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1. Full Text The prognostic value of BAP1, PBRM1, pS6, PTEN, TGase2, PD-L1, CA9, PSMA, and Ki-67 tissue markers in localized renal cell carcinoma: A retrospective study of tissue microarrays using immunohistochemistry
by Kim, Sung Han and Park, Weon Seo and Park, Eun Young and Park, Boram and Joo, Jungnam and Joung, Jae Young and Seo, Ho Kyung and Lee, Kang Hyun and Chung, Jinsoo
PLoS ONE, ISSN 1932-6203, 06/2017, Volume 12, Issue 6, pp. e0179610 - e0179610
Objective To assess the prognostic roles of BAP1, PBRM1, pS6, PTEN, TGase2, PD-L1, CA9, PSMA, and Ki-67 tissue biomarkers in localized renal cell carcinoma... 
SURVIVAL | MORTALITY | CARBONIC-ANHYDRASE-IX | PROTEIN | MULTIDISCIPLINARY SCIENCES | CANCER INCIDENCE | METASTASES | OUTCOMES | KI67 | EXPRESSION | TUMORS | Immunohistochemistry | Prognosis | Tissue Array Analysis | Humans | Middle Aged | Ki-67 Antigen - metabolism | Male | Kidney Neoplasms - metabolism | Porphyrins - metabolism | Neoplasm Recurrence, Local - mortality | Neoplasm Recurrence, Local - pathology | Glutamate Carboxypeptidase II - metabolism | Neoplasm Grading | Antigens, Neoplasm - metabolism | Antigens, Surface - metabolism | Biomarkers, Tumor - metabolism | Ubiquitin Thiolesterase - metabolism | Adult | Female | Carbonic Anhydrase IX - metabolism | Retrospective Studies | Tumor Suppressor Proteins - metabolism | Neoplasm Recurrence, Local - metabolism | Carcinoma, Renal Cell - pathology | PTEN Phosphohydrolase - metabolism | Nuclear Proteins - metabolism | Survival Rate | Kidney Neoplasms - mortality | Transcription Factors - metabolism | Carcinoma, Renal Cell - metabolism | Carcinoma, Renal Cell - mortality | Disease-Free Survival | B7-H1 Antigen - metabolism | Transglutaminases - metabolism | Sulfonamides - metabolism | Kidney Neoplasms - pathology | Aged | Neoplasm Staging | GTP-Binding Proteins - metabolism | Genetic aspects | Carcinoma, Renal cell | Research | Biological markers | Biometrics | Slopes | Metastasis | Kinases | Epidemiology | Cancer therapies | Urology | Proteins | Nephrectomy | Quality | Bioindicators | Growth factors | Age | Antigens | Markers | Hazards | Patients | Survival | Disease prevention | Hospitals | Medical prognosis | PD-L1 protein | Biomarkers | Death | Mutation | Diabetes | Prostate cancer | PTEN protein | Clear cell-type renal cell carcinoma | Cancer | Kidney transplantation | Tumors | Index Medicus
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2. Full Text Urea-induced ROS cause endothelial dysfunction in chronic renal failure
by D'Apolito, Maria and Du, Xueliang and Pisanelli, Daniela and Pettoello-Mantovani, Massimo and Campanozzi, Angelo and Giacco, Ferdinando and Maffione, Angela Bruna and Colia, Anna Laura and Brownlee, Michael and Giardino, Ida
Atherosclerosis, ISSN 0021-9150, 2015, Volume 239, Issue 2, pp. 393 - 400
Abstract Objective The pathogenic events responsible for accelerated atherosclerosis in patients with chronic renal failure (CRF) are poorly understood. Here... 
Cardiovascular | MnTBAP | chronic renal failure | UCP-1 | Endothelial cells | uncoupling protein 1 | Urea | O-linked-N-acetylglucosamine | manganese tetrakis (4-benzoic acid) porphyrin | CRF | ROS | reactive oxygen species | GlcNAc | Prostacyclin synthase | Reactive oxygen species | Chronic renal failure | Manganese tetrakis (4-benzoic acid) porphyrin | Uncoupling protein 1 | CELLS | OXIDATIVE STRESS | ATHEROSCLEROSIS | INSULIN-RESISTANCE | CARDIOVASCULAR-DISEASE | GENE-EXPRESSION | HIGH GLUCOSE | PERIPHERAL VASCULAR DISEASE | CHRONIC KIDNEY-DISEASE | HYPERGLYCEMIC DAMAGE | Tumor Necrosis Factor-alpha - metabolism | Reactive Oxygen Species - metabolism | Oxidative Stress | Humans | Cytochrome P-450 Enzyme System - metabolism | Endothelium, Vascular - drug effects | Aorta - metabolism | Urea - chemistry | Antigens, CD - metabolism | Endoglin | Atherosclerosis - enzymology | Kidney Failure, Chronic - chemically induced | Chemokine CCL2 - metabolism | Endothelium - enzymology | Intramolecular Oxidoreductases - metabolism | Interleukin-6 - metabolism | Superoxide Dismutase - metabolism | Atherosclerosis - physiopathology | Endothelial Cells - metabolism | Mice, Inbred C57BL | Receptors, Cell Surface - metabolism | Random Allocation | Atherosclerosis - metabolism | Kidney Failure, Chronic - metabolism | Catalase - metabolism | Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating) - metabolism | Animals | Endothelium, Vascular - pathology | Mice | Vascular Cell Adhesion Molecule-1 - metabolism | Chronic kidney failure | Atherosclerosis | Endothelium | Index Medicus
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3. Full Text XPO1-dependent nuclear export is a druggable vulnerability in KRAS-mutant lung cancer
by Kim, Jimi and McMillan, Elizabeth and Kim, Hyun Seok and Venkateswaran, Niranjan and Makkar, Gurbani and Rodriguez-Canales, Aime and Villalobos, Pamela and Neggers, Jasper Edgar and Mendiratta, Saurabh and Wei, Shuguang and Landesman, Yosef and Senapedis, William and Baloglu, Erkan and Chow, Chi-Wan B and Frink, Robin E and Gao, Boning and Roth, Michael and Minna, John D and Daelemans, Dirk and Wistuba, Ignacio I and Posner, Bruce A and Scaglioni, Pier Paolo and White, Michael A
Nature, ISSN 0028-0836, 09/2016, Volume 538, Issue 7623, pp. 114 - 117
The common participation of oncogenic KRAS proteins in many of the most lethal human cancers, together with the ease of detecting somatic KRAS mutant alleles... 
TARGET | CRM1/XPO1 | ACTIVATION | MODELS | MULTIDISCIPLINARY SCIENCES | KINASE | YAP | MUTATIONS | INHIBITORS | IDENTIFICATION | Lung Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Lung Neoplasms - metabolism | Cell Survival - genetics | Lung Neoplasms - pathology | NF-kappa B - metabolism | Phosphoproteins - antagonists & inhibitors | Phosphoproteins - metabolism | DNA-Binding Proteins - metabolism | Cell Nucleus - metabolism | RNA Interference | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | Female | Verteporfin | Protein-Serine-Threonine Kinases - metabolism | Carcinoma, Non-Small-Cell Lung - pathology | Follistatin-Related Proteins - genetics | Lung Neoplasms - genetics | Cell Survival - drug effects | NF-kappa B - antagonists & inhibitors | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Porphyrins - pharmacology | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Animals | Karyopherins - metabolism | Active Transport, Cell Nucleus - drug effects | Genes, Lethal - genetics | NF-KappaB Inhibitor alpha - metabolism | Nuclear Proteins - antagonists & inhibitors | Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | RNA, Small Interfering | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Cell Nucleus - drug effects | Karyopherins - antagonists & inhibitors | Receptors, Cytoplasmic and Nuclear - metabolism | Care and treatment | Genetic aspects | Gene mutations | Health aspects | Guanosine triphosphatase | Lung cancer | Genomics | Genomes | Kinases | Drug resistance | Gene expression | Drug dosages | Index Medicus
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4. The metabolism of porphyrins
: the effects of inducing chemicals on porphyrin biosynthesis in the photosynthetic bacterium Rhodopseudomonas spheroides
by Cooper, Stanley David, 1942 and Toronto, Ont. University.Theses (M.Sc.)
1968, 114 leaves
Metabolism | Porphyrins | Rhodopseudomonas spheroides
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5. Full Text Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice
by Jinu Kim and Young Mi Seok and Kyong-Jin Jung and Kwon Moo Park
American Journal of Physiology - Renal Physiology, ISSN 1931-857X, 08/2009, Volume 297, Issue 2, pp. 461 - 470
Recently, kidney fibrosis following transplantation has become recognized as a main contributor of chronic allograft nephropathy. In transplantation, transient... 
Ischemia-reperfusion | α-smooth muscle actin | Superoxide | Manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin | Interstitial fibrosis | alpha-smooth muscle actin | manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin | OXIDATIVE STRESS | ISCHEMIA/REPERFUSION INJURY | PHYSIOLOGY | REPERFUSION INJURY | ischemia-reperfusion | interstitial fibrosis | MAPK KINASE ACTIVATION | NITRIC-OXIDE | UROLOGY & NEPHROLOGY | INDUCED FUNCTIONAL INJURY | superoxide | SUPEROXIDE-DISMUTASE | URETERAL OBSTRUCTION | CHRONIC ALLOGRAFT NEPHROPATHY | IMMUNOSTIMULATED MACROPHAGES | Kidney - blood supply | Reactive Oxygen Species - metabolism | Kidney - pathology | Apoptosis - drug effects | S100 Calcium-Binding Protein A4 | Actins - metabolism | Male | Metalloporphyrins - pharmacology | Tyrosine - analogs & derivatives | Antigens, CD - metabolism | Kidney - metabolism | Time Factors | Lipid Peroxidation - drug effects | Reperfusion Injury - metabolism | Ischemia - pathology | Superoxide Dismutase - metabolism | Disease Models, Animal | Kidney - drug effects | Oxidation-Reduction | Reperfusion Injury - pathology | Ischemia - metabolism | S100 Proteins - metabolism | Antioxidants - pharmacology | Disease Progression | Hydrogen Peroxide - metabolism | Collagen - metabolism | Tyrosine - metabolism | Animals | Reperfusion Injury - prevention & control | Antigens, Differentiation, Myelomonocytic - metabolism | Fibrosis | Glucosephosphate Dehydrogenase - metabolism | HSP47 Heat-Shock Proteins - metabolism | Mice | Mice, Inbred BALB C | Oxidative Stress - drug effects | Proliferating Cell Nuclear Antigen - metabolism | Vitamin E - pharmacology | Proteins | Studies | Rodents | Oxidation | Kidney diseases | Gene expression | Cells | Index Medicus
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6. Diseases of porphyrin metabolism
by Goldberg, Abraham and Rimington, C
1962, American lecture series, publication no. 481. A monograph in the Bannerstone Division in American lectures in living chemistry, 231
Porphyria
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7. Disorders of porphyrin metabolism
by Moore, Michael R and Wintrobe, Maxwell Myer
1987, ISBN 0306426250, xv, 374 p., [1] leaf of plates
Porphyria
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8. Full Text TMEM14C is required for erythroid mitochondrial heme metabolism
by Yien, Yvette Y and Robledo, Raymond F and Schultz, Iman J and Takahashi-Makise, Naoko and Gwynn, Babette and Bauer, Daniel E and Dass, Abhishek and Yi, Gloria and Li, Liangtao and Hildick-Smith, Gordon J and Cooney, Jeffrey D and Pierce, Eric L and Mohler, Kyla and Dailey, Tamara A and Miyata, Non and Kingsley, Paul D and Garone, Caterina and Hattangadi, Shilpa M and Huang, Hui and Chen, Wen and Keenan, Ellen M and Shah, Dhvanit I and Schlaeger, Thorsten M and Dimauro, Salvatore and Orkin, Stuart H and Cantor, Alan B and Palis, James and Koehler, Carla M and Lodish, Harvey F and Kaplan, Jerry and Ward, Diane M and Dailey, Harry A and Phillips, John D and Peters, Luanne L and Paw, Barry H
Journal of Clinical Investigation, ISSN 0021-9738, 10/2014, Volume 124, Issue 10, pp. 4294 - 4304
The transport and intracellular trafficking of heme biosynthesis intermediates are crucial for hemoglobin production, which is a critical process in developing... 
CHIP-SEQ | MEDICINE, RESEARCH & EXPERIMENTAL | IRON TRAFFICKING | PROTEIN | GENE | ABCB6 | ERYTHROPOIESIS | MOUSE | LOCI | FERROCHELATASE | IDENTIFICATION | Cell Line | Mitochondrial Membrane Transport Proteins - metabolism | Heme - metabolism | Membrane Proteins - genetics | Erythroid Cells - metabolism | Gene Expression Regulation | Hemoglobins - metabolism | Protoporphyrins - metabolism | Mitochondria - metabolism | Porphyrins - metabolism | Liver - embryology | Mitochondrial Membrane Transport Proteins - genetics | Mitochondrial Membranes - metabolism | Anemia - metabolism | Animals | Membrane Proteins - metabolism | Mice | Erythropoiesis - genetics | RNA, Small Interfering - metabolism | Mitochondria | Cell metabolism | Genetic research | Genetic aspects | Research | Gene expression | Observations | Proteins | Studies | Enzymes | Genes | Rodents | Cloning | Stem cells | Metabolism | Laboratory animals | Index Medicus | Abridged Index Medicus
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9. Full Text Genetic and pharmacological disruption of the TEAD-YAP complex suppresses the oncogenic activity of YAP
by Liu-Chittenden, Yi and Huang, Bo and Shim, Joong Sup and Chen, Qian and Lee, Se-Jin and Anders, Robert A and Liu, Jun O and Pan, Duojia
Genes and Development, ISSN 0890-9369, 06/2012, Volume 26, Issue 12, pp. 1300 - 1305
The Drosophila TEAD ortholog Scalloped is required for Yki-mediated overgrowth but is largely dispensable for normal tissue growth, suggesting that its... 
Chemical biology | YAP | Hippo signaling | Oncogene | APOPTOSIS | GROWTH-CONTROL | ORGAN SIZE CONTROL | HIPPO SIGNALING PATHWAY | CELL-PROLIFERATION | DEVELOPMENTAL BIOLOGY | oncogene | CANCER | DROSOPHILA | CELL BIOLOGY | INHIBITION | chemical biology | GENETICS & HEREDITY | TUMORIGENESIS | MAMMALS | Hepatomegaly - pathology | Liver - pathology | Humans | Phosphoproteins - metabolism | DNA-Binding Proteins - metabolism | Multiprotein Complexes - metabolism | Liver - drug effects | Protein Binding - drug effects | HEK293 Cells | Neurofibromin 2 - metabolism | Liver - metabolism | Mice, Transgenic | Phosphoproteins - genetics | Porphyrins - pharmacology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Transcription Factors - metabolism | Phenotype | Animals | Adaptor Proteins, Signal Transducing - genetics | Hepatomegaly - metabolism | Mice | Adaptor Proteins, Signal Transducing - metabolism | Cell Transformation, Neoplastic - pathology | Genes, Dominant - genetics | Index Medicus | Research Communication
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10. Full Text Synthetic ion transporters can induce apoptosis by facilitating chloride anion transport into cells
by Ko, Sung-Kyun and Kim, Sung Kuk and Share, Andrew and Lynch, Vincent M and Park, Jinhong and Namkung, Wan and Van Rossom, Wim and Busschaert, Nathalie and Gale, Philip A and Sessler, Jonathan L and Shin, Injae
Nature Chemistry, ISSN 1755-4330, 10/2014, Volume 6, Issue 10, pp. 885 - 892
Anion transporters based on small molecules have received attention as therapeutic agents because of their potential to disrupt cellular ion homeostasis.... 
ANTICANCER ACTIVITY | TRANSMEMBRANE TRANSPORT | SMALL-MOLECULE | PATHWAY | ANALOGS | PRODIGIOSIN | CHANNELS | DEATH | BINDING PROPERTIES | CANCER | CHEMISTRY, MULTIDISCIPLINARY | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Pyridines - chemistry | Humans | Porphyrins - chemistry | Small Molecule Libraries - metabolism | Chlorides - chemistry | Porphyrins - metabolism | Anion Transport Proteins - chemistry | Calixarenes - chemistry | Caspases - metabolism | Amino Acid Chloromethyl Ketones - metabolism | Ion Transport | Caspases - chemistry | Cell Line | Chlorides - pharmacology | Amino Acid Chloromethyl Ketones - chemistry | Cytochromes c - metabolism | HCT116 Cells | Rats | Mitochondria - metabolism | Anion Transport Proteins - metabolism | Calixarenes - metabolism | Liposomes - chemistry | Animals | Diamide - chemistry | HeLa Cells | Index Medicus
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11. Full Text Role of mitochondrial oxidative stress in modulating the expressions of aquaporins in obstructive kidney disease
by Liu, Mi and Sun, Ying and Xu, Man and Yu, Xiaowen and Zhang, Yue and Huang, Songming and Ding, Guixia and Zhang, Aihua and Jia, Zhanjun
American journal of physiology. Renal physiology, ISSN 1931-857X, 04/2018, Volume 314, Issue 4, pp. F658 - F666
Downregulation of aquaporins (AQPs) in obstructive kidney disease has been well demonstrated with elusive mechanisms. Our previous study indicated that... 
Free Radical Scavengers - pharmacology | Ureteral Obstruction - complications | Kidney - pathology | Receptors, Vasopressin - metabolism | Male | Ureteral Obstruction - metabolism | Metalloporphyrins - pharmacology | Aquaporin 1 - metabolism | Aquaporins - genetics | Kidney Diseases - genetics | Kidney - metabolism | Cyclooxygenase 2 - genetics | Aquaporin 4 - genetics | Ureteral Obstruction - genetics | Superoxide Dismutase - metabolism | Disease Models, Animal | Kidney Diseases - metabolism | Kidney - drug effects | Prostaglandin-E Synthases - metabolism | Signal Transduction | Kidney Diseases - pathology | Down-Regulation | Mice, Inbred C57BL | Aquaporins - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Aquaporin 3 - genetics | Aquaporin 1 - genetics | Aquaporin 2 - metabolism | Dinoprostone - metabolism | Aquaporin 3 - metabolism | Animals | Aquaporin 4 - metabolism | Ureteral Obstruction - pathology | Cyclooxygenase 2 - metabolism | Kidney Diseases - etiology | Oxidative Stress - drug effects | Aquaporin 2 - genetics | Oxidative stress | Mitochondria | Genetic aspects | Kidney diseases | Health aspects | Aquaporins | Aquaporin 4 | Benzoic acid | Prostaglandin E2 | Superoxide dismutase | Mitochondrial DNA | Tetrakis(4-benzoic acid)porphyrin | Western blotting | Prostaglandin endoperoxide synthase | Prostaglandin E | Thiobarbituric acid | Aquaporin 1 | Aquaporin 2 | Aquaporin 3 | Urine | Kidneys | Secretion | Prostaglandin-E synthase | Polymerase chain reaction | Cyclooxygenase-1 | Cyclooxygenase-2 | Manganese | Index Medicus
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12. Full Text YAP activation is an early event and a potential therapeutic target in liver cancer development
by Perra, Andrea and Kowalik, Marta Anna and Ghiso, Elena and Ledda-Columbano, Giovanna Maria and Di Tommaso, Luca and Angioni, Maria Maddalena and Raschioni, Carlotta and Testore, Elena and Roncalli, Massimo and Giordano, Silvia and Columbano, Amedeo
Journal of Hepatology, ISSN 0168-8278, 2014, Volume 61, Issue 5, pp. 1088 - 1096
Background & Aims Although the growth suppressing Hippo pathway has been implicated in hepatocellular carcinoma (HCC) pathogenesis, it is unknown at which... 
Gastroenterology and Hepatology | Preneoplastic stages | HCC | Verteporfin | TCPOBOP | Hippo pathway | YES-ASSOCIATED PROTEIN | RAT | ORGAN SIZE CONTROL | REGENERATION | CELL-PROLIFERATION | LESIONS | CARCINOGENESIS | PATHWAY | HEPATOCELLULAR-CARCINOMA DEVELOPMENT | GASTROENTEROLOGY & HEPATOLOGY | TUMORIGENESIS | Adenoma, Liver Cell - drug therapy | Precancerous Conditions - etiology | Adenoma, Liver Cell - etiology | Humans | Middle Aged | Rats, Inbred F344 | Male | MicroRNAs - metabolism | Precancerous Conditions - metabolism | Phosphoproteins - metabolism | Liver Neoplasms - etiology | Precancerous Conditions - drug therapy | Young Adult | Liver Neoplasms, Experimental - metabolism | Carcinoma, Hepatocellular - drug therapy | Apoptosis Regulatory Proteins - genetics | Adult | Female | Antineoplastic Agents - pharmacology | Carcinoma, Hepatocellular - etiology | Protein-Serine-Threonine Kinases - metabolism | Gene Expression | Signal Transduction | Adenoma, Liver Cell - metabolism | Liver Neoplasms - drug therapy | Rats | Porphyrins - pharmacology | Liver Neoplasms, Experimental - etiology | Apoptosis Regulatory Proteins - metabolism | Animals | Liver Neoplasms, Experimental - drug therapy | Apoptosis Regulatory Proteins - antagonists & inhibitors | Liver Neoplasms - metabolism | Cell Line, Tumor | Aged | Cell Proliferation - drug effects | Mice | MicroRNAs - genetics | Adaptor Proteins, Signal Transducing - metabolism | Carcinoma, Hepatocellular - metabolism | Liver cancer | Health aspects | Index Medicus
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13. Full Text Cancer Cell Membrane Camouflaged Cascade Bioreactor for Cancer Targeted Starvation and Photodynamic Therapy
by Li, Shi-Ying and Cheng, Hong and Xie, Bo-Ru and Qiu, Wen-Xiu and Zeng, Jing-Yue and Li, Chu-Xin and Wan, Shuang-Shuang and Zhang, Lu and Liu, Wen-Long and Zhang, Xian-Zheng
ACS Nano, ISSN 1936-0851, 07/2017, Volume 11, Issue 7, pp. 7006 - 7018
Selectively cuting off the nutrient supply and the metabolism pathways of cancer cells would be a promising approach to improve the efficiency of cancer... 
homotypic targeting | photodynamic therapy | starvation therapy | cell membrane | metal-organic framework | CLEARANCE | PHOTOSENSITIZER | MATERIALS SCIENCE, MULTIDISCIPLINARY | CHEMISTRY, PHYSICAL | NANOSCIENCE & NANOTECHNOLOGY | HYPOXIA | CHEMISTRY, MULTIDISCIPLINARY | DELIVERY | FUNCTIONALIZATION | NANOPARTICLES | PEG | METABOLISM | LIPOSOMES | Neoplasms - metabolism | Catalase - therapeutic use | Photosensitizing Agents - chemistry | Photosensitizing Agents - therapeutic use | Humans | Porphyrins - chemistry | Cercopithecus aethiops | Metal-Organic Frameworks - chemistry | Photochemotherapy | Oxygen - metabolism | Cell Membrane - metabolism | Cell Membrane - drug effects | Glucose Oxidase - therapeutic use | Glucose Oxidase - metabolism | Porphyrins - therapeutic use | Hydrogen Peroxide - metabolism | Neoplasms - drug therapy | Catalase - metabolism | Animals | Cell Line, Tumor | Glucose - metabolism | RAW 264.7 Cells | Mice | Mice, Inbred BALB C | COS Cells | Metal-Organic Frameworks - therapeutic use | Index Medicus
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14. Full Text Targeting YAP in malignant pleural mesothelioma
by Zhang, Wen‐Qian and Dai, Yu‐Yuan and Hsu, Ping‐Chih and Wang, Hui and Cheng, Li and Yang, Yi‐Lin and Wang, Yu‐Cheng and Xu, Zhi‐Dong and Liu, Shu and Chan, Geraldine and Hu, Bin and Li, Hui and Jablons, David M and You, Liang
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 11/2017, Volume 21, Issue 11, pp. 2663 - 2676
Malignant mesothelioma is an aggressive cancer that is resistant to current therapy. The poor prognosis of mesothelioma has been associated with elevated... 
YAP | therapeutic target | Hippo pathway | mesothelioma | MEDICINE, RESEARCH & EXPERIMENTAL | HIPPO SIGNALING CASCADE | CANCER STEM-CELLS | CELL BIOLOGY | TISSUE GROWTH-FACTOR | MELANOMA | TEAD | GENE | PATHWAY | DYSREGULATION | MUTATIONS | PROGRESSION | RNA, Small Interfering - genetics | Phosphorylation | Epithelial Cells - metabolism | Prognosis | Mesothelioma - pathology | Epithelial Cells - drug effects | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Spheroids, Cellular - pathology | Lung Neoplasms - pathology | rhoA GTP-Binding Protein - metabolism | Phosphoproteins - antagonists & inhibitors | rhoA GTP-Binding Protein - genetics | Phosphoproteins - metabolism | RNA, Messenger - metabolism | DNA-Binding Proteins - metabolism | rho-Associated Kinases - metabolism | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Spheroids, Cellular - drug effects | 3' Untranslated Regions | Nuclear Proteins - genetics | Genes, Reporter | Lung Neoplasms - genetics | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | RNA, Messenger - genetics | Spheroids, Cellular - metabolism | rho-Associated Kinases - genetics | Epithelial Cells - pathology | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Mesothelioma - genetics | Phosphoproteins - genetics | Porphyrins - pharmacology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Transcription Factors - metabolism | Mesothelioma - metabolism | Nuclear Proteins - antagonists & inhibitors | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Adaptor Proteins, Signal Transducing - metabolism | RNA, Small Interfering - metabolism | Immunohistochemistry | Yuan (China) | Mesothelioma | RNA | Analysis | Biotechnology | Transcription | siRNA | Yes-associated protein | Proteins | Signaling | 3' Untranslated regions | Cell lines | Inhibition | Viability | Cancer | Index Medicus | Original
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