Mitch Raponi
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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: 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: Supplementary Figure 7 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
Supplementary Figure 7 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC Open
Supplementary Figure 7 - PDF file 352K, H&E and immunohistochemical (Ki67) staining of tumors derived from EGFR mutant GEM models
View article: Supplementary Table 2 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
Supplementary Table 2 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC Open
Supplementary Table 2 - PDF file 113K, Mutant EGFR cell panel profiling of CO-1686
View article: Supplementary Table 1 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
Supplementary Table 1 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC Open
Supplementary Table 1 - PDF file 114K, Kinase selectivity profiling of CO-1686
View article: Supplementary Figure 9 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
Supplementary Figure 9 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC Open
Supplementary Figure 9 - PDF file 168K, NCI-H1975 parental and CO-1686 resistant clones cluster into distinct groups using an RNA-based EMT signature
View article: Supplementary Tables 1 through 4 and Supplementary Figures 1 through 5 from <i>In Vitro</i> and <i>In Vivo</i> Characterization of Irreversible Mutant-Selective EGFR Inhibitors That Are Wild-Type Sparing
Supplementary Tables 1 through 4 and Supplementary Figures 1 through 5 from <i>In Vitro</i> and <i>In Vivo</i> Characterization of Irreversible Mutant-Selective EGFR Inhibitors That Are Wild-Type Sparing Open
PDF - 252K, Supplemental Table 1. Mass spectrometry on EGFR-L858R/T790M protein. Supplemental Table 2. EGFR modulation in A431, H1975 and HCC827 cells by compound 3. Supplemental Table 3. Kinase selectivity profile of compound 3, afatinib …
View article: Data from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
Data from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC Open
Patients with non–small cell lung cancer (NSCLC) with activating EGF receptor (EGFR) mutations initially respond to first-generation reversible EGFR tyrosine kinase inhibitors. However, clinical efficacy is limited by acquired resistance, …
View article: Supplementary Figure 8 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
Supplementary Figure 8 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC Open
Supplementary Figure 8 - PDF file 215K, Photomicrographs of CO-1686 resistant NCI-H1975 cell (COR) clones and quantification of EGFR siRNA knockdown in COR clones
View article: Supplementary Tables 1 through 4 and Supplementary Figures 1 through 5 from <i>In Vitro</i> and <i>In Vivo</i> Characterization of Irreversible Mutant-Selective EGFR Inhibitors That Are Wild-Type Sparing
Supplementary Tables 1 through 4 and Supplementary Figures 1 through 5 from <i>In Vitro</i> and <i>In Vivo</i> Characterization of Irreversible Mutant-Selective EGFR Inhibitors That Are Wild-Type Sparing Open
PDF - 252K, Supplemental Table 1. Mass spectrometry on EGFR-L858R/T790M protein. Supplemental Table 2. EGFR modulation in A431, H1975 and HCC827 cells by compound 3. Supplemental Table 3. Kinase selectivity profile of compound 3, afatinib …
View article: Supplementary Figure 11 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
Supplementary Figure 11 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC Open
Supplementary Figure 11 - PDF file 255K, Analysis of the role of AXL in mediating CO-1686 resistance in COR cell clones.