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View article: Supplementary Figure 4 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Supplementary Figure 4 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
PDF file - 766K
View article: Data from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Data from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
Following the discovery of NVP-BEZ235, our first dual pan-PI3K/mTOR clinical compound, we sought to identify additional phosphoinositide 3-kinase (PI3K) inhibitors from different chemical classes with a different selectivity profile. The k…
View article: Supplementary Figure and Table Legends from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Supplementary Figure and Table Legends from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Supplementary Figure and Table Legends
View article: Data from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
Data from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors Open
Focal amplification and activating point mutation of the MET gene are well-characterized oncogenic drivers that confer susceptibility to targeted MET inhibitors. Recurrent somatic splice site alterations at MET exon 14 (METex14) that resul…
View article: Data from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Data from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
Following the discovery of NVP-BEZ235, our first dual pan-PI3K/mTOR clinical compound, we sought to identify additional phosphoinositide 3-kinase (PI3K) inhibitors from different chemical classes with a different selectivity profile. The k…
View article: Supplementary Figure Legends, Supplementary Table Legends, and Supplementary Tables 1 through 7 from Characterization of the Novel and Specific PI3Kα Inhibitor NVP-BYL719 and Development of the Patient Stratification Strategy for Clinical Trials
Supplementary Figure Legends, Supplementary Table Legends, and Supplementary Tables 1 through 7 from Characterization of the Novel and Specific PI3Kα Inhibitor NVP-BYL719 and Development of the Patient Stratification Strategy for Clinical Trials Open
PDF - 129K, Legends for Supplementary Figures 1 through 4 and Supplementary Tables 1 through 7. Supplementary Table 1. Determination of NVP-BYL719 in vitro effects on human protein kinases. Supplementary Table 2. Activity profile of NVP-BY…
View article: Supplementary Figure 3 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Supplementary Figure 3 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
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View article: Supplementary Figure 7 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Supplementary Figure 7 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
PDF file - 579K
View article: Data from Characterization of the Novel and Specific PI3Kα Inhibitor NVP-BYL719 and Development of the Patient Stratification Strategy for Clinical Trials
Data from Characterization of the Novel and Specific PI3Kα Inhibitor NVP-BYL719 and Development of the Patient Stratification Strategy for Clinical Trials Open
Somatic PIK3CA mutations are frequently found in solid tumors, raising the hypothesis that selective inhibition of PI3Kα may have robust efficacy in PIK3CA-mutant cancers while sparing patients the side-effects associated with broader inhi…
View article: Data from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Data from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Activating mutations in either KIT or PDGFRA are present in approximately 90% of gastrointestinal stromal tumors (GIST). Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patient…
View article: Supplementary Figure 4 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Supplementary Figure 4 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
PDF file - 766K
View article: Supplementary Figure 2 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Figure 2 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
Mechanisms of TSC2 loss in HCC cell lines and xenografts. (A) Taqman RT-PCR analysis of TSC1 and TSC2 mRNA levels in HCC cell lines. (B) Taqman RT-PCR analysis of MZB1, TSC1 and TSC2 mRNA levels in TSC2-null Li-7 cells treated with epigene…
View article: Supplementary Figure 1 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Supplementary Figure 1 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
PDF file - 419K
View article: Supplementary Table S2 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Supplementary Table S2 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Annotation of cell lines.
View article: Supplementary Table S3 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Supplementary Table S3 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Differentially expressed genes (DEGs) identified from RNA-Seq by DeSeq between control and imatinib-treated GIST cell lines.
View article: Supplementary Table S1 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Supplementary Table S1 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Annotation of primary tumor tissues.
View article: Supplementary Table S1 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Supplementary Table S1 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Annotation of primary tumor tissues.
View article: Supplementary Figure 5 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Figure 5 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
Model of mTOR activation and everolimus sensitivity caused by TSC2 loss.
View article: Supplementary Table S4 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
Supplementary Table S4 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors Open
Co- and anti-occurrence of genomic alterations in lung adenocarcinoma.
View article: Supplementary Table S2 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
Supplementary Table S2 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors Open
Summary of MET exon 14 alterations.
View article: Supplementary Table S4 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
Supplementary Table S4 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors Open
Co- and anti-occurrence of genomic alterations in lung adenocarcinoma.
View article: Supplementary Figure 5 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Figure 5 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
Model of mTOR activation and everolimus sensitivity caused by TSC2 loss.
View article: Supplementary Figure 3 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Figure 3 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
TSC2 immunohistochemistry assay validation and analysis of HCC xenograft and primary tumors. (A) TSC2 immunohistochemistry (IHC) assay with HCC cell lines. (B) TSC2 IHC assay with HCC xenograft tumors. (C) TSC2 expression by IHC assay in H…
View article: Supplementary Materials, Tables 1-2, Figure Legends 1-8 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor
Supplementary Materials, Tables 1-2, Figure Legends 1-8 from Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor Open
PDF file - 180K
View article: Supplementary Figure and Table Legends from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Supplementary Figure and Table Legends from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Supplementary Figure and Table Legends
View article: Supplementary Figure Legends, Tables 1 - 3 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Figure Legends, Tables 1 - 3 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
Supplementary Table 1. Quantification of phospho-protein levels in Figure 1B. Supplementary Table 2. Everolimus IC50 and growth inhibition at 1uM in HCC cell lines. Supplementary Table 3. Quantification of phospho-protein levels in Figure …
View article: Supplementary Figure 4 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Figure 4 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
Race distribution of HCC patients in EVOLVE-1 trial. Percentage of Caucasian, Asian and other race in different groups of EVOLVE-1 patients (A) and TSC2 IHC H-score ranges (B).
View article: Supplemantary Figure S1 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors
Supplemantary Figure S1 from FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors Open
Expression of FGFR1-4, FGF1-23, KIT, ETV1, PRKCQ, ANO1, EGFR, ERBB2-4, MET, IGF1R, HGF, EGF and NRG1 in multiple primary tumor types and cancer cell lines.
View article: Supplementary Figure 3 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Figure 3 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
TSC2 immunohistochemistry assay validation and analysis of HCC xenograft and primary tumors. (A) TSC2 immunohistochemistry (IHC) assay with HCC cell lines. (B) TSC2 IHC assay with HCC xenograft tumors. (C) TSC2 expression by IHC assay in H…
View article: Supplementary Table 4 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus
Supplementary Table 4 from Loss of Tuberous Sclerosis Complex 2 (TSC2) Is Frequent in Hepatocellular Carcinoma and Predicts Response to mTORC1 Inhibitor Everolimus Open
Genetic characterization of 35 established HCC PTX models by targeted DNA sequencing (Excel file).