Redefining p53: Entering the Tumor Suppressor Era
نویسندگان
چکیده
منابع مشابه
Regulation of the p53 tumor suppressor protein.
Mutations in the p53 tumor suppressor gene occur in about 50% of all human tumors, making it the most frequent target for genetic alterations in cancer (for recent reviews on p53 see Refs. 1–5). Such mutations probably facilitate carcinogenesis primarily through abrogating the tumor suppressor activities of the wild type p53 protein, although at least some forms of tumor-associated mutant p53 p...
متن کاملThe p53 tumor suppressor protein: meeting review.
The p53 protein is finally swimming into focus. This became clear at the Sixth International p53 meeting, which was held in Israel in Tiberias on the shores of the Sea of Galilee in early November 1992. In recent years, the p53 protein has captured the imagination of a broad spectrum of biomedical researchers. Because of its potentially central role in human cancer, there is considerable impetu...
متن کاملTumor suppressor p53: regulation and function.
The p53 protein is a transcription factor involved in maintaining genomic integrity by controlling cell cycle progression and cell survival. Mutations in p53 are the most frequently seen genetic alterations in human cancer. The function of p53 is critical to the way many cancer treatments kill cells because radiotherapy and chemotherapy act in part by triggering programmed cell death in respons...
متن کاملP53 is a tumor suppressor gene
Arnold J. Levine, 1. Cathy A. Finlay, 2 and Philip W. Hinds 3 1Institute for Advanced Study Einstein Drive Princeton, New Jersey 08540 and Cancer Institute of New Jersey 195 Little Albany St. New Brunswick, New Jersey 08903 2 Department of High Throughput Biology GlaxoSmithKline 5 Moore Drive Research Triangle Park, North Carolina 27709 3Harvard Medical School Department of Pathology Armenise 4...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Cell Cycle
سال: 2003
ISSN: 1538-4101,1551-4005
DOI: 10.4161/cc.2.1.288