Katelyn J. Noronha
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View article: NAPRT expression and epigenetic regulation in pediatric rhabdomyosarcoma as a potential biomarker for NAMPT inhibition
NAPRT expression and epigenetic regulation in pediatric rhabdomyosarcoma as a potential biomarker for NAMPT inhibition Open
Purpose New treatments are needed to improve survival in children with rhabdomyosarcoma (RMS). NAD⁺ biosynthesis, regulated by the enzymes NAPRT and NAMPT, represents a metabolic vulnerability due to high NAD⁺ turnover in cancers. Although…
View article: Supplementary Table 2 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Table 2 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Results from GO Pathway Analysis in FH-deficient cell lines.
View article: Supplementary Figure 8 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 8 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
NAPRT silencing confers sensitivity to NAMPTis in IDH1/2 mutant cancer cell line models.
View article: Supplementary Figure 11 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 11 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Combination of PARPi and NAMPTi lead to unresolved double stranded breaks NAPRT silenced models.
View article: Supplementary Figure 1 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 1 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Additional cell line validation.
View article: Supplementary Figure 3 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 3 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Patient methylation and protein expression of NAPRT.
View article: Supplementary Figure 10 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 10 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
NAMPTis and PARPis synergize in IDH1/2 NAPRT-deficient tumor models.
View article: Supplementary Table 7 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Table 7 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Summary of statistics and data used to generate NAD+ pathway gene expression correlation plots.
View article: Supplementary Figure 12 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 12 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Combination of FK866 and olaparib leads to sustained cell cycle arrest in G2.
View article: Supplementary Table 4 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Table 4 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Differentially methylated gene lists in common as depicted in Supplementary Figure 2.
View article: Supplementary Table 1 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Table 1 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Mycoplasma testing information.
View article: Supplementary Figure 5 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 5 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Relationships between NAPRT, NAMPT, PARP, and QPRT expression in cancer cell lines.
View article: Supplementary Table 5 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Table 5 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Detailed pathology and FH mutation information for HLRCC patients' samples.
View article: Supplementary Table 6 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Table 6 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Detailed information for RCC PDX samples.
View article: Supplementary Figure 9 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 9 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
BLISS synergy scores for FH-deficient renal cell lines.
View article: Supplementary Figure 2 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 2 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Hypermethylation of patient derived cell line models and patient samples impacts various cancer related pathways and NAPRT expression.
View article: Supplementary Figure 6 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 6 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
NAPRT protein expression is associated with response to NAMPTi alone and in combination with PARPi.
View article: Supplementary Table 3 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Table 3 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Statistics for CpG island comparisons between mean methylation of probes in FH-deficient cell lines.
View article: Supplementary Figure 7 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 7 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
NAPRT is silenced in IDH1R132H U87 glioma model by promoter hypermethylation.
View article: Supplementary Figure 4 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Supplementary Figure 4 from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Patient derived FH-deficient, NAPRT silenced cell line models are sensitive to multiple NAMPTis.
View article: Data from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion
Data from NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD<sup>+</sup> Depletion Open
Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is caused by loss of function mutations in fumarate hydratase (FH) and results in an aggressive subtype of renal cell carcinoma with limited treatment options. Loss of FH leads to …
View article: Data from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Data from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors Open
The treatment of primary central nervous system tumors is challenging due to the blood–brain barrier and complex mutational profiles, which is associated with low survival rates. However, recent studies have identified common mutations in …
View article: Data from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Data from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors Open
The treatment of primary central nervous system tumors is challenging due to the blood–brain barrier and complex mutational profiles, which is associated with low survival rates. However, recent studies have identified common mutations in …
View article: Figure S1 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Figure S1 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors Open
Validation of PLA-PEG GMX1778 efficacy in an IDH1-R132H model.
View article: Figure S1 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Figure S1 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors Open
Validation of PLA-PEG GMX1778 efficacy in an IDH1-R132H model.
View article: Figure S2 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Figure S2 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors Open
Efficacy of BNP GMX1778 in PPM1Dtrnc. isogenic model.
View article: Figure S2 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Figure S2 from Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors Open
Efficacy of BNP GMX1778 in PPM1Dtrnc. isogenic model.
View article: NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD+ Depletion
NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD+ Depletion Open
Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is caused by loss of function mutations in fumarate hydratase (FH) and results in an aggressive subtype of renal cell carcinoma with limited treatment options. Loss of FH leads to …
View article: Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors Open
The treatment of primary central nervous system tumors is challenging due to the blood–brain barrier and complex mutational profiles, which is associated with low survival rates. However, recent studies have identified common mutations in …