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Cited by 287

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells.

Open access
Lowe, S W, Jacks, T, Housman, D E, Ruley, H E·1994·Proceedings of the National Academy of Sciences

Abstract

p53-deficient mouse embryonic fibroblasts were used to establish a direct mechanism of tumor suppression by p53 involving the destruction of oncogene-expressing cells by apoptosis. The absence of p53 enhanced cell growth, appeared sufficient for immortalization, and allowed a single oncogene [adenovirus early region 1A (E1A)] to transform cells to a tumorigenic state. p53 suppressed transformation of E1A-expressing cells by apoptosis. Apoptosis was associated with p53 stabilization and was triggered by environmental signals that normally suppress cell growth. Absence of even a single p53 allele significantly enhanced cell growth and survival. Although abrogation of apoptosis allowed transformation by E1A alone, escape from apoptosis susceptibility was not a prerequisite for tumor growth. Consequently, p53 mutation could enhance the survival of malignant cells expressing oncogenes activated early in tumor progression.

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Crossref · 10.1073/pnas.91.6.2026

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Metadata

Authors
Lowe, S. W., Jacks, T., Housman, D. E., & Ruley, H. E.
Venue
Proceedings of the National Academy of Sciences
Published
1994-03-15
Volume
91
Issue
6
Pages
2026-2030
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2005677707
Cited by
287
References
4
FWCI
12.52
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells. https://app.cochat.ai/papers/10.1073/pnas.91.6.2026
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Lowe, S. W., Jacks, T., Housman, D. E., & Ruley, H. E. (1994). Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.91.6.2026

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