiogenic drug that targets VEGFR1, VEGFR2, VEGFR3, PDGFRβ, PDGFRα, and c-kit, for p…
View article: Supplementary Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis
Supplementary Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis Open
Supplementary Figures S1-S5; Supplementary Materials and Methods.
View article: Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis
Data from Pazopanib Reveals a Role for Tumor Cell B-Raf in the Prevention of HER2<sup>+</sup> Breast Cancer Brain Metastasis Open
Purpose: Brain metastases of breast cancer contribute significantly to patient morbidity and mortality. We have tested pazopanib, a recently approved antiangiogenic drug that targets VEGFR1, VEGFR2, VEGFR3, PDGFRβ, PDGFRα, and c-kit, for p…
View article: Supplementary Figure from Chemopreventive Activity of Plant Flavonoid Isorhamnetin in Colorectal Cancer Is Mediated by Oncogenic Src and β-Catenin
Supplementary Figure from Chemopreventive Activity of Plant Flavonoid Isorhamnetin in Colorectal Cancer Is Mediated by Oncogenic Src and β-Catenin Open
PDF file, 34K, Isorhamnetin has little affect on cell growth of HT29 cells on plastic, but inhibits anchor independent growth.