Abstract
The p53 protein is the product of a tumor suppressor gene, whose inactivation is most probably involved in the development of many types of cancer (for recent reviews on p53 see 1–6). In most cases, tumor cells harbor point mutations in the p53 gene, resulting in the overproduction of mutant forms of the protein. Whereas the wild-type (wt) form of p53 can exhibit a variety of anti-proliferative and tumor-inhibitory activities, mutants of the types found in cancer cells are typically devoid of such activities. Hence, the principal outcome of such mutations is probably the inactivation of the tumor suppressor function of wt p53. In addition, at least certain mutations may also confer a distinct gain of function7, thereby possibly contributing a novel oncogenic activity to the affected cell.
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Gottlieb, E., Haffner, R., Yonish-Rouach, E., von Ruden, T., Wagner, E., Oren, M. (1994). Wild Type p53 Activity Contributes to Dependence on Hematopoietic Survival Factors. In: Mihich, E., Schimke, R.T. (eds) Apoptosis. Pezcoller Foundation Symposia, vol 5. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9217-1_3
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DOI: https://doi.org/10.1007/978-1-4757-9217-1_3
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