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The current year (2004) marks the Silver Anniversary of the discovery of the p53 tumor suppressor. The emerging ?eld ?rst considered p53 as a viral antigen and then as an oncogene that cooperates with activated ras in transforming primary cells in culture. Fueling the concept of p53 acting as a transforming factor, p53 expression was markedly elevated in various transformed and tumorigenic cell lines when compared to normal cells. In a simple twist of fate, most of the studies conducted in those early years inadvertently relied on a point mutant of p53 that had been cloned from a normal mouse genomic library. A bona ?de wild-type p53 cDNA was subsequently isolated, ironically, from a mouse teratocarcinoma cell line. A decade after its discovery, p53 was shown to be a tumor suppressor that protects against cancer. It is now recognized that approximately half of all human tumors arise due to mutations within the p53 gene. As remarkable as this number may seem, it signi?cantly underrepresents how often the p53 pathway is targeted during tumorigenesis. It is my personal view, as well as many in the p53 ?eld, that the p53-signaling pathway is corrupted in nearly 100% of tumors. If you are interested in understanding cancer and how it develops, you must begin by studying p53 and its pathway. After demonstrating that p53 functions as a tumor suppressor the ?eld exploded and p53 became a major focus of scientists around the world.

p53 antioncogene. --- p53 protein. --- Protein p53 --- Protein TP53 --- TP53 protein --- DNA-binding proteins --- Phosphoproteins --- Tumor suppressor proteins --- p53 gene --- p53 suppressor gene --- Antioncogenes --- Oncology. --- Oncology  . --- Biochemistry. --- Cytology. --- Human genetics. --- Cancer Research. --- Biochemistry, general. --- Cell Biology. --- Medical Biochemistry. --- Human Genetics. --- Cell biology --- Cellular biology --- Biology --- Cells --- Cytologists --- Biological chemistry --- Chemical composition of organisms --- Organisms --- Physiological chemistry --- Chemistry --- Medical sciences --- Tumors --- Genetics --- Heredity, Human --- Human biology --- Physical anthropology --- Composition --- Cancer research. --- Cell biology. --- Medical biochemistry. --- Medical biochemistry --- Pathobiochemistry --- Pathological biochemistry --- Biochemistry --- Pathology --- Cancer research

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Since the discovery of p53 as a tumor suppressor, numerous methods have evolved to reveal its unique structural features and biochemical functions. In p53 Protocols, Sumitra and Swati Palit Deb have assembled an indispensable collection of novel techniques that have proven most useful for studying the physiological properties of p53 both in vitro and in vivo. Described by leading basic and clinical researchers who have successfully used the methods, the techniques provide proven solutions to problems in studying the purification, target identification, gene expression, quantitation, interaction, signaling, transactivation, and transrepression of p53. The methods are also useful for delineating the functions of other proteins that may act as tumor or growth suppressors. Each technique includes step-by-step instructions, troubleshooting notes, a theoretical review, and discussion of associated problems that might arise during the course of investigation. Special effort has been made to discuss problems and their solutions to help ease the learning curve when standardizing a new method. Diverse and highly practical, p53 Protocols offers both beginning and experienced researchers in cancer biology a gold-standard compendium of readily reproducible techniques for studying p53 and related proteins.

Protein p53 --- Tumor Suppressor Proteins --- Genes, p53 --- Neoplasms --- p53 protein --- p53 antioncogene --- Protéine p53 --- Gène p53 --- analysis --- therapeutic use --- physiology --- genetics --- Laboratory manuals --- Manuels de laboratoire --- Electronic books. -- local. --- p53 antioncogene -- Laboratory manuals. --- p53 protein -- Laboratory manuals. --- Tumor Suppressor Protein p53 --- Genetics --- Physiology --- Biological Science Disciplines --- Phosphoproteins --- DNA-Binding Proteins --- Biology --- Genes, Tumor Suppressor --- Nuclear Proteins --- Neoplasm Proteins --- Diseases --- Proteins --- Genes, Recessive --- Natural Science Disciplines --- Genes, Neoplasm --- Disciplines and Occupations --- Amino Acids, Peptides, and Proteins --- Genes --- Chemicals and Drugs --- Genome Components --- Genome --- Genetic Structures --- Genetic Phenomena --- Phenomena and Processes --- Animal Biochemistry --- Cytology --- Human Anatomy & Physiology --- Health & Biological Sciences --- Protéine p53 --- Gène p53 --- p53 gene --- p53 suppressor gene --- Antioncogenes --- Protein TP53 --- TP53 protein --- DNA-binding proteins --- Tumor suppressor proteins --- analysis. --- physiology. --- genetics. --- Cytology. --- Cell Biology. --- Cell biology --- Cellular biology --- Cells --- Cytologists

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Squamous cell cancer (SCC) development and recent preclinical and clinical advances for the effective prevention and treatment of the disease are covered in this book. Experts in the field describe here the cellular and molecular events in SCC development, recurrence, and metastasis, and provide an updated snapshot on our understanding of the heterogeneity of SCC pathogenesis with novel opportunities in precision therapeutics to achieve better clinical outcomes.

Medicine --- Oncology --- n/a --- oral cancer --- tobacco --- alcohol --- human papilloma virus --- targeted sequencing --- DNA copy number --- TP53 --- CDKN2A --- EGFR --- PIK3CA --- anal cancer --- radiation therapy --- chemoradiation --- de-escalation of therapy --- pain --- cathepsin S --- protease-activated receptor-2 --- PAR2 --- cancer pain --- oral squamous cell carcinoma --- differentiation --- terminal differentiation --- oral epithelium --- epithelial integrity --- epithelial transformation --- genetic alterations --- therapy response biomarkers --- cutaneous squamous cell carcinoma --- immunotherapy --- anti-PD1 --- biomarkers --- predictive medicine --- personalized medicine --- cancer --- immune system --- HNSCC --- farnesyl transferase --- tipifarnib --- combination regimen --- oropharynx --- neoplasm --- squamous cell carcinoma --- human papillomavirus --- therapeutic management --- treatment selection --- CSCC --- treatment --- advances --- biology --- immunocompromised --- immune checkpoint inhibition

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The number of males diagnosed with prostate cancer (PCa) is increasing all over the world. Most patients with early-stage PCa can be treated with appropriate therapy, such as radical prostatectomy or irradiation. On the other hand, androgen deprivation therapy (ADT) is the standard systemic therapy given to patients with advanced PCa. ADT induces temporary remission, but the majority of patients (approximately 60%) eventually progress to castration-resistant prostate cancer (CRPC), which is associated with a high mortality rate. Generally, well-differentiated PCa cells are androgen dependent, i.e., androgen receptor (AR) signalling regulates cell cycle and differentiation. The loss of AR signalling after ADT triggers androgen-independent outgrowth, generating poorly differentiated, uncontrollable PCa cells. Once PCa cells lose their sensitivity to ADT, effective therapies are limited. In the last few years, however, several new options for the treatment of CRPC have been approved, e.g., the CYP17 inhibitor, the AR antagonist, and the taxane. Despite this progress in the development of new drugs, there is a high medical need for optimizing the sequence and combination of approved drugs. Thus, the identification of predictive biomarkers may help in the context of personalized medicine to guide treatment decisions, improve clinical outcomes, and prevent unnecessary side effects. In this Special Issue Book, we focused on the cytobiology of human PCa cells and its clinical applications to develop a major step towards personalized medicine matched to the individual needs of patients with early-stage and advanced PCa and CRPC. We hope that this Special Issue Book attracts the attention of readers with expertise and interest in the cytobiology of PCa cells.

Medicine --- androgen receptor --- docetaxel --- cabazitaxel --- castration-resistant prostate cancer --- chemotherapy --- P-glycoprotein --- EPI-002 --- splice variant --- prostate-specific antigen --- androgen deprivation therapy --- time to PSA nadir --- fibroblasts --- prostate cancer --- androgen sensitivity --- pirfenidone --- TGFβ1 --- G1 cell cycle arrest --- fibroblast growth factor --- fibroblast growth factor receptor --- obesity --- inflammation --- immune cells --- cytokine --- high-fat diet --- KIFC1 --- docetaxel resistance --- apoptosis --- CW069 --- Caveolin-1 --- TP53-regulated inhibitor of apoptosis 1 --- tumour stroma --- tumour microenvironment --- fibroblast --- CAF --- resistance --- radiotherapy --- CCL2 --- CCL22 --- CCL5 --- migration --- LSD1 --- epigenetics --- autophagy --- abiraterone --- enzalutamide --- testosterone --- castration resistant prostate cancer --- animal model --- diet --- fat --- in vitro --- in vivo --- mouse --- AKR1C3 --- hormone-naïve prostate cancer --- immunohistochemistry --- tissue microarray --- androgen receptor dependency --- fibroblast-dependent androgen receptor activation

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Our common knowledge on oxidative stress has evolved substantially over the years and has been mostly focused on the fundamental chemical reactions and the most relevant chemical species involved in the human pathophysiology of oxidative stress-associated diseases. Thus, reactive oxygen species and reactive nitrogen species (ROS and RNS) were identified as the key players initiating, mediating, and regulating the cellular and biochemical complexity of oxidative stress either as physiological (acting pro-hormetic) or as pathogenic (causing destructive vicious circle) process. The papers published in this particular Special Issue of the Cells demonstrate the impressive pathophysiological relevance of ROS and RNS in a range of contexts, including the relevance of second messengers of free radicals like 4-hydroxynonenal, allowing us to assume that even more detailed mechanisms of their positive and negative effects lie in wait, and should assist in better monitoring of the major modern diseases and the development of advanced integrative biomedicine treatments.

toxicity --- toll-like receptors --- acrolein --- hydroxyapatite-based biomaterials --- LC-MS/MS --- blood–brain barrier --- NADPH-oxidase --- human neuroblastoma SH-SY5Y cells --- NRF2-NQO1 axis --- granulocytes --- free radicals --- antioxidant --- plaque vulnerability --- bEnd.3 --- relaxation --- Ca2+ --- keratinocytes --- oxidative metabolism of the cells --- lipid peroxidation --- intermittent hypoxia --- osteoblast growth --- UV radiation --- ROS --- bEnd5 --- cyclopurines --- NF?B --- glucose deprivation --- antimicrobial --- endothelial cells --- 4-hydroxynonenal (4-HNE) --- histamine --- glutamine deprivation --- optical coherence tomography --- antioxidants --- DNA damage --- glutathione --- NQO1 transcript variants --- xeroderma pigmentosum --- cancer cells --- VAS2870 --- reactive oxygen species (ROS) --- TP53 mutation --- DNA and RNA polymerases --- viability --- oxidative burst --- macrophages --- inflammation --- Nrf2 --- von Willebrand factor --- reactive oxygen species --- growth control --- intracellular signaling --- MFN2 --- nuclear factor erythroid 2–related factor 2 --- fusion/fission --- IMR-90 --- calcium --- proliferation --- mitochondria --- pathophysiology of oxidative stress --- redox balance --- 4-hydroxynonenal --- cannabidiol --- oxidative homeostasis --- rs1800566 --- neuronal cell death --- heme-oxygenase-1 --- vitamins --- cell signaling --- TRPM2 channel --- aorta --- cancer --- growth --- cancer regression --- oxidative stress --- nucleotide excision repair