Vijayashree Ramesh
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View article: Supplementary Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 2). Epithelial and myeloid cell contributions to gene expression and 13C labeling features.
View article: Supplementary Table 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 3). Overall and recurrence-free survival summary.
View article: Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
13C enrichment in the TCA cycle distinguishes tumors but not benign pulmonary lesions from the adjacent lung. A, Summary of patients with pulmonary lesions. B, Schematic of labeling from [U-13C]glucose, …
View article: Supplementary Table 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
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View article: Supplementary Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 1). TCA cycle labeling and metabolite abundance in tumors and lungs from NSCLC patents.
View article: Supplementary Table 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 1). Patient Isotopologue Data.
View article: Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
PDXs derived from primary NSCLC retain histological, molecular, and metabolic characteristics. A and B, Summary of histological and molecular characterization of donor tumors (A) and PDX models (B). C, H&…
View article: Supplementary Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 4). Development of patient-derived xenografts from malignant tumors in the lung.
View article: Supplementary Table 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 1). Clinical and pathological data from patients recruited to this study.
View article: Supplementary Table 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 2). Transcriptomic data for NSCLC and adjacent lung tissue fragments.
View article: Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
PDXs generated from primary NSCLCs spontaneously metastasize in NSG mice. A, Flow cytometry analysis of lung tissue from a mouse engrafted with mx73. Cells were stained with mouse lineage markers (CD45, CD31, and TER119) and HLA.
View article: Supplementary Table 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Related to Figures 4 and 6). PDX Isotopologue Data.
View article: Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Increased 13C enrichment in the TCA cycle predicts reduced survival. A,13C enrichment in the adjacent lung and tumors with high or low TCA cycle labeling. Fractional enrichments of glycolytic (M+3) and TCA cycl…
View article: Supplementary Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 3). TCA cycle metabolite abundance does not correlate with overall survival.
View article: Data from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Data from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
In patients with non–small cell lung cancer (NSCLC), the relationship between tumor metabolism and clinical outcomes is unknown. Here, 13C-labeled nutrients were intraoperatively infused into more than 90 patients with surgicall…
View article: Supplementary Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figures 5 and 6): Treatment with IACS-010759 reduces distant metastasis.
View article: Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Cancer cells drive an OXPHOS expression signature in tumors. A, Heatmap of TCA cycle and ETC transcript differences between primary NSCLC and adjacent lung samples. B, RNA scores comparing matched tumor and adjacent lung for …
View article: Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Inhibition of complex I with IACS-010759 limits metastasis in NSCLC PDXs. A and B, Tumor-bearing mice were treated daily with DMSO or IACS-010759 (5 mg/kg) by oral gavage for 3–4 weeks and then infused with [U-13C]…
View article: Supplementary Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 3). Relationships between TCA cycle labeling and clinical factors.
View article: Supplemental figures from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Supplemental figures from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplemental data file contains Table S1, S2 and Figures S1-S7
View article: Data from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Data from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Evolutionarily conserved selenoprotein O (SELENOO) catalyzes a posttranslational protein modification known as AMPylation that is essential for the oxidative stress response in bacteria and yeast. Given that oxidative stress experienced in…
View article: Table S3 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Table S3 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Data table of AMPylated substrates identified by mass spectrometry analysis.
View article: Figure S6 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S6 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S6 depicts markers of subcellular fractionation used to isolate crude mitochondria.
View article: Figure S2 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S2 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S2 correlates SelenoO expression with survival and metastasis
View article: Figure S1 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S1 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S1 shows expressions of SelenoO in cancer subtypes
View article: Figure S7 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S7 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S7 shows mass spectra of SdhA and Aco2
View article: Figure S4 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S4 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S4 depicts characterization of SelenoO deficient cell lines
View article: Figure S3 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S3 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S3 depicts expression of SelenoO in cell lines used in this study
View article: Figure S5 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S5 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S5 shows redox metabolite levels in wildtype and SelenoO deficient cell lines.
View article: High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
In patients with non–small cell lung cancer (NSCLC), the relationship between tumor metabolism and clinical outcomes is unknown. Here, 13C-labeled nutrients were intraoperatively infused into more than 90 patients with surgically resectabl…