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Functional evidence obtained from somatic cell fusion studies indicated that a group of genes from normal cells might replace or correct a defective function of cancer cells. Tumorigenesis that could be initiated by two mutations was established by the analysis of hereditary retinoblastoma, which led to the eventual cloning of RB1 gene. The two-hit hypothesis helped isolate many tumor suppressor genes (TSG) since then. More recently, the roles of haploinsufficiency, epigenetic control, and gene dosage effects in some TSGs, such as P53, P16 and PTEN, have been studied extensively. It is now widely recognized that deregulation of growth control is one of the major hallmarks of cancer biological capabilities, and TSGs play critical roles in many cellular activities through signaling transduction networks. This book is an excellent review of current understanding of TSGs, and indicates that the accumulated TSG knowledge has opened a new frontier for cancer therapies.

Antioncogenes. --- Anti-oncogenes --- Cancer suppressor genes --- Emerogenes --- Tumor suppressing genes --- Tumor suppressor genes --- Cancer genes --- Tumor suppressor proteins --- Oncology

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The Second Edition of The Oncogene and Tumour Suppressor Gene FactsBook has been completely revised, updated, and expanded by 60%. The book contains more than 80 entries on oncogenes including JUN, MYC, and RAS, as well as DNA tumour viruses, tumour suppressor genes, including p53, retinoblastoma, BRCA1, BRCA2, VHL, F2FL, and essential material on angiogenesis and metastasis, apoptosis, cell cycle control, and gene therapy.Key Features* Includes much new data on this fast-moving field, including newly discovered oncogenes* Summarizes the clinical associatio

Oncogenes. --- Antioncogenes. --- Anti-oncogenes --- Cancer suppressor genes --- Emerogenes --- Tumor suppressing genes --- Tumor suppressor genes --- Onc genes --- Cancer genes --- Tumor suppressor proteins --- Proto-oncogenes --- Antioncogenes --- Oncogenes

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Pathological biochemistry --- Human medicine --- medische biochemie --- biomedische wetenschappen --- geneeskunde --- Tumor suppressor proteins. --- Tumor Suppressor Proteins. --- Antioncoproteins --- Growth suppressor proteins --- Metastasis suppressor proteins --- Proteins --- Antioncogenes --- Growth Suppressor Proteins --- Metastasis Suppressor Proteins --- Proteins, Growth Suppressor --- Proteins, Metastasis Suppressor --- Proteins, Tumor Suppressor --- Genes, Tumor Suppressor --- Tumors --- Carcinomes --- Malalties neoplàstiques --- Neoplàsies --- Neoplasmes --- Patologia --- Càncer --- Feocromocitoma --- Fibromes --- Marcadors tumorals --- Mesotelioma --- Miomes --- Pòlips (Patologia) --- Sarcoïdosi --- Teratoma --- Tumors de parts toves --- Tumors en els animals --- Classificació de tumors --- Oncologia --- Quistos

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This thesis presents the first report of the comprehensive and quantitative analysis of the effects of tumor-derived mutations on the tetrameric structure of tumor suppressor protein p53, which plays a central role in maintaining genomic integrity. Inactivation of p53 via mutation of its gene is a key step in tumorigenesis. Biophysical analyses revealed that the stability of the mutant peptides varied widely. Formation of a tetrameric structure is to be critical for protein–protein interactions, DNA binding, and the post-translational modification of p53. A small destabilization of the tetrameric structure therefore could result in dysfunction of tumor suppressor activity. This work suggests that the threshold for loss of tumor suppressor activity, in terms of the disruption of p53’s tetrameric structure, could be extremely low. Furthermore, functional control of p53 via tetramer formation was demonstrated, based on the structure–function analysis of mutant p53. The results disclosed that relatively small changes in tetramer formation, induced by the stabilization or inhibition of homo-tetramerization, could control p53 function.

Drugs -- Structure-activity relationships. --- Medicine. --- Proteomics. --- Tumor suppressor proteins. --- p53 antioncogene --- Tumor suppressor proteins --- Human Anatomy & Physiology --- Medicine --- Chemistry --- Health & Biological Sciences --- Physical Sciences & Mathematics --- Organic Chemistry --- Oncology --- Animal Biochemistry --- p53 antioncogene. --- Tumor suppresor proteins. --- p53 gene --- p53 suppressor gene --- Chemistry. --- Bioorganic chemistry. --- Medicinal chemistry. --- Bioorganic Chemistry. --- Medicinal Chemistry. --- Antioncogenes --- Biochemistry. --- Molecular biology --- Proteins --- Biological chemistry --- Chemical composition of organisms --- Organisms --- Physiological chemistry --- Biology --- Medical sciences --- Bio-organic chemistry --- Biological organic chemistry --- Biochemistry --- Chemistry, Organic --- Composition --- Chemistry, Medical and pharmaceutical --- Chemistry, Pharmaceutical --- Drug chemistry --- Drugs --- Medical chemistry --- Medicinal chemistry --- Pharmacochemistry

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Our understanding of human cancer in the past 40 years has been driven by linking innovative concepts and cutting edge technologies to key problems identified by clinical research. Some of the successes in cancer genetics identified from clinical work have been the identification of specific gene deletions in human chromosomes, the use of PCR-based cloning methodologies to identify and clone human cancer genes, the validation of the human cancer genes using transgenetic technologies in the mouse, and the ability to sequence whole genomes that has recently allowed a collation of all somatic and germline mutations in a human genome. In the same generation, entirely different disciplines involved in basic life science research have used model organisms like yeast, flies, worms, and cancer causing animal viruses as tools to develop windows to see into the machinery of the cell life cycle. The discoveries of pro-apoptotic genes, oncogenes, and covalent control mechanisms like phosphorylation and ubiquitination using the tools of science and technology have all been awarded Nobel prizes for their contribution to our understanding of how cells work. The discovery of p53 using the tumor causing animal virus SV40 falls into this pioneering period of biological and medical research.

Cell Transformation, Neoplastic -- genetics. --- Genes, p53. --- p53 antioncogene. --- p53 protein. --- p53 antioncogene --- p53 protein --- Neoplastic Processes --- Biology --- Genes, Tumor Suppressor --- Biological Science Disciplines --- Genes, Neoplasm --- Pathologic Processes --- Genes, Recessive --- Neoplasms --- Natural Science Disciplines --- Pathological Conditions, Signs and Symptoms --- Genes --- Diseases --- Genome Components --- Disciplines and Occupations --- Genome --- Genetic Structures --- Genetic Phenomena --- Phenomena and Processes --- Genetics --- Genes, p53 --- Cell Transformation, Neoplastic --- Medicine --- Health & Biological Sciences --- Oncology --- Protein p53 --- Protein TP53 --- TP53 protein --- p53 gene --- p53 suppressor gene --- Medicine. --- Cancer research. --- Biomedicine. --- Cancer Research. --- Cancer research --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- DNA-binding proteins --- Phosphoproteins --- Tumor suppressor proteins --- Antioncogenes --- Oncology. --- Tumors