Institution
Novartis
Company•Basel, Switzerland•
About: Novartis is a company organization based out in Basel, Switzerland. It is known for research contribution in the topics: Alkyl & Population. The organization has 41930 authors who have published 50566 publications receiving 1978996 citations. The organization is also known as: Novartis International AG.
Topics: Alkyl, Population, Alkoxy group, Tolerability, Receptor
Papers published on a yearly basis
Papers
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University of Melbourne1, Université libre de Bruxelles2, Katholieke Universiteit Leuven3, St. Vincent's Health System4, University of Victoria5, La Trobe University6, Royal Melbourne Hospital7, Netherlands Cancer Institute8, University of California, San Diego9, Vanderbilt University10, Peter MacCallum Cancer Centre11, University of Antwerp12, French Institute of Health and Medical Research13, University of Paris14, Medical University of Vienna15, Cornell University16, University of Texas MD Anderson Cancer Center17, Mayo Clinic18, Royal Brisbane and Women's Hospital19, University of Queensland20, Harvard University21, Novartis22, Indiana University – Purdue University Indianapolis23, Fred Hutchinson Cancer Research Center24, University of Milan25, University of Auvergne26, Kansai Medical University27, Yeshiva University28, Yonsei University29, Brown University30, Rhode Island Hospital31, Curie Institute32, Charité33, Yale University34, University of British Columbia35, Garvan Institute of Medical Research36, Université Paris-Saclay37, Autonomous University of Madrid38, University of Ottawa39, National Institutes of Health40, New York University41, University of Adelaide42, Stanford University43, Anschutz Medical Campus44, University of Padua45, European Organisation for Research and Treatment of Cancer46, Medical University of Graz47, Hoffmann-La Roche48, Genentech49, MedImmune50, Merck & Co.51, Memorial Sloan Kettering Cancer Center52
TL;DR: Standardization of TIL assessment will help clinicians, researchers and pathologists to conclusively evaluate the utility of this simple biomarker in the current era of immunotherapy.
Abstract: Assessment of the immune response to tumors is growing in importance as the prognostic implications of this response are increasingly recognized, and as immunotherapies are evaluated and implemented in different tumor types. However, many different approaches can be used to assess and describe the immune response, which limits efforts at implementation as a routine clinical biomarker. In part 1 of this review, we have proposed a standardized methodology to assess tumor-infiltrating lymphocytes (TILs) in solid tumors, based on the International Immuno-Oncology Biomarkers Working Group guidelines for invasive breast carcinoma. In part 2 of this review, we discuss the available evidence for the prognostic and predictive value of TILs in common solid tumors, including carcinomas of the lung, gastrointestinal tract, genitourinary system, gynecologic system, and head and neck, as well as primary brain tumors, mesothelioma and melanoma. The particularities and different emphases in TIL assessment in different tumor types are discussed. The standardized methodology we propose can be adapted to different tumor types and may be used as a standard against which other approaches can be compared. Standardization of TIL assessment will help clinicians, researchers and pathologists to conclusively evaluate the utility of this simple biomarker in the current era of immunotherapy.
477 citations
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TL;DR: The results reveal a new post‐translational regulation of SOD2 by means of acetylation and SIRT3‐dependent deacetylation in response to oxidative stress.
Abstract: Mitochondria manganese superoxide dismutase (SOD2) is an important antioxidant enzyme, deficiency of which is associated with various human diseases. The known primary regulation of SOD2 is through transcriptional activation. Here, we report that SOD2 is acetylated at Lys 68 and that this acetylation decreases SOD2 activity. Mitochondrial deacetylase SIRT3 binds to, deacetylates and activates SOD2. Increase of reactive oxygen species (ROS) levels stimulates SIRT3 transcription, leading to SOD2 deacetylation and activation. SOD2-mediated ROS reduction is synergistically increased by SIRT3 co-expression, but is cancelled by SIRT3 depletion. These results reveal a new post-translational regulation of SOD2 by means of acetylation and SIRT3-dependent deacetylation in response to oxidative stress.
476 citations
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TL;DR: Systematic literature review of all English-language studies evaluating the epidemiology and visual burden of pathologic myopia or myopic CNV found older age, subfoveal CNV location, and larger baseline lesion size were predictors of worse visual outcomes.
475 citations
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University of Texas MD Anderson Cancer Center1, Rabin Medical Center2, Sarah Cannon Research Institute3, Netherlands Cancer Institute4, Sheba Medical Center5, Duke University6, Harvard University7, University of Ulm8, Tom Baker Cancer Centre9, University of Padua10, Vanderbilt University11, Edinburgh Cancer Research Centre12, Novartis13, Texas Oncology14
TL;DR: Improved efficacy outcomes and manageable tolerability observed with first-line ribociclib plus letrozole monotherapy are maintained with longer follow-up, relative to letrozo monotherapy.
475 citations
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TL;DR: It is found that GluR6-deficient mice are less susceptible to systemic administration of kainate, as judged by onset of seizures and by the activation of immediate early genes in the hippocampus.
Abstract: L-glutamate, the neurotransmitter of the majority of excitatory synapses in the brain, acts on three classes of ionotropic receptors: NMDA (N-methyl-D-aspartate), AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) and kainate receptors. Little is known about the physiological role of kainate receptors because in many experimental situations it is not possible to distinguish them from AMPA receptors. Mice with disrupted kainate receptor genes enable the study of the specific role of kainate receptors in synaptic transmission as well as in the neurotoxic effects of kainate. We have now generated mutant mice lacking the kainate-receptor subunit GluR6. The hippocampal neurons in the CA3 region of these mutant mice are much less sensitive to kainate. In addition, a postsynaptic kainate current evoked in CA3 neurons by a train of stimulation of the mossy fibre system is absent in the mutant. We find that GluR6-deficient mice are less susceptible to systemic administration of kainate, as judged by onset of seizures and by the activation of immediate early genes in the hippocampus. Our results indicate that kainate receptors containing the GluR6 subunit are important in synaptic transmission as well as in the epileptogenic effects of kainate.
475 citations
Authors
Showing all 41972 results
Name | H-index | Papers | Citations |
---|---|---|---|
Irving L. Weissman | 201 | 1141 | 172504 |
Peter J. Barnes | 194 | 1530 | 166618 |
Paul G. Richardson | 183 | 1533 | 155912 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Jie Zhang | 178 | 4857 | 221720 |
Lei Jiang | 170 | 2244 | 135205 |
Marc A. Pfeffer | 166 | 765 | 133043 |
Jorge E. Cortes | 163 | 2784 | 124154 |
Ian A. Wilson | 158 | 971 | 98221 |
Peter G. Schultz | 156 | 893 | 89716 |
Bruce D. Walker | 155 | 779 | 86020 |
Timothy P. Hughes | 145 | 831 | 91357 |
Kurt Wüthrich | 143 | 739 | 103253 |
Leonard Guarente | 143 | 352 | 80169 |
Christopher D.M. Fletcher | 138 | 674 | 82484 |