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Genes, tumor suppressor --- Tumor suppressor proteins

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Cancer --- Oncogenes --- Transcription factors --- Tumor proteins --- Drug Design --- Genes, Tumor Suppressor --- Neoplasms --- Oncogene Proteins --- Receptors, Cytoplasmic and Nuclear --- Transcription Factors --- Chemotherapy --- physiology --- drug therapy

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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

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Cancer cells --- Growth. --- Cells --- Pathology, Cellular --- Cancer cell growth --- Tumor Suppressor Proteins. --- Apoptosis. --- Apoptosis, Extrinsic Pathway --- Apoptosis, Intrinsic Pathway --- Caspase-Dependent Apoptosis --- Classic Apoptosis --- Classical Apoptosis --- Programmed Cell Death --- Programmed Cell Death, Type I --- Apoptoses, Extrinsic Pathway --- Apoptoses, Intrinsic Pathway --- Apoptosis, Caspase-Dependent --- Apoptosis, Classic --- Apoptosis, Classical --- Caspase Dependent Apoptosis --- Cell Death, Programmed --- Classic Apoptoses --- Extrinsic Pathway Apoptoses --- Extrinsic Pathway Apoptosis --- Intrinsic Pathway Apoptoses --- Intrinsic Pathway Apoptosis --- Necrosis --- Cell Death --- Clonal Deletion --- Superantigens --- Caspases --- Caspase 1 --- In Situ Nick-End Labeling --- Cellular Apoptosis Susceptibility Protein --- Genes, Transgenic, Suicide --- Growth Suppressor Proteins --- Metastasis Suppressor Proteins --- Proteins, Growth Suppressor --- Proteins, Metastasis Suppressor --- Proteins, Tumor Suppressor --- Genes, Tumor Suppressor --- Apoptosi

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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.