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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
Journal Article
Nature, ISSN 0028-0836, 10/2014, Volume 514, Issue 7524, pp. 628 - 632
Journal Article
Journal Article
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
Journal Article
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
Journal Article
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
Journal Article
Molecular Cancer Therapeutics, ISSN 1535-7163, 12/2015, Volume 14, Issue 12 Supplement 2, pp. C157 - C157
Journal Article
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
Journal Article
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
Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 4945 - 13
Journal Article