TY - BOOK ID - 206977 TI - The p53 tumor suppressor pathway and cancer PY - 2005 SN - 1280945052 9786610945054 0387301275 0387241353 1489998799 PB - New York, NY : Springer, DB - UniCat KW - p53 antioncogene. KW - p53 protein. KW - Protein p53 KW - Protein TP53 KW - TP53 protein KW - DNA-binding proteins KW - Phosphoproteins KW - Tumor suppressor proteins KW - p53 gene KW - p53 suppressor gene KW - Antioncogenes KW - Oncology. KW - Oncology  . KW - Biochemistry. KW - Cytology. KW - Human genetics. KW - Cancer Research. KW - Biochemistry, general. KW - Cell Biology. KW - Medical Biochemistry. KW - Human Genetics. KW - Cell biology KW - Cellular biology KW - Biology KW - Cells KW - Cytologists KW - Biological chemistry KW - Chemical composition of organisms KW - Organisms KW - Physiological chemistry KW - Chemistry KW - Medical sciences KW - Tumors KW - Genetics KW - Heredity, Human KW - Human biology KW - Physical anthropology KW - Composition KW - Cancer research. KW - Cell biology. KW - Medical biochemistry. KW - Medical biochemistry KW - Pathobiochemistry KW - Pathological biochemistry KW - Biochemistry KW - Pathology KW - Cancer research UR - https://www.unicat.be/uniCat?func=search&query=sysid:206977 AB - 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. ER -