C. Patrick
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View article: TMOD-20. Growth rates of patient-derived tumor organoids reflect glioblastoma patients’ heterogeneity in survival
TMOD-20. Growth rates of patient-derived tumor organoids reflect glioblastoma patients’ heterogeneity in survival Open
The generation of patient-derived glioblastoma explant organoids (GBOs) is a recent advancement in patient-focused research. Much like their parent tumors, GBOs exhibit heterogeneity in growth rate and cellular composition. As interest in …
View article: Figure S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Expression of key ferroptosis evasion genes SCD1 and SLC7A11 is higher in KRAS/STK11/KEAP1 co-mutant LUADs which causes poor clinical outcomes.
View article: Figure S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
SCD1 inhibition modulate several kinases in LUAD and SCD1 knockdown induces ferroptotic cell death in DKO.
View article: Figure S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Survival analysis of different treatment group of mice harboring Isogenic H358 NTC and H358 STK11/KEAP1 KO cells and de novo A549 and H460 cells induced tumors.
View article: Supplementary Table S7 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S7 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the lung cancer clinical samples with high SCD1 expression.
View article: Supplementary Table S5 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S5 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the list of primers used in the study.
View article: Supplementary Table S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows details of the drugs used in the study.
View article: Figure S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
SCD1 inhibition augments the cytotoxic response of SLC7A11 inhibitor, erastin, in KRAS/STK11/KEAP1 co-mutant LUADs.
View article: Supplementary Table S6 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S6 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the list of antibodies used in the study.
View article: Supplementary Table S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the details of the cell lines used in the study.
View article: Data from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Data from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Concurrent inactivating mutations in STK11 and KEAP1 drive primary resistance to therapies, leading to worse outcomes in KRAS-mutated lung adenocarcinoma (KRASmut LUAD), and are associated with metabolic alterations. Elucidation of the und…
View article: Supplementary Table S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the details and number of the clinical samples used in the study.
View article: Supplementary Table S8 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S8 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the percentage of the SCD1 high population in KRAS mutant LUADs.
View article: Supplementary Table S9 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S9 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the percentage of LUAD cases with SCD1 and SLC7A11 expression.
View article: Supplementary Table S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows details of the kits, assays used in the study.
View article: Quantitative peripheral live single T-cell dynamic polyfunctionality profiling predicts lung cancer checkpoint immunotherapy treatment response and clinical outcomes
Quantitative peripheral live single T-cell dynamic polyfunctionality profiling predicts lung cancer checkpoint immunotherapy treatment response and clinical outcomes Open
Our study nominates single peripheral T-cell polyfunctionality dynamics analysis to be a promising liquid biopsy platform to determine potential ICI predictive biomarker in NSCLC. It warrants further studies in larger prospective cohorts t…
View article: Impact of Bone Metastasis in Stage IV Non–Small Cell Lung Cancer Treated With Durvalumab and Tremelimumab With or Without Chemotherapy: A Retrospective Analysis of the CCTG BR.34 Trial
Impact of Bone Metastasis in Stage IV Non–Small Cell Lung Cancer Treated With Durvalumab and Tremelimumab With or Without Chemotherapy: A Retrospective Analysis of the CCTG BR.34 Trial Open
PURPOSE This retrospective analysis examines the impact of bone metastasis on outcomes in patients with non–small cell lung cancer (NSCLC) from the CCTG BR.34 trial, which investigated the combined immune checkpoint blockade. MATERIALS AND…
View article: Proceedings of the 1st biannual bridging the gaps in lung cancer conference
Proceedings of the 1st biannual bridging the gaps in lung cancer conference Open
Lung cancer is the leading cause of cancer death in the US and globally. The mortality from lung cancer has been declining, due to a reduction in incidence and advances in treatment. Although recent success in developing targeted and immun…
View article: Supplementary Figure 14 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Figure 14 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Western blot analysis of MET and ERK1/2 phosphorylation in MET R1170Q cell models. MET and ERK1/2 phosphorylation in (A) Ba/F3 cells stably transduced with MET R1170Q and (B) 293T cells transiently overexpressing MET R1170Q. Cells were tre…
View article: Supplementary Table 4 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 4 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
List of missense mutations with unknown biologic function and their pathogenicity scores using all three in silico tools in cohort #1
View article: Supplementary Table 6 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 6 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Prevalence of MET tyrosine kinase domain (TKD) mutations across cancer types in cohort #1.
View article: Supplementary Table 10 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 10 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Characteristics of 44 NSCLC cases harboring oncogenic / likely oncogenic MET TKD mutations in cohort #1.
View article: Supplementary Table 13 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 13 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Concurrent driver mutations according to oncogenic / likely oncogenic MET TKD mutations detected in cohort #2.
View article: Supplementary Table 22 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 22 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Oncogenic / likely oncogenic MET TKD mutations in RCC compared to those detected in NSCLC in cohort #1.
View article: Supplementary Figure 10 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Figure 10 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
MET TKD mutations in NSCLC cohort of Caris Life Sciences. (A) Flowchart of the NSCLC subgroup in the Caris Life Sciences dataset. (B) Prevalence of MET TKD mutations in NSCLC cases in the Caris Life Sciences dataset (MET TKD mutations in 2…
View article: Data from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Data from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Activating point mutations in the MET tyrosine kinase domain (TKD) are oncogenic in a subset of papillary renal cell carcinomas. Here, using comprehensive genomic profiling among >600,000 patients, we identify activating MET TKD point muta…
View article: Supplementary Table 6 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 6 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Prevalence of MET tyrosine kinase domain (TKD) mutations across cancer types in cohort #1.
View article: Supplementary Table 14 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 14 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Concurrent genomic drivers in cases with oncogenic / likely oncogenic MET tyrosine kinase domain (TKD) mutations and co-occurring MET gene amplification in cohort #2.
View article: Supplementary Figure 19 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Figure 19 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Equilibration of interactions that drives ATP affinity in the presence MET F1200I mutant. (A) Representative structure of ATP bound MET F1200I with the regions of interest highlighted [alpha C helix (red), DFG site (green), mutation site (…
View article: Supplementary Table 11 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors
Supplementary Table 11 from Activating Point Mutations in the <i>MET</i> Kinase Domain Represent a Unique Molecular Subset of Lung Cancer and Other Malignancies Targetable with MET Inhibitors Open
Detailed genomic characteristics for each case of NSCLC with oncogenic / likely oncogenic MET tyrosine kinase domain (TKD) mutations in cohort #1.