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Cited by 292

The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.

Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53

Open access
Sugrue, Mary M., Shin, Deug Y., Lee, Sam W., Aaronson, Stuart A.·1997·Proceedings of the National Academy of Sciences

Abstract

The p53 tumor suppressor gene has been shown to play an important role in determining cell fate. Overexpression of wild-type p53 in tumor cells has been shown to lead to growth arrest or apoptosis. Previous studies in fibroblasts have provided indirect evidence for a link between p53 and senescence. Here we show, using an inducible p53 expression system, that wild-type p53 overexpression in EJ bladder carcinoma cells, which have lost functional p53, triggers the rapid onset of G 1 and G 2 /M growth arrest associated with p21 up-regulation and repression of mitotic cyclins (cyclin A and B) and cdc2. Growth arrest in response to p53 induction became irreversible within 48-72 h, with cells exhibiting morphological features as well as specific biochemical and ultrastructural markers of the senescent phenotype. These findings provide direct evidence that p53 overexpression can activate the rapid onset of senescence in tumor cells.

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Metadata

Authors
Sugrue, M. M., Shin, D. Y., Lee, S. W., & Aaronson, S. A.
Venue
Proceedings of the National Academy of Sciences
Published
1997-09-02
Volume
94
Issue
18
Pages
9648-9653
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2058135827
Cited by
292
References
13
FWCI
11.86
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53. https://app.cochat.ai/papers/10.1073/pnas.94.18.9648
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Sugrue, M. M., Shin, D. Y., Lee, S. W., & Aaronson, S. A. (1997). Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.94.18.9648

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