Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Pathology of the organs of movement --- Immunology. Immunopathology --- Neuropathology --- Myasthenia Gravis. --- 616.8 --- 577.27 --- Glass --- -Glass transition temperature --- -Polymers --- -Polymere --- Polymeride --- Polymers and polymerization --- Macromolecules --- Glass transformation temperature --- Glass transitions --- Materials --- Phase transformations (Statistical physics) --- Transition temperature --- Amorphous substances --- Ceramics --- Glazing --- Myasthenia Gravis, Generalized --- Myasthenia Gravis, Ocular --- Generalized Myasthenia Gravis --- Ocular Myasthenia Gravis --- Thymus Hyperplasia --- Myasthenic Syndromes, Congenital --- Neurologie. Neuropathologie. Zenuwstelsel. Neurologische aandoeningen --- Molecular bases of immunity. Molecular immunology --- Congresses --- Thermal properties --- 666.1 --- -Myasthenia gravis --- -Neuromuscular transmission --- Motoneuron transmission --- Motor neuron transmission --- Muscles --- Nerve endings --- Neural transmission --- Neuromuscular diseases --- Glass industry. Glass technology. Glass manufacture in general. Glass in the comprehensive sense --- Immunological aspects --- -Congresses --- -Neurologie. Neuropathologie. Zenuwstelsel. Neurologische aandoeningen --- -Glass industry. Glass technology. Glass manufacture in general. Glass in the comprehensive sense --- 577.27 Molecular bases of immunity. Molecular immunology --- 666.1 Glass industry. Glass technology. Glass manufacture in general. Glass in the comprehensive sense --- -666.1 Glass industry. Glass technology. Glass manufacture in general. Glass in the comprehensive sense --- Polymere --- -577.27 Molecular bases of immunity. Molecular immunology --- -Motoneuron transmission --- Anti-MuSK Myasthenia Gravis --- MuSK MG --- MuSK Myasthenia Gravis --- Muscle-Specific Receptor Tyrosine Kinase Myasthenia Gravis --- Muscle-Specific Tyrosine Kinase Antibody Positive Myasthenia Gravis --- Anti MuSK Myasthenia Gravis --- Muscle Specific Receptor Tyrosine Kinase Myasthenia Gravis --- Muscle Specific Tyrosine Kinase Antibody Positive Myasthenia Gravis --- Myasthenia Gravis, Anti-MuSK --- Myasthenia Gravis, MuSK --- Myasthenia Gravis

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

In the era of precision medicine, the use of molecularly targeted therapies in selected patients has led to a paradigm change in cancer treatment. Multiple studies have demonstrated the benefits of therapies that are chosen based on the molecular profile of the tumor and also from the liquid biopsy. With genomics' increasing ability, a routine transcriptomics analysis of advanced/metastatic cancers is now feasible in most cancer hospitals, including community cancer centers. This is an unprecedented shift in the management of cancers irrespective of their organ types, which not only improved the outcome but also opened several new avenues in research and practice, such as immune-check-point inhibitors, tumor-TME co-evolution in the development of resistance, longitudinal liquid biopsies, biomarkers screening and the management of electronic medical records.This book brings together these crucial areas of investigation. The research presented here attempts to address the current issues to provoke thoughts for the future. The future of precision medicine will have to embrace a shift from in vitro, in vivo/PDX models for the mechanistic study to a more functional test based on the scientific interrogation of genomic data, in the form of functional precision medicine. We will also have to combat the element of noise in the multitudes of data and impart the regulatory structure to make judicious use of the data. The expectations for functional precision medicine are high. We aspire to witness a tremendous improvement in patient outcomes, from better to best, down the road that will match the clinical guidelines.

pediatric tumors --- tumor mutational burden --- TMB --- whole-exome sequencing --- gene panel sequencing --- immune checkpoint inhibitors --- glioblastoma prognosis --- overall survival --- extent of resection --- random forest --- Decision tree --- personalized precision oncology --- circulating free DNA --- liquid biopsy --- epidermal growth factor receptor --- tyrosine kinase inhibitor --- osimertinib --- comprehensive genomic profiling --- molecular genotyping --- intratumor heterogeneity --- multiple biopsies --- tumor evolution --- clonality classification --- strategic therapeutic intervention --- thymoma --- driver mutation --- sequencing --- molecular barcoding --- EGFR mutation --- EGFR-TKI --- cfDNA --- NGS --- digital enrichment --- next-generation sequencing --- solid cancer --- universal health-care system --- precision medicine --- presumed germline findings --- clinical guideline --- non-small cell lung cancer --- outcome --- adjuvant chemotherapy --- anaplastic lymphoma receptor tyrosine kinase --- HNSCC --- ctDNA --- tDNA --- DDR genes --- PARP inhibitors --- new drug development --- next-generation sequencing (NGS) --- open data --- regulatory reform --- tumor profiling test --- triple-negative breast cancer (TNBC) --- breast cancer --- targeted therapy --- TNBC subtypes --- immunotherapy --- cancer --- screening --- smoking --- electronic records --- PD-L1 --- cancer-associated fibroblasts --- resistance --- chemotherapy --- CTC --- immunocytochemistry --- parallel double-detection --- laboratory-friendly --- n/a

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Cellular Responses to Stress brings together a group of scientists who work on different but interrelated aspects of cellular stress responses. The book provides state-of-the-art information on the wide spectrum of ways in which cells can respond to different forms of stress induced by chemicals, oxidants, and DNA-damaging agents. Mechanisms are described that involve altered uptake and efflux of chemical agents, intracellular detoxification, and DNA damage responses. Many of these changes trigger a cascade of reactions mediated by stress-activated signaling pathways, which have the capacity to determine whether a cell will survive or die. The spectrum of topics covered in this book aims to provide a broad overview of our current knowledge of the different forms of adaptive response systems.It is hoped that this text will stimulate further research to establish the relative cellular role of specific response pathways and will enable us to gain a deeper understanding of the mechanisms that allow cells to live or die. This book will be valued by university researchers at all levels, industrial scientists in the pharmaceutical and biotechnology industries, and clinical researchers.Originally published in 1999.The Princeton Legacy Library uses the latest print-on-demand technology to again make available previously out-of-print books from the distinguished backlist of Princeton University Press. These editions preserve the original texts of these important books while presenting them in durable paperback and hardcover editions. The goal of the Princeton Legacy Library is to vastly increase access to the rich scholarly heritage found in the thousands of books published by Princeton University Press since its founding in 1905.

Stress (Physiology) --- Cell metabolism --- Cellular control mechanisms --- Cells --- Metabolism --- Regulation --- AMPK. --- ASK1. --- Actin. --- Activation. --- Angiogenesis. --- Antibody. --- Antigen. --- Apoptosis. --- Autoimmunity. --- Autophosphorylation. --- C-Fos. --- C-Jun N-terminal kinases. --- C-terminus. --- Cell Cycle Arrest. --- Cell Line, Transformed. --- Cell cycle. --- Cell membrane. --- Cell migration. --- Cell surface receptor. --- Cellular differentiation. --- Cellular stress response. --- Conformational change. --- Cytochrome P450. --- Cytokine receptor. --- Cytokine. --- Cytotoxicity. --- DNA-PKcs. --- Drug metabolism. --- Ectopic expression. --- Effector (biology). --- Endonuclease. --- Enzyme. --- Epidermal growth factor receptor. --- Epidermal growth factor. --- Extracellular signal–regulated kinases. --- Fibroblast growth factor. --- Gene expression. --- Gene therapy. --- Gene. --- Germinal center. --- Glutathione S-transferase. --- HMG-CoA reductase. --- Heat shock. --- Histidine kinase. --- Hormone-sensitive lipase. --- Hsp27. --- Immortalised cell line. --- Immunodeficiency. --- Immunoglobulins. --- Immunoprecipitation. --- In vitro. --- Inducer. --- Inflammation. --- Jurkat cells. --- Kinase. --- Lymphotoxin. --- Macrophage colony-stimulating factor. --- Mechanism of action. --- Mechanistic target of rapamycin. --- Metabolism. --- Mitogen-activated protein kinase kinase. --- Mitogen-activated protein kinase. --- Mitogen. --- Mitosis. --- Model organism. --- Neuropeptide. --- Neurotoxin. --- Osmotic shock. --- Oxidative phosphorylation. --- Oxidative stress. --- P38 mitogen-activated protein kinases. --- Pathogenesis. --- Peptide. --- Peroxidase. --- Phosphatase. --- Phosphoinositide 3-kinase. --- Phosphorylation cascade. --- Phosphorylation. --- Post-translational modification. --- Protease. --- Protein kinase. --- Protein phosphorylation. --- Protein synthesis inhibitor. --- Protein. --- Proteolysis. --- RNA interference. --- Receptor (biochemistry). --- Receptor tyrosine kinase. --- Repressor. --- Response element. --- Signal transduction. --- Ternary Complex Factors. --- Thrombin. --- Transcription factor. --- Transcriptional regulation. --- Transfection. --- Transposable element. --- Tumor necrosis factor superfamily. --- Turgor pressure. --- Vascular endothelial growth factor.