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Cellular signal transduction. --- Tumor suppressor proteins --- Cancer --- Research. --- Treatment --- Technological innovations. --- Chemotherapy.
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Antioncogenes. --- Tumor suppressor proteins. --- Antioncoproteins --- Growth suppressor proteins --- Metastasis suppressor proteins --- Proteins --- Antioncogenes --- Anti-oncogenes --- Cancer suppressor genes --- Emerogenes --- Tumor suppressing genes --- Tumor suppressor genes --- Cancer genes --- Tumor suppressor proteins
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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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Tumor suppressor genes (TSGs) and their signaling networks are fast growing areas in current biomedical science. These groups of genes, which are not limited to tumor suppression, play critical roles in many cellular activities. This book, "Future Aspects of Tumor Suppressor Genes", contains some fascinating fields, from basic to translational researches, in recent TSG studies. For example, several TSG signaling pathways are addressed in this book, and both mouse and Drosophila models used for the exploration of these genes are described based on the experimental evidence. A detailed review for current knowledge of microRNA studies in the regulation of tumor growth is introduced. Additionally, how natural compounds interfere with the progression of cancer development via TSG pathways is systemically summarized. Recent progresses in cell reprogramming and stemness transition processes regulated by TSG pathways are also included in this book.
Antioncogenes. --- Anti-oncogenes --- Cancer suppressor genes --- Emerogenes --- Tumor suppressing genes --- Tumor suppressor genes --- Cancer genes --- Tumor suppressor proteins --- Molecular biology
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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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With over 60,000 referenced publications, p53 has emerged as one of the most important factors in human cancer. Research on p53 has led to a complete overhaul of our understanding of the molecular basis of human cancer. In recent years, these major advances in knowledge are starting to impact on cancer management and therapy. This book thus captures a critical turning point in p53 research, from basic to translational research and clinical application. p53 in the Clinics follows the success of 25 Years of p53 Research and condensates in a series of authoritative chapters the considerable progress on the applications of p53 into the clinics and the substantial advances on diseases caused by inheritance of p53 defects, on somatic p53 mutations as biomarkers in molecular pathology, on progress in gene therapy and on developments of innovative drugs and clinical trials. This volume will appeal to a wide audience of students and professionals in basic and clinical cancer research and treatment, and will highlight the exciting “next steps” in p53 research and applications.
p53 antioncogene. --- p53 protein. --- Protein p53 --- Protein TP53 --- TP53 protein --- p53 gene --- p53 suppressor gene --- Medicine. --- Cancer research. --- Pharmacology. --- Biomedicine. --- Cancer Research. --- Pharmacology/Toxicology. --- DNA-binding proteins --- Phosphoproteins --- Tumor suppressor proteins --- Antioncogenes
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The underlying idea that cancer is a genetic disease at the cellular level was postulated over 75 years ago when Boveri hypothesised that the malignant cell was one that had obtained an abnormal chromatin content. However, it has been only the last decade where enormous strides have been made toward understanding neoplastic development. Explosive growth in the discipline of cancer genetics is so rapid that any attempt to review this subject becomes rapidly outdated and continuous revisions are warranted. Conclusive evidence has been reached associating specific chromosomal abnormalities to var
Antioncogenes. --- Cancer --- Oncogenes. --- Tumors --- Onc genes --- Cancer genes --- Proto-oncogenes --- Cancer genetics --- Anti-oncogenes --- Cancer suppressor genes --- Emerogenes --- Tumor suppressing genes --- Tumor suppressor genes --- Tumor suppressor proteins --- Genetic aspects.
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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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The initial identification of the Adenomatous polyposis coli (Apc) gene as the site of mutations in familial adenomatous polyposis (FA P) was described in 1992. A causal relationship between Apc mutations and intestinal tract tumours was confirmed three years later with the establishment of the Min mouse model. These mice are heterozygous for Apc and develop numerous intestinal tumours that mimic FA P. Subsequently, Apc has emerged as the most commonly mutated gene in colorectal cancer with reports varying between 50-80 per cent of sporadic tumours carrying such mutations. The search for how m
Adenomatous Polyposis Coli Protein. --- Adenomatous Polyposis Coli. --- Colon (Anatomy) -- Cancer. --- Colorectal Neoplasms -- Metabolism. --- Genes, APC. --- Tumor suppressor proteins. --- Colon (Anatomy) --- Tumor suppressor proteins --- Adenomatous Polyposis Coli --- Colorectal Neoplasms --- Genes, APC --- Metabolism --- Adenomatous Polyposis Coli Protein --- Intestinal Polyposis --- Intestinal Neoplasms --- Colonic Neoplasms --- Neoplastic Syndromes, Hereditary --- Colonic Diseases --- Metabolic Phenomena --- Cytoskeletal Proteins --- Genes, Tumor Suppressor --- Tumor Suppressor Proteins --- Rectal Diseases --- Adenomatous Polyps --- Proteins --- Neoplasm Proteins --- Intestinal Diseases --- Neoplasms --- Genes, Neoplasm --- Phenomena and Processes --- Gastrointestinal Neoplasms --- Genes, Recessive --- Adenoma --- Genetic Diseases, Inborn --- Gastrointestinal Diseases --- Digestive System Neoplasms --- Genes --- Diseases --- Neoplasms, Glandular and Epithelial --- Congenital, Hereditary, and Neonatal Diseases and Abnormalities --- Amino Acids, Peptides, and Proteins --- Chemicals and Drugs --- Digestive System Diseases --- Genome Components --- Neoplasms by Site --- Neoplasms by Histologic Type --- Genome --- Genetic Structures --- Genetic Phenomena --- Oncology --- Medicine --- Health & Biological Sciences --- Cancer --- Cancer. --- Antioncoproteins --- Growth suppressor proteins --- Metastasis suppressor proteins --- Colon cancer --- Colorectal cancer --- Medicine. --- Biomedicine. --- Biomedicine general. --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Antioncogenes --- Health Workforce --- Biomedicine, general.
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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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