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1. Full Text Ribociclib as First-Line Therapy for HR-Positive, Advanced Breast Cancer
by Hortobagyi, Gabriel N and Stemmer, Salomon M and Burris, Howard A and Yap, Yoon-Sim and Sonke, Gabe S and Paluch-Shimon, Shani and Campone, Mario and Blackwell, Kimberly L and André, Fabrice and Winer, Eric P and Janni, Wolfgang and Verma, Sunil and Conte, Pierfranco and Arteaga, Carlos L and Cameron, David A and Petrakova, Katarina and Hart, Lowell L and Villanueva, Cristian and Chan, Arlene and Jakobsen, Erik and Nusch, Arnd and Burdaeva, Olga and Grischke, Eva-Maria and Alba, Emilio and Wist, Erik and Marschner, Norbert and Favret, Anne M and Yardley, Denise and Bachelot, Thomas and Tseng, Ling-Ming and Blau, Sibel and Xuan, Fengjuan and Souami, Farida and Miller, Michelle and Germa, Caroline and Hirawat, Samit and O’Shaughnessy, Joyce
The New England Journal of Medicine, ISSN 0028-4793, 11/2016, Volume 375, Issue 18, pp. 1738 - 1748
In patients with advanced HR-positive, HER2-negative breast cancer, the addition of the cyclin-dependent kinase inhibitor ribociclib to letrozole was... 
CRITERIA | CONTROLLED-TRIAL | PALBOCICLIB | MEDICINE, GENERAL & INTERNAL | PLACEBO | CDK4/6 | CLINICAL-TRIALS | DOUBLE-BLIND | ESTROGEN | POSTMENOPAUSAL WOMEN | Aminopyridines - administration & dosage | Triazoles - administration & dosage | Double-Blind Method | Drug Administration Schedule | Receptors, Estrogen | Humans | Middle Aged | Kaplan-Meier Estimate | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Purines - administration & dosage | Breast Neoplasms - drug therapy | Nitriles - administration & dosage | Disease-Free Survival | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Breast Neoplasms - pathology | Receptors, Progesterone | Aged, 80 and over | Adult | Female | Aged | Receptor, ErbB-2 | Neoplasm Staging | Letrozole | Care and treatment | Postmenopausal women | Breast cancer | Health aspects | Leukopenia | Estrogen | Endocrine therapy | Metastasis | Kinases | Cancer therapies | Survival | Patients | ErbB-2 protein | Cyclin-dependent kinase 4 | Post-menopause | Metastases | Proteins | Epidermal growth factor | Womens health | Myelosuppression | Neutropenia
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2. Full Text Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation
by Kaufman, Bella and Shapira-Frommer, Ronnie and Schmutzler, Rita K and Audeh, M. William and Friedlander, Michael and Balmaña, Judith and Mitchell, Gillian and Fried, Georgeta and Stemmer, Salomon M and Hubert, Ayala and Rosengarten, Ora and Steiner, Mariana and Loman, Niklas and Bowen, Karin and Fielding, Anitra and Domchek, Susan M
Journal of Clinical Oncology, ISSN 0732-183X, 01/2015, Volume 33, Issue 3, pp. 244 - 250
Purpose Olaparib is an oral poly (ADP-ribose) polymerase inhibitor with activity in germline BRCA1 and BRCA2 (BRCA1/2) -associated breast and ovarian cancers.... 
BREAST-CANCER | POLY(ADP-RIBOSE) POLYMERASE | MULTICENTER | FOLFIRINOX | ONCOLOGY | ADENOCARCINOMA | PANCREATIC-CANCER | OPEN-LABEL | PARP INHIBITORS | TUMORS | GEMCITABINE | Piperazines - administration & dosage | Prospective Studies | Humans | Middle Aged | Male | Antineoplastic Agents - therapeutic use | Antineoplastic Agents - administration & dosage | Ovarian Neoplasms - genetics | Pancreatic Neoplasms - drug therapy | Prostatic Neoplasms - genetics | Neoplasms - genetics | Antineoplastic Agents - adverse effects | Germ-Line Mutation | Adult | Female | Ovarian Neoplasms - drug therapy | Prostatic Neoplasms - drug therapy | Phthalazines - administration & dosage | Drug Administration Schedule | Kaplan-Meier Estimate | Pancreatic Neoplasms - genetics | Treatment Outcome | Piperazines - therapeutic use | Breast Neoplasms - drug therapy | Piperazines - adverse effects | Neoplasms - drug therapy | BRCA1 Protein - genetics | Disease-Free Survival | Phthalazines - therapeutic use | Breast Neoplasms - genetics | Aged | Neoplasms - pathology | BRCA2 Protein - genetics | Phthalazines - adverse effects | ORIGINAL REPORTS
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3. Full Text Resistance to checkpoint blockade therapy through inactivation of antigen presentation
by Sade-Feldman, Moshe and Jiao, Yunxin J and Chen, Jonathan H and Rooney, Michael S and Barzily-Rokni, Michal and Eliane, Jean-Pierre and Bjorgaard, Stacey L and Hammond, Marc R and Vitzthum, Hans and Blackmon, Shauna M and Frederick, Dennie T and Hazar-Rethinam, Mehlika and Nadres, Brandon A and Van Seventer, Emily E and Shukla, Sachet A and Yizhak, Keren and Ray, John P and Rosebrock, Daniel and Livitz, Dimitri and Adalsteinsson, Viktor and Getz, Gad and Duncan, Lyn M and Li, Bo and Corcoran, Ryan B and Lawrence, Donald P and Stemmer-Rachamimov, Anat and Boland, Genevieve M and Landau, Dan A and Flaherty, Keith T and Sullivan, Ryan J and Hacohen, Nir
Nature Communications, ISSN 2041-1723, 12/2017, Volume 8, Issue 1, pp. 1136 - 11
Treatment with immune checkpoint blockade (CPB) therapies often leads to prolonged responses in patients with metastatic melanoma, but the common mechanisms of... 
PLATFORM | METASTATIC MELANOMA | CTLA-4 BLOCKADE | PEMBROLIZUMAB | GENOMICS | PD-1 BLOCKADE | MULTIDISCIPLINARY SCIENCES | ACQUIRED-RESISTANCE | CANCER-IMMUNOTHERAPY | MUTATIONS | TUMORS | Humans | Mice, Inbred C57BL | Antibodies, Monoclonal - therapeutic use | Antigen Presentation - genetics | Melanoma - pathology | CTLA-4 Antigen - immunology | Loss of Heterozygosity | Mice, Knockout | Neoplasms, Experimental - pathology | Point Mutation | Drug Resistance, Neoplasm - genetics | Neoplasm Metastasis | Animals | Melanoma - genetics | Melanoma - drug therapy | Neoplasms, Experimental - genetics | Female | Antigen Presentation - drug effects | Programmed Cell Death 1 Receptor - immunology | Neoplasms, Experimental - drug therapy | Antibodies, Monoclonal - immunology | beta 2-Microglobulin - genetics | Drug Resistance, Neoplasm - drug effects | Antigen presentation | Deactivation | PD-1 protein | Melanoma | Metastasis | Inactivation | Patients | Metastases | Heterozygosity | CTLA-4 protein | Major histocompatibility complex | Immune checkpoint | Loss of heterozygosity | Mutation | Target acquisition
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4. Full Text The Reprogramming of Tumor Stroma by HSF1 Is a Potent Enabler of Malignancy
by Scherz-Shouval, Ruth and Santagata, Sandro and Mendillo, Marc L and Sholl, Lynette M and Ben-Aharon, Irit and Beck, Andrew H and Dias-Santagata, Dora and Koeva, Martina and Stemmer, Salomon M and Whitesell, Luke and Lindquist, Susan
Cell, ISSN 0092-8674, 07/2014, Volume 158, Issue 3, pp. 564 - 578
Stromal cells within the tumor microenvironment are essential for tumor progression and metastasis. Surprisingly little is known about the factors that drive... 
BREAST-CANCER | HEAT-SHOCK FACTOR-1 | LUNG-CANCER | TGF-BETA | TRANSCRIPTION FACTOR HSF1 | MICROENVIRONMENT | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | GENE-EXPRESSION | FIBROBLASTS | PROGRESSION | CELL BIOLOGY | Heat shock proteins | Development and progression | Bone morphogenetic proteins | Transforming growth factors | Lung cancer | Cancer
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5. Full Text Insulator dysfunction and oncogene activation in IDH mutant gliomas
by Flavahan, William A and Drier, Yotam and Liau, Brian B and Gillespie, Shawn M and Venteicher, Andrew S and Stemmer-Rachamimov, Anat O and Suvà, Mario L and Bernstein, Bradley E
Nature, ISSN 0028-0836, 01/2016, Volume 529, Issue 7584, pp. 110 - 114
Gain-of-function IDH mutations are initiating events that define major clinical and prognostic classes of gliomas(1,2). Mutant IDH protein produces a new... 
MAINTENANCE | METHYLATION | LANDSCAPE | DEMETHYLATION | MULTIDISCIPLINARY SCIENCES | INTEGRATED GENOMIC ANALYSIS | ARCHITECTURE | PHENOTYPE | EXPRESSION | 2-HYDROXYGLUTARATE | PRINCIPLES | Chromatin - metabolism | Up-Regulation | Humans | Glioma - genetics | Base Sequence | Glioma - pathology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | Chromatin - drug effects | Repressor Proteins - metabolism | Oncogenes - genetics | Insulator Elements - genetics | Glioma - enzymology | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Isocitrate Dehydrogenase - genetics | DNA Methylation - genetics | Down-Regulation - drug effects | Mutation - genetics | CRISPR-Cas Systems - genetics | Insulator Elements - drug effects | Phenotype | Isocitrate Dehydrogenase - chemistry | Receptor, Platelet-Derived Growth Factor alpha - genetics | CCCTC-Binding Factor | CpG Islands - genetics | Protein Binding | Isocitrate Dehydrogenase - metabolism | Cell Proliferation - drug effects | Enhancer Elements, Genetic - genetics | Glutarates - metabolism | Cell Transformation, Neoplastic - drug effects | Chromatin - genetics | DNA Methylation - drug effects | Glioma - drug therapy | Complications and side effects | Care and treatment | Platelet-derived growth factor | Gliomas | Analysis | Influence | Genetic aspects | Research | Methylation | Oncogenes | DNA methylation | Epigenetics | Genomes | Mutation | Gene expression | Binding sites | Deoxyribonucleic acid--DNA | Tumors
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6. Full Text Randomized Phase II Study of the Anti–Epidermal Growth Factor Receptor Monoclonal Antibody Cetuximab With Cisplatin Versus Cisplatin Alone in Patients With Metastatic Triple-Negative Breast Cancer
by José Baselga and Patricia Gómez and Richard Greil and Sofia Braga and Miguel A. Climent and Andrew M. Wardley and Bella Kaufman and Salomon M. Stemmer and António Pêgo and Arlene Chan and Jean-Charles Goeminne and Marie-Pascale Graas and M. John Kennedy and Eva Maria Ciruelos Gil and Andreas Schneeweiss and Angela Zubel and Jutta Groos and Helena Melezínková and Ahmad Awada
Journal of Clinical Oncology, ISSN 0732-183X, 07/2013, Volume 31, Issue 20, pp. 2586 - 2592
Purpose Epidermal growth factor receptor is overexpressed in metastatic triple-negative breast cancers (mTNBCs), an aggressive subtype of breast cancer. Our... 
TRIAL | MULTICENTER | EFFICACY | ONCOLOGY | SUBTYPES | COLORECTAL-CANCER | PLATINUM-BASED CHEMOTHERAPY | OXALIPLATIN | COMBINATION | EXPRESSION | CARCINOMA | Multivariate Analysis | Confidence Intervals | Receptors, Estrogen - metabolism | Antineoplastic Combined Chemotherapy Protocols - administration & dosage | Prognosis | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Breast Neoplasms - metabolism | Cisplatin - administration & dosage | Receptors, Progesterone - metabolism | Dose-Response Relationship, Drug | Antibodies, Monoclonal, Humanized - administration & dosage | Neoplasm Invasiveness - pathology | Adult | Female | Cetuximab | Antibodies, Monoclonal, Humanized - adverse effects | ErbB Receptors - metabolism | Drug Administration Schedule | Risk Assessment | Proportional Hazards Models | Treatment Outcome | ErbB Receptors - drug effects | Breast Neoplasms - drug therapy | Disease-Free Survival | Maximum Tolerated Dose | Receptors, Estrogen - drug effects | Breast Neoplasms - pathology | Receptors, Progesterone - drug effects | Survival Analysis | Cisplatin - adverse effects | Breast Neoplasms - mortality | Aged | Neoplasm Staging | ORIGINAL REPORTS
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7. Full Text Fibroblast growth factor 21 mediates specific glucagon actions
by Habegger, Kirk M and Stemmer, Kerstin and Cheng, Christine and Müller, Timo D and Heppner, Kristy M and Ottaway, Nickki and Holland, Jenna and Hembree, Jazzminn L and Smiley, David and Gelfanov, Vasily and Krishna, Radha and Arafat, Ayman M and Konkar, Anish and Belli, Sara and Kapps, Martin and Woods, Stephen C and Hofmann, Susanna M and D'Alessio, David and Pfluger, Paul T and Perez-Tilve, Diego and Seeley, Randy J and Konishi, Morichika and Itoh, Nobuyujki and Kharitonenkov, Alexei and Spranger, Joachim and DiMarchi, Richard D and Tschöp, Matthias H
Diabetes, ISSN 0012-1797, 05/2013, Volume 62, Issue 5, pp. 1453 - 1463
Glucagon, an essential regulator of glucose homeostasis, also modulates lipid metabolism and promotes weight loss, as reflected by the wasting observed in... 
PPAR-ALPHA | BODY-WEIGHT | METABOLISM | FIBROBLAST-GROWTH-FACTOR-21 | PHARMACOLOGY | INCREASES ENERGY-EXPENDITURE | ENDOCRINOLOGY & METABOLISM | DEGRADATION | MICE | INSULIN SENSITIVITY | FGF21 | Obesity - drug therapy | Humans | Peptides - pharmacokinetics | Fibroblast Growth Factors - genetics | Male | Fibroblast Growth Factors - secretion | Obesity - blood | Anti-Obesity Agents - therapeutic use | Glucagon - agonists | Fibroblast Growth Factors - metabolism | Anti-Obesity Agents - pharmacokinetics | Peptides - chemical synthesis | Hepatocytes - secretion | Hypoglycemic Agents - therapeutic use | Receptors, Glucagon - agonists | Receptors, Glucagon - genetics | Hypoglycemic Agents - pharmacokinetics | Peptides - physiology | Rats | Hypoglycemic Agents - pharmacology | Mice, Knockout | Cross-Over Studies | Anti-Obesity Agents - chemical synthesis | Mice | Anti-Obesity Agents - pharmacology | Hepatocytes - pathology | Diabetes Mellitus, Type 2 - metabolism | Hepatocytes - metabolism | Molecular Targeted Therapy | Mice, Mutant Strains | HEK293 Cells | Adult | Female | Hepatocytes - drug effects | Recombinant Proteins - metabolism | Double-Blind Method | Cells, Cultured | Insulin Resistance | Receptors, Glucagon - metabolism | Recombinant Proteins - agonists | Glucagon - pharmacology | Obesity - metabolism | Diabetes Mellitus, Type 2 - blood | Animals | Fibroblast Growth Factors - blood | Hypoglycemic Agents - chemical synthesis | Glucagon - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Peptides - therapeutic use | Physiological aspects | Fibroblast growth factors | Research | Glucagon | Analysis | Original Research
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8. Full Text Genomic characterization of brain metastases reveals branched evolution and potential therapeutic targets
by Brastianos, Priscilla K and Carter, Scott L and Santagata, Sandro and Cahill, Daniel P and Taylor-Weiner, Amaro and Jones, Robert T and Van Allen, Eliezer M and Lawrence, Michael S and Horowitz, Peleg M and Cibulskis, Kristian and Ligon, Keith L and Tabernero, Josep and Seoane, Joan and Martinez-Saez, Elena and Curry, William T and Dunn, Ian F and Paek, Sun Ha and Park, Sung-Hye and McKenna, Aaron and Chevalier, Aaron and Rosenberg, Mara and Barker, Frederick G and Gill, Corey M and Van Hummelen, Paul and Thorner, Aaron R and Johnson, Bruce E and Hoang, Mai P and Choueiri, Toni K and Signoretti, Sabina and Sougnez, Carrie and Rabin, Michael S and Lin, Nancy U and Winer, Eric P and Stemmer-Rachamimov, Anat and Meyerson, Matthew and Garraway, Levi and Gabriel, Stacey and Lander, Eric S and Beroukhim, Rameen and Batchelor, Tracy T and Baselga, Jose and Louis, David N and Getz, Gad and Hahn, William C
Cancer Discovery, ISSN 2159-8274, 11/2015, Volume 5, Issue 11, pp. 1164 - 1177
Brain metastases are associated with a dismal prognosis. Whether brain metastases harbor distinct genetic alterations beyond those observed in primary tumors... 
CELL LUNG-CANCER | GROWTH-FACTOR RECEPTOR | PTEN LOSS | DEPENDENT KINASE 4/6 | PI3K | ONCOLOGY | BREAST-CANCER METASTASIS | SINGLE METASTASES | MUTATIONS | ANTITUMOR-ACTIVITY | INHIBITOR | Neoplasms - metabolism | Genome-Wide Association Study | Lymph Nodes - pathology | Brain Neoplasms - diagnosis | Humans | Brain Neoplasms - genetics | Lymph Nodes - metabolism | Brain Neoplasms - drug therapy | Molecular Targeted Therapy | Disease Progression | Genetic Heterogeneity | Exome | Genetic Variation | Brain Neoplasms - secondary | Drug Resistance, Neoplasm - genetics | Neoplasms - genetics | Signal Transduction - drug effects | High-Throughput Nucleotide Sequencing | Mutation | Neoplasms - pathology | Cluster Analysis | evolutionary patterns | precision medicine | CDK inhibitors | PI3K inhibitors | Genomics | brain metastases
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9. Full Text Chemical Hybridization of Glucagon and Thyroid Hormone Optimizes Therapeutic Impact for Metabolic Disease
by Finan, Brian and Clemmensen, Christoffer and Zhu, Zhimeng and Stemmer, Kerstin and Gauthier, Karine and Müller, Luisa and Müller, Timo D and De Angelis, Meri and Moreth, Kristin and Neff, Frauke and Perez-Tilve, Diego and Fischer, Katrin and Lutter, Dominik and Sánchez-Garrido, Miguel A and Liu, Fa and Liu, Peng and Tuckermann, Jan and Malehmir, Mohsen and Healy, Marc E and Weber, Christian and Weber, Achim and Heikenwalder, Mathias and Jastroch, Martin and Kleinert, Maximilian and Jall, Sigrid and Brandt, Sara and Flamant, Frédéric and Schramm, Karl-Werner and Biebermann, Heike and Döring, Yvonne and Habegger, Kirk M and Keuper, Michaela and Gelfanov, Vasily and Köhrle, Josef and Rozman, Jan and Fuchs, Helmut and Gailus-Durner, Valerie and Hrabě de Angelis, Martin and Hofmann, Susanna M and Yang, Bin and Tschöp, Matthias H and DiMarchi, Richard
Cell, ISSN 0092-8674, 10/2016, Volume 167, Issue 3, pp. 843 - 857.e14
Glucagon and thyroid hormone (T ) exhibit therapeutic potential for metabolic disease but also exhibit undesired effects. We achieved synergistic effects of... 
conjugate | co-agonist | thyroid hormone | polypharmacology | glucagon | dyslipidemia | NASH | obesity | BODY-WEIGHT | ACTIVATION | OBESITY | TRIIODOTHYRONINE | CHOLESTEROL | BIOCHEMISTRY & MOLECULAR BIOLOGY | ATHEROSCLEROSIS | RECEPTOR | GROWTH-FACTOR 21 | FGF21 | PROTECTS | CELL BIOLOGY | Triiodothyronine - adverse effects | Obesity - drug therapy | Body Weight - drug effects | Metabolic Diseases - drug therapy | Molecular Targeted Therapy | Hyperglycemia - drug therapy | Bone and Bones - drug effects | Drug Delivery Systems | Liver - drug effects | Triiodothyronine - drug effects | Glucagon - chemistry | Disease Models, Animal | Triiodothyronine - pharmacology | Atherosclerosis - drug therapy | Liver - metabolism | Cholesterol - metabolism | Glucagon - pharmacology | Triiodothyronine - chemistry | Non-alcoholic Fatty Liver Disease - drug therapy | Drug Synergism | Animals | Glucagon - therapeutic use | Mice | Diabetes Mellitus, Type 2 - drug therapy | Chemical Engineering - methods | Glucagon - adverse effects | Drug Combinations | Type 2 diabetes | Physiological aspects | Glucagon | Health aspects | Atherosclerosis | Life Sciences
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10. Full Text Incidence, risk factors, and outcomes of osteonecrosis of the jaw: Integrated analysis from three blinded active-controlled phase III trials in cancer patients with bone metastases
by Saad, F and Brown, J.E and Van Poznak, C and Ibrahim, T and Stemmer, S.M and Stopeck, A.T and Diel, I.J and Takahashi, S and Shore, N and Henry, D.H and Barrios, C.H and Facon, T and Senecal, F and Fizazi, K and Zhou, L and Daniels, A and Carrière, P and Dansey, R
Annals of Oncology, ISSN 0923-7534, 05/2012, Volume 23, Issue 5, pp. 1341 - 1347
Osteonecrosis of the jaw (ONJ) has been reported in patients receiving bisphosphonates for metastatic bone disease. ONJ incidence, risk factors, and outcomes... 
Zoledronic acid | Denosumab | Osteonecrosis of the jaw | Bone metastases | NECROSIS | osteonecrosis of the jaw | ONCOLOGY | MULTIPLE-MYELOMA PATIENTS | zoledronic acid | BISPHOSPHONATE-RELATED OSTEONECROSIS | bone metastases | IMPLEMENTATION | EXPERIENCE | ONJ | denosumab | PREVENTIVE MEASURES | Prognosis | Humans | Middle Aged | Bone Neoplasms - secondary | Bone Neoplasms - epidemiology | Male | Neoplasms - diagnosis | Incidence | Clinical Trials, Phase III as Topic - statistics & numerical data | Diphosphonates - therapeutic use | Female | Imidazoles - therapeutic use | Diphosphonates - adverse effects | Data Interpretation, Statistical | Randomized Controlled Trials as Topic - statistics & numerical data | Bone Neoplasms - diagnosis | Bone Density Conservation Agents - adverse effects | Double-Blind Method | Imidazoles - adverse effects | Risk Factors | Bone Density Conservation Agents - therapeutic use | Bisphosphonate-Associated Osteonecrosis of the Jaw - epidemiology | Neoplasms - drug therapy | Algorithms | Bisphosphonate-Associated Osteonecrosis of the Jaw - diagnosis | Bisphosphonate-Associated Osteonecrosis of the Jaw - etiology | Neoplasms - pathology | Neoplasms - epidemiology
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11. Full Text Efficacy and safety of olaparib monotherapy in germline BRCA1 / 2 mutation carriers with advanced ovarian cancer and three or more lines of prior therapy
by Domchek, Susan M and Aghajanian, Carol and Shapira-Frommer, Ronnie and Schmutzler, Rita K and Audeh, M. William and Friedlander, Michael and Balmaña, Judith and Mitchell, Gillian and Fried, Georgeta and Stemmer, Salomon M and Hubert, Ayala and Rosengarten, Ora and Loman, Niklas and Robertson, Jane D and Mann, Helen and Kaufman, Bella and Onkologi och Patologi, MV and Oncology and Pathology, Kamprad Lab and Lund University and Oncology and Pathology, MV and Lunds universitet and Onkologi och Patologi, Kampradlab
Gynecologic Oncology, ISSN 0090-8258, 2016, Volume 140, Issue 2, pp. 199 - 203
Abstract Objective The efficacy and safety of olaparib, an oral poly(ADP-ribose) polymerase (PARP) inhibitor, was investigated in a subgroup of patients with... 
Hematology, Oncology and Palliative Medicine | Obstetrics and Gynecology | Olaparib | Phase II | BRCA1/2 mutation | Ovarian cancer | PEGYLATED LIPOSOMAL DOXORUBICIN | POLY(ADP-RIBOSE) POLYMERASE | MULTICENTER | OPEN-LABEL | PHASE-2 | PLUS CARBOPLATIN | OBSTETRICS & GYNECOLOGY | TRIAL | ONCOLOGY | PLATINUM-BASED CHEMOTHERAPY | BRCAI/2 mutation | CARCINOMA | Prospective Studies | Humans | Middle Aged | Drug Resistance, Neoplasm | Antineoplastic Agents - therapeutic use | Piperazines - therapeutic use | Piperazines - adverse effects | Organoplatinum Compounds - pharmacology | Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use | Ovarian Neoplasms - genetics | Phthalazines - therapeutic use | Genes, BRCA2 | Germ-Line Mutation | Female | Aged | Genes, BRCA1 | Ovarian Neoplasms - drug therapy | Phthalazines - adverse effects | Chemotherapy | Genetic aspects | Cancer | 2 mutation | BRCA1 | ovarian cancer | olaparib | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Cancer and Oncology | Medicin och hälsovetenskap | Cancer och onkologi
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