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1. Full Text Abstract 437: Stromal support of pancreatic tumor metabolism
by Lyssiotis, Costas A
Cancer Research, ISSN 0008-5472, 07/2017, Volume 77, Issue 13 Supplement, pp. 437 - 437
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2. Full Text Abstract A85: Metabolic wiring dictates GOT1 dependency in pancreatic cancer
by Lyssiotis, Costas A
Cancer Research, ISSN 0008-5472, 12/2016, Volume 76, Issue 24 Supplement, pp. A85 - A85
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3. Full Text Metabolic Interactions in the Tumor Microenvironment
by Lyssiotis, Costas A and Kimmelman, Alec C
Trends in Cell Biology, ISSN 0962-8924, 11/2017, Volume 27, Issue 11, pp. 863 - 875
Tumors are dynamic pseudoorgans that contain numerous cell types interacting to create a unique physiology. Within this network, the malignant cells encounter... 
hypoxia | cancer-associated fibroblasts | immune | crosstalk | stroma | ADENOSINE RECEPTORS | PANCREATIC DUCTAL ADENOCARCINOMA | CANCER-ASSOCIATED FIBROBLASTS | ARYL-HYDROCARBON RECEPTOR | PYRUVATE-CARBOXYLASE | ONCOGENIC KRAS | GLUTAMINE-SYNTHETASE | CELL-PROLIFERATION | MITOCHONDRIAL TRANSFER | LACTATE METABOLISM | CELL BIOLOGY | Neoplasms - metabolism | Amino Acids - metabolism | Macrophages - metabolism | Energy Metabolism | Cancer-Associated Fibroblasts - metabolism | Humans | Cell Communication | Glucose - metabolism | Tumor Microenvironment | Neoplasms - pathology | Fatty Acids - metabolism | Physiological aspects | Development and progression | Metabolites | Tumors
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4. Full Text Employing Metabolism to Improve the Diagnosis and Treatment of Pancreatic Cancer
by Halbrook, Christopher J and Lyssiotis, Costas A
Cancer Cell, ISSN 1535-6108, 01/2017, Volume 31, Issue 1, pp. 5 - 19
Pancreatic ductal adenocarcinoma is on pace to become the second leading cause of cancer-related death. The high mortality rate results from a lack of methods... 
FDG-PET | pancreatic cancer | PDAC | HP-MRI | stroma | Kras | metabolic crosstalk | metabolic imaging | tumor metabolism | metabolic reprogramming | POSITRON-EMISSION-TOMOGRAPHY | MAGNETIC-RESONANCE-SPECTROSCOPY | T-CELL IMMUNITY | AUTOPHAGY INHIBITION | ONCOLOGY | DUCTAL ADENOCARCINOMA | IN-VIVO | MOUSE MODEL | AEROBIC GLYCOLYSIS | MR SPECTROSCOPY | GLUTAMINE-METABOLISM | CELL BIOLOGY | Metformin - therapeutic use | Pancreatic Neoplasms - metabolism | Pancreatic Neoplasms - diagnosis | Humans | Carcinoma, Pancreatic Ductal - metabolism | Glutamine - metabolism | Tumor Microenvironment | Carcinoma, Pancreatic Ductal - therapy | Positron-Emission Tomography | Cellular Reprogramming | Carcinoma, Pancreatic Ductal - diagnosis | Glucose - metabolism | Fluorodeoxyglucose F18 | Pancreatic Neoplasms - therapy | Physiological aspects | Care and treatment | Diagnosis | Pancreatic cancer | Cancer | Diagnostic imaging
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5. Metabolic Interactions in the Tumor Microenvironment
by Costas A Lyssiotis and Alec C Kimmelman
Trends in Cell Biology, ISSN 0962-8924, 11/2017, Volume 27, Issue 11, p. 863
Tumors are dynamic pseudoorgans that contain numerous cell types interacting to create a unique physiology. Within this network, the malignant cells encounter... 
Signaling | Metabolites | Nutrients | Physiology | Metabolism | Drug development | Cancer therapies | Cells | Tumors | Cancer
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6. Full Text Auditory metabolomics, an approach to identify acute molecular effects of noise trauma
by Ji, Lingchao and Lee, Ho-Joon and Wan, Guoqiang and Wang, Guo-Peng and Zhang, Li and Sajjakulnukit, Peter and Schacht, Jochen and Lyssiotis, Costas A and Corfas, Gabriel
Scientific Reports, ISSN 2045-2322, 12/2019, Volume 9, Issue 1, pp. 9273 - 9
Animal-based studies have provided important insights into the structural and functional consequences of noise exposure on the cochlea. Yet, less is known... 
REPAIR | ACID | COCHLEA | MULTIDISCIPLINARY SCIENCES | ADENOSINE | GATED ION CHANNELS | UP-REGULATION | EXPRESSION | ATP | INDUCED HEARING-LOSS | PIG INNER-EAR | Oxidative stress | Metabolomics | Noise | Mass spectroscopy | Liquid chromatography | Hearing protection | Hearing impairment | Metabolism | Trauma | Inner ear | Hearing loss | Molecular modelling | Metabolites | Cochlea | Ears & hearing | Metabolic pathways | Neurotransmission | Structure-function relationships
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7. Full Text Acetate Fuels the Cancer Engine
by Lyssiotis, Costas A and Cantley, Lewis C
Cell, ISSN 0092-8674, 12/2014, Volume 159, Issue 7, pp. 1492 - 1494
Cancer cells have distinctive nutrient demands to fuel growth and proliferation, including the disproportionate use of glucose, glutamine, and fatty acids.... 
METABOLISM | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL BIOLOGY | Glucose metabolism | Glucose | Fatty acids | Acetates | Dextrose | Cancer | Glutamine
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8. Full Text New tricks for an old drug
by Nelson, Barbara S and Kremer, Daniel M and Lyssiotis, Costas A
Nature Chemical Biology, ISSN 1552-4450, 11/2018, Volume 14, Issue 11, pp. 990 - 991
The prodrug dimethyloxalylglycine (DMOG) is a well-known tool compound used to study hypoxia. New findings reveal that DMOG also inhibits glutamine metabolism... 
BIOCHEMISTRY & MOLECULAR BIOLOGY | INHIBITORS | Hypoxia | Metabolism | Glutamine | Cancer
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9. Full Text Metabolic syndrome: F stands for fructose and fat
by Lyssiotis, Costas A and Cantley, Lewis C
Nature, ISSN 0028-0836, 2013, Volume 502, Issue 7470, pp. 181 - 182
SWEETENED BEVERAGES | MULTIDISCIPLINARY SCIENCES | ADIPOSITY | Liver - pathology | Animals | Humans | Liver - metabolism | Fructose - biosynthesis | Metabolic Syndrome - metabolism | Metabolic Syndrome - pathology | Fructose - metabolism
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10. Full Text Running the Light: Nucleotide Metabolism Drives Bypass of Senescence in Cancer
by Halbrook, Christopher J and Wahl, Daniel R and Lyssiotis, Costas A
Trends in Biochemical Sciences, ISSN 0968-0004, 12/2019, Volume 44, Issue 12, pp. 991 - 993
Senescence is engaged in response to oncogenes to suppress proliferation. Cancers rewire metabolism to facilitate proliferation; however, it is not well... 
RPIA | p16 | nucleotide metabolism | mTORC1 | pentose phosphate pathway | SUPPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MTOR
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11. Full Text Macrophage-Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer
by Halbrook, Christopher J and Pontious, Corbin and Kovalenko, Ilya and Lapienyte, Laura and Dreyer, Stephan and Lee, Ho-Joon and Thurston, Galloway and Zhang, Li and Zhang, Yaqing and Lazarus, Jenny and Sajjakulnukit, Peter and Hong, Hanna S and Kremer, Daniel M and Nelson, Barbara S and Kemp, Samantha and Chang, David and Biankin, Andrew and Shi, Jiaqi and Frankel, Timothy L and Crawford, Howard C and Morton, Jennifer P and Pasca di Magliano, Marina and Lyssiotis, Costas A
Cell Metabolism, ISSN 1550-4131, 06/2019, Volume 29, Issue 6, pp. 1390 - 1399.e6
Pancreatic ductal adenocarcinoma (PDA) is characterized by abundant infiltration of tumor-associated macrophages (TAMs). TAMs have been reported to drive... 
pancreatic cancer | gemcitabine resistance | deoxycytidine | immunometabolism | metabolomics | macrophage | tumor-associated macrophage | tumor microenvironment | metabolic crosstalk | pancreatic ductal adenocarcinoma | Pyrimidines | Chemotherapy | Metabolites | Gemcitabine | Analysis | Pancreatic cancer | Resveratrol | Nucleosides | Macrophages | Health aspects | Cancer
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12. Full Text Enhanced oxidative phosphorylation in NKT cells is essential for their survival and function
by Kumar, A and Pyaram, K and Yarosz, EL and Hong, HN and Lyssiotis, CA and Giri, S and Chang, CH
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, ISSN 0027-8424, 04/2019, Volume 116, Issue 15, pp. 7439 - 7448
Cellular metabolism and signaling pathways are key regulators to determine conventional T cell fate and function, but little is understood about the role of... 
MAMMALIAN TARGET | glucose | ACTIVATION | MULTIDISCIPLINARY SCIENCES | C-MYC | OXPHOS | PLZF | CUTTING EDGE | METABOLISM | NKT | DIFFERENTIATION | EXPRESSION | REQUIREMENT | Cell Proliferation | Glucose - immunology | CD4-Positive T-Lymphocytes - cytology | Oxidative Phosphorylation | Cell Survival - genetics | Natural Killer T-Cells - cytology | Glucose - genetics | Mitochondria - metabolism | Pentose Phosphate Pathway - immunology | Cell Survival - immunology | Promyelocytic Leukemia Zinc Finger Protein - immunology | Mice, Knockout | CD4-Positive T-Lymphocytes - immunology | Animals | Mitochondria - genetics | Promyelocytic Leukemia Zinc Finger Protein - genetics | Mice | Pentose Phosphate Pathway - genetics | Natural Killer T-Cells - immunology | Physiological aspects | Phosphorylation | Killer cells | Research | Immunological research | Cell proliferation | Regulators | Leukemia | Effector cells | Lymphocytes T | Glucose | Promyeloid leukemia | Glucose metabolism | Mitochondria | Cell activation | Cell fate | Lymphocytes | Pentose | Zinc finger proteins | Natural killer cells | Pentose phosphate | Cell survival | Metabolism | Gene expression | Survival | Zinc | CD4 antigen | Oxidative phosphorylation | γ-Interferon | Pentose phosphate pathway | Lactic acid | Biological Sciences | PNAS Plus
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13. Full Text ERK1/2-dependent phosphorylation and nuclear translocation of PKM2 promotes the Warburg effect
by Yang, Weiwei and Zheng, Yanhua and Xia, Yan and Ji, Haitao and Chen, Xiaomin and Guo, Fang and Lyssiotis, Costas A and Aldape, Kenneth and Cantley, Lewis C and Lu, Zhimin
Nature Cell Biology, ISSN 1465-7392, 2012, Volume 14, Issue 12, pp. 1295 - 1304
Pyruvate kinase M2 (PKM2) is upregulated in multiple cancer types and contributes to the Warburg effect by unclear mechanisms. Here we demonstrate that... 
APOPTOSIS | TRANSCRIPTIONAL ACTIVITY | ACTIVATION | METABOLISM | PROTEIN-KINASE | PYRUVATE-KINASE M2 | DOWN-REGULATION | BETA-CATENIN | CANCER | GENE-TRANSCRIPTION | CELL BIOLOGY | Phosphorylation | Immunoprecipitation | Humans | Glucose Transporter Type 1 - metabolism | Protein Transport - physiology | Cell Nucleus - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Female | Peptidylprolyl Isomerase - metabolism | Membrane Proteins - metabolism | Peptidylprolyl Isomerase - genetics | Cell Line | Mitogen-Activated Protein Kinase 3 - genetics | Membrane Proteins - genetics | Cells, Cultured | NIMA-Interacting Peptidylprolyl Isomerase | Thyroid Hormones - genetics | beta Catenin - metabolism | Protein Transport - genetics | beta Catenin - genetics | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Glucose Transporter Type 1 - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Mice, Nude | Thyroid Hormones - metabolism | Cell Line, Tumor | Protein Binding | Mice | Mitogen-Activated Protein Kinase 1 - metabolism | Translocation (Genetics) | Cancer cells | Physiological aspects | Cytogenetics | Genetic aspects | Research | Health aspects
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14. Full Text Erratum: Acetate fuels the cancer engine (Cell (2014) 159 (1492-1494))
by Lyssiotis, Costas A and Cantley, Lewis C
Cell, ISSN 0092-8674, 01/2015, Volume 160, Issue 3, p. 567
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15. Full Text Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion
by Sousa, Cristovão M and Biancur, Douglas E and Wang, Xiaoxu and Halbrook, Christopher J and Sherman, Mara H and Zhang, Li and Kremer, Daniel and Hwang, Rosa F and Witkiewicz, Agnes K and Ying, Haoqiang and Asara, John M and Evans, Ronald M and Cantley, Lewis C and Lyssiotis, Costas A and Kimmelman, Alec C
Nature, ISSN 0028-0836, 08/2016, Volume 536, Issue 7617, pp. 479 - 483
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease characterized by an intense fibrotic stromal response and deregulated metabolism(1-4). The... 
PROTEIN | CANCER | MULTIDISCIPLINARY SCIENCES | FIBROBLASTS | PROGRESSION | GROWTH | Carbon - metabolism | Neoplasm Transplantation | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Humans | Pancreatic Neoplasms - pathology | Carcinoma, Pancreatic Ductal - metabolism | Alanine - metabolism | Biosynthetic Pathways | Tumor Microenvironment - physiology | Autophagy | Carcinoma, Pancreatic Ductal - pathology | Citric Acid Cycle | Adenocarcinoma - metabolism | Animals | Heterografts | Pancreatic Stellate Cells - cytology | Pancreatic Stellate Cells - secretion | Glucose - metabolism | Female | Alanine - secretion | Mice | Physiological aspects | Alanine | Metabolism | Health aspects | Pancreatic cancer | Tumors | Metabolites | Amino acids | Biosynthesis | Carbon
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16. Full Text Glutamine supports pancreatic cancer growth through a KRAS-regulated metabolic pathway
by Son, Jaekyoung and Lyssiotis, Costas A and Ying, Haoqiang and Wang, Xiaoxu and Hua, Sujun and Ligorio, Matteo and Perera, Rushika M and Ferrone, Cristina R and Mullarky, Edouard and Shyh-Chang, Ng and Kang, Ya'An and Fleming, Jason B and Bardeesy, Nabeel and Asara, John M and Haigis, Marcia C and Depinho, Ronald A and Cantley, Lewis C and Kimmelman, Alec C
Nature, ISSN 0028-0836, 04/2013, Volume 496, Issue 7443, pp. 101 - 105
Cancer cells have metabolic dependencies that distinguish them from their normal counterparts(1). Among these dependencies is an increased use of the amino... 
GLUCOSE | MULTIDISCIPLINARY SCIENCES | MASS-SPECTROMETRY | ADDICTION | TRANSFORMED-CELLS | Care and treatment | Pancreatic cancer | Physiological aspects | Development and progression | Research | Health aspects | Guanosine triphosphatase | Glutamine | Cancer | Enzymes | Oxidative stress | Glucose | Metabolites | Cancer therapies
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