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1. 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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2. 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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3. Full Text Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function
by Viale, Andrea and Viale, Andrea and Pettazzoni, Piergiorgio and Lyssiotis, Costas A and Ying, Haoqiang and Sánchez, Nora and Marchesini, Matteo and Carugo, Alessandro and Green, Tessa and Seth, Sahil and Giuliani, Virginia and Kost-Alimova, Maria and Muller, Florian and Colla, Simona and Nezi, Luigi and Genovese, Giannicola and Deem, Angela K and Kapoor, Avnish and Yao, Wantong and Brunetto, Emanuela and Kang, Ya'an and Yuan, Min and Asara, John M and Wang, Y Alan and Heffernan, Timothy P and Kimmelman, Alec C and Wang, Huamin and Fleming, Jason B and Cantley, Lewis C and DePinho, Ronald A and Draetta, Giulio F
Nature, ISSN 0028-0836, 10/2014, Volume 514, Issue 7524, pp. 628 - 632
Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers in western countries, with a median survival of 6 months and an extremely low... 
STEM-CELLS | INHIBITION | MELANOMA | METABOLISM | GLUCOSE | MULTIDISCIPLINARY SCIENCES | IMATINIB | LEUKEMIA | AUTOPHAGY | INDUCTION | TUMOR-GROWTH | Recurrence | Pancreatic Neoplasms - metabolism | Neoplastic Stem Cells - drug effects | Proto-Oncogene Proteins p21(ras) - genetics | Carcinoma, Pancreatic Ductal - metabolism | Gene Expression Regulation, Neoplastic | Autophagy | Carcinoma, Pancreatic Ductal - genetics | Oxidative Phosphorylation - drug effects | Pancreatic Neoplasms - drug therapy | Lysosomes - metabolism | Neoplastic Stem Cells - metabolism | Cell Respiration - drug effects | Neoplastic Stem Cells - pathology | Female | Disease Models, Animal | Proto-Oncogene Proteins p21(ras) - metabolism | Cell Survival - drug effects | Neoplasm Recurrence, Local - prevention & control | Signal Transduction | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Mitochondria - metabolism | Genes, p53 - genetics | Mitochondria - drug effects | Mutation - genetics | Carcinoma, Pancreatic Ductal - pathology | Carcinoma, Pancreatic Ductal - drug therapy | Animals | Glycolysis | Mice | Protein research | Ablation (Surgery) | Care and treatment | Pancreatic cancer | Oncology, Experimental | Genetic aspects | Research | Cancer | Mitochondria | Stem cells | Cell cycle | Lipids | Metabolism | Tumors | Apoptosis
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4. Full Text Pancreatic cancers require autophagy for tumor growth
by Yang, Shenghong and Wang, Xiaoxu and Contino, Gianmarco and Liesa, Marc and Sahin, Ergun and Ying, Haoqiang and Bause, Alexandra and Li, Yinghua and Stomme, Jayne M and Dell'Antonio, Giacomo and Mautner, Josef and Tonon, Giovanni and Haigis, Marcia and Shirihai, Orian S and Doglioni, Claudio and Bardeesy, Nabeel and Kimmelman, Alec C
Genes and Development, ISSN 0890-9369, 04/2011, Volume 25, Issue 7, pp. 717 - 729
Macroautophagy (autophagy) is a regulated catabolic pathway to degrade cellular organelles and macromolecules. The role of autophagy in cancer is complex and... 
Kras | Metabolism | Autophagy | Chloroquine | DNA damage | Pancreatic cancer | autophagy | ADENOCARCINOMA | ELIMINATION | DEVELOPMENTAL BIOLOGY | INDUCTION | CELL-DEATH | CELL BIOLOGY | chloroquine | pancreatic cancer | INHIBITION | MOUSE MODEL | DISEASE | GENETICS & HEREDITY | RESISTANCE | metabolism | TUMORIGENESIS | PROGRESSION | Reactive Oxygen Species - metabolism | Humans | Pancreatic Neoplasms - pathology | Transplantation, Heterologous | Random Allocation | Carcinoma, Pancreatic Ductal - pathology | Autophagy - drug effects | Chloroquine - pharmacology | Animals | RNA Interference | Mice, Nude | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Mice | DNA Damage | Autophagy (Cytology) | Usage | Care and treatment | Growth | Cancer cells | Genetic aspects | Research | Research Paper
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5. Full Text Glucose Metabolism in Pancreatic Cancer
by Yan, Liang and Raj, Priyank and Yao, Wantong and Ying, Haoqiang
Cancers, ISSN 2072-6694, 09/2019, Volume 11, Issue 10, p. 1460
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal cancers, with a five-year survival rate of around 5% to 8%. To date, very few... 
glucose metabolism | pancreatic cancer
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6. Full Text Coactivation of Receptor Tyrosine Kinases Affects the Response of Tumor Cells to Targeted Therapies
by Jayne M. Stommel and Alec C. Kimmelman and Haoqiang Ying and Roustem Nabioullin and Aditya H. Ponugoti and Ruprecht Wiedemeyer and Alexander H. Stegh and James E. Bradner and Keith L. Ligon and Cameron Brennan and Lynda Chin and Ronald A. DePinho
Science, ISSN 0036-8075, 10/2007, Volume 318, Issue 5848, pp. 287 - 290
Targeted therapies that inhibit receptor tyrosine kinases (RTKs) and the downstream phosphatidylinositol 3-kinase (PI3K) signaling pathway have shown promising... 
Tumor cell line | Cell growth | Glioma | Cell lines | Antibodies | Small interfering RNA | Reports | Viability | Endothelial cells | Medical schools | Tumors | GLIOBLASTOMA | GENE | CONFERS ENHANCED TUMORIGENICITY | MARKER | MULTIDISCIPLINARY SCIENCES | COMMON | INHIBITORS | CANCER | MET | DIFFUSE GLIOMAS | BRAIN | Erlotinib Hydrochloride | Glioblastoma - enzymology | Phosphorylation | Humans | Phosphatidylinositol 3-Kinases - metabolism | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Receptor, Epidermal Growth Factor - metabolism | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins - metabolism | PTEN Phosphohydrolase - genetics | Brain Neoplasms - enzymology | Signal Transduction | Cell Survival | Proto-Oncogene Proteins c-met | PTEN Phosphohydrolase - metabolism | Brain Neoplasms - drug therapy | Receptor Protein-Tyrosine Kinases - metabolism | Sulfonamides - pharmacology | Piperazines - pharmacology | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Glioblastoma - drug therapy | Quinazolines - pharmacology | Receptors, Growth Factor - metabolism | Tyrosine | Care and treatment | Physiological aspects | Properties | Phosphotransferases | Health aspects | Signal transduction | Brain | Hypotheses | Inhibitor drugs | Oncology | Kinases | Molecular biology
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7. Full Text p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation
by Wang, Y. Alan and Tonon, Giovanni and Chen, An-Jou and Ying, Haoqiang and Brennan, Cameron and Wong, Wing H and Hiller, David J and Ligon, Keith L and Kimmelman, Alec C and Chin, Lynda and Stommel, Jayne M and Yan, Haiyan and Wiedemeyer, Ruprecht and Ding, Zhihu and Perry, Samuel R and Chu, Gerald C and You, Mingjian J and DePinho, Ronald A and Dunn, Katherine L and Zheng, Hongwu
Nature, ISSN 0028-0836, 10/2008, Volume 455, Issue 7216, pp. 1129 - 1133
Glioblastoma (GBM) is a highly lethal brain tumour presenting as one of two subtypes with distinct clinical histories and molecular profiles. The primary GBM... 
INITIATING CELLS | PATHWAYS | GLIOBLASTOMA | MULTIDISCIPLINARY SCIENCES | BIOLOGY | C-MYC | SELF-RENEWAL | RECEPTOR | TUMORS | EXPRESSION | CANCER STEM-CELLS | Cell proliferation | Gliomas | Physiological aspects | Genetic aspects | Research | Cell differentiation | Tumor proteins | Health aspects | Histology | Mutation | Cancer | Tumors
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8. Full Text Abstract C157: Syndecan1 is required for oncogenic Kras-driven PDAC tumorigenesis and maintenance
by Yao, Wantong and Ying, Haoqiang and Draetta, Giulio
Molecular Cancer Therapeutics, ISSN 1535-7163, 12/2015, Volume 14, Issue 12 Supplement 2, pp. C157 - C157
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9. Full Text FoxO3 coordinates metabolic pathways to maintain redox balance in neural stem cells
by Yeo, Hyeonju and Lyssiotis, Costas A and Zhang, Yuqing and Ying, Haoqiang and Asara, John M and Cantley, Lewis C and Paik, Ji‐Hye
The EMBO Journal, ISSN 0261-4189, 10/2013, Volume 32, Issue 19, pp. 2589 - 2602
Forkhead Box O (FoxO) transcription factors act in adult stem cells to preserve their regenerative potential. Previously, we reported that FoxO maintains the... 
FoxO3 | oxidative stress | pentose phosphate pathway | glutaminolysis | MAMMALIAN TARGET | FORKHEAD TRANSCRIPTION FACTOR | MITOCHONDRIAL HEXOKINASE | HOMEOSTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | GLUTAMINE-METABOLISM | CELL BIOLOGY | SIGNALING PATHWAY | GLUCOSE-METABOLISM | AEROBIC GLYCOLYSIS | GENE-EXPRESSION | Animals, Newborn | Reactive Oxygen Species - metabolism | Oxidation-Reduction | Oxidative Stress | TOR Serine-Threonine Kinases - metabolism | Cells, Cultured | Glutamine - metabolism | Mice, Transgenic | Forkhead Transcription Factors - genetics | Animals | Metabolic Networks and Pathways | Forkhead Transcription Factors - metabolism | Glucose - metabolism | Mice | NADP - metabolism | Forkhead Box Protein O3 | Neural Stem Cells - metabolism | Pentose Phosphate Pathway | Neural networks | Metabolic disorders | Stem cells
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10. Full Text Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer
by Dey, Prasenjit and Baddour, Joelle and Muller, Florian and Wu, Chia Chin and Wang, Huamin and Liao, Wen-Ting and Lan, Zangdao and Chen, Alina and Gutschner, Tony and Kang, Yaan and Fleming, Jason and Satani, Nikunj and Zhao, Di and Achreja, Abhinav and Yang, Lifeng and Lee, Jiyoon and Chang, Edward and Genovese, Giannicola and Viale, Andrea and Ying, Haoqiang and Draetta, Giulio and Maitra, Anirban and Wang, Y. Alan and Nagrath, Deepak and Depinho, Ronald A
Nature, ISSN 0028-0836, 02/2017, Volume 542, Issue 7639, pp. 119 - 123
The genome of pancreatic ductal adenocarcinoma (PDAC) frequently contains deletions of tumour suppressor gene loci, most notably SMAD4, which is homozygously... 
SREBP ACTIVITY | PATHWAYS | AMINO-ACID-METABOLISM | ACTIVATED PROTEIN-KINASE | GLUTAMINE | GENE | ADENOCARCINOMA | MULTIDISCIPLINARY SCIENCES | BIOLOGY | GROWTH | TARGETS | Mitochondria - enzymology | AMP-Activated Protein Kinases - metabolism | Reactive Oxygen Species - metabolism | Amino Acids, Branched-Chain - metabolism | Humans | Pregnancy Proteins - genetics | Male | Carcinoma, Pancreatic Ductal - genetics | Malate Dehydrogenase - genetics | Carcinoma, Pancreatic Ductal - psychology | Gene Deletion | Minor Histocompatibility Antigens - genetics | NADP - metabolism | Ketoglutaric Acids - metabolism | Sterol Regulatory Element Binding Protein 1 - metabolism | Transaminases - biosynthesis | Biocatalysis | Transaminases - genetics | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - enzymology | Pancreatic Neoplasms - genetics | Carcinoma, Pancreatic Ductal - therapy | Malate Dehydrogenase - deficiency | Mitochondria - pathology | NADP - biosynthesis | Pregnancy Proteins - biosynthesis | Carcinoma, Pancreatic Ductal - enzymology | Minor Histocompatibility Antigens - biosynthesis | Animals | Mice | Pancreatic Neoplasms - therapy | Enzymes | Complications and side effects | Pancreatic cancer | Genetic aspects | Chromosome deletion | Health aspects | Risk factors | Cell growth | Mitochondria | Metabolites | Homeostasis | Collateral | Biosynthesis | Tumors | Cancer | Apoptosis
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11. Full Text Cancer signaling: When phosphorylation meets methylation
by Ying, Haoqiang and Depinho, Ronald A
Cell Research, ISSN 1001-0602, 11/2014, Volume 24, Issue 11, pp. 1282 - 1283
The propagation of kinase-mediated phosphorylation signals is central to the oncogenic activity of the RAS-MAPK pathway in human cancers. A recent study shows... 
RAS | ACTIVATION | CELL BIOLOGY | MAP Kinase Kinase Kinase 2 - metabolism | Animals | Histone-Lysine N-Methyltransferase - metabolism | Humans | Lysine - metabolism | MAP Kinase Kinase Kinases - metabolism | Cell Transformation, Neoplastic - metabolism | Oncogene Protein p21(ras) - metabolism | Research Highlight
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12. Full Text Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis
by Santana-Codina, Naiara and Roeth, Anjali A and Zhang, Yi and Zhang, Yi and Yang, Annan and Mashadova, Oksana and Mashadova, Oksana and Asara, John M and Wang, Xiaoxu and Bronson, Roderick T and Bronson, Roderick T and Lyssiotis, Costas A and Lyssiotis, Costas A and Ying, Haoqiang and Ying, Haoqiang and Kimmelman, Alec C and Kimmelman, Alec C
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 4945 - 13
Oncogenic KRAS is the key driver of pancreatic ductal adenocarcinoma (PDAC). We previously described a role for KRAS in PDAC tumor maintenance through rewiring... 
INHIBITION | METABOLISM | RAS | MULTIDISCIPLINARY SCIENCES | EPITHELIAL-CELL LINES | AUTOPHAGY | PYRIMIDINE SYNTHESIS | LEFLUNOMIDE | TUMORS | ADDICTION | Pentose Phosphate Pathway - drug effects | Pancreatic Neoplasms - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Carcinoma, Pancreatic Ductal - metabolism | Gene Expression Regulation, Neoplastic | Pancreatic Neoplasms - genetics | Pyrimidines - biosynthesis | Carcinoma, Pancreatic Ductal - genetics | Pancreatic Neoplasms - drug therapy | Carcinoma, Pancreatic Ductal - drug therapy | Protein Kinase Inhibitors - administration & dosage | Animals | MAP Kinase Signaling System - drug effects | Mice, Nude | Female | Mice | Proto-Oncogene Proteins p21(ras) - metabolism | Adenocarcinoma | Pentose phosphate | Transcription | MEK inhibitors | MAP kinase | Biosynthesis | Myc protein | Metabolism | Signal transduction | Rewiring | Pancreatic cancer | Pentose | Dependence | Pentose phosphate pathway
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