Absence of p53 permits propagation of mutant cells following genotoxic damage
نویسندگان
چکیده
منابع مشابه
A new approach to identifying genotoxic carcinogens: p53 induction as an indicator of genotoxic damage.
The tumor suppressor gene p53 encodes a nuclear phosphoprotein which is critical for cell cycle control and prevention of uncontrolled cell proliferation that can lead to cancer. Previous studies have shown that cells respond to DNA damage by increasing their levels of p53, which then acts to prevent replication of damaged DNA. This study examined the effects on p53 protein levels of several di...
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We have previously shown that p53 mutations are associated with cisplatin resistance in ovarian carcinoma IGROV-1/Pt 1 cells. The relationship between p53 status and the development of resistance has not been completely elucidated; in particular, the biological mechanisms behind the acquired drug-resistant p53-mutant phenotype were not clearly explained. Thus, in this study, we investigated whe...
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چکیده هدف اصلی از طراحی لرزه ای تامین ایمنی جانی در هنگام وقوع زلزله و تعمیر پذیر بودن سازه خسارت دیده، پس از وقوع زلزله است. تجربه زلزله های اخیر نشان داده است که ساختمان های طراحی شده با آیین نامه های مبتنی بر نیرو از نظر محدود نمودن خسارت وارده بر سازه دقت لازم را ندارند. این امر سبب پیدایش نسل جدید آیین نامه های مبتنی بر عملکرد شده است. در این آیین نامه ها بر اساس تغییرشکل های غیرارتجاعی ...
15 صفحه اولPolyploid giant cells provide a survival mechanism for p53 mutant cells after DNA damage.
The relationships between delayed apoptosis, polyploid 'giant' cells and reproductive survivors were studied in p53-mutated lymphoma cells after DNA damage. Following severe genotoxic insult with irradiation or chemotherapy, cells arrest at the G(2)-M cell cycle check-point for up to 5 days before undergoing a few rounds of aberrant mitoses. The cells then enter endoreduplication cycles resulti...
متن کاملDNA damage-specific control of cell death by cryptochrome in p53-mutant ras-transformed cells.
The main feedback loop driving circadian rhythm in mice is controlled, in part, by the genes encoding the cryptochromes Cry1 and Cry2. Targeted mutation of both Cry1 and Cry2 delay the early onset of tumor formation in p53-null mutant mice. Furthermore, Ras-transformed p53- and Cry-null mouse skin fibroblasts are more sensitive than p53 mutants to apoptotic cell death initiated by agents that a...
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ژورنال
عنوان ژورنال: Oncogene
سال: 1997
ISSN: 0950-9232,1476-5594
DOI: 10.1038/sj.onc.1200871