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ABSTRACT Testicular teratocarcinomas never contain _p53_ gene mutations even though these tumors express high levels of nuclear p53 protein. We have characterized two murine teratocarcinoma
cell lines and find no evidence that endogenous p53–regulated genes are correspondingly upregulated. Differentiation of these teratocarcinoma cells with retinoic acid results in a marked
decrease in p53 protein levels but is accompanied by a marked increase in p53–mediated transcriptional activity. Together these results support the hypothesis that the p53 protein in
undifferentiated teratocarcinoma cells is transcriptionally inactive and accounts for the lack of selection for _p53_ gene mutations in this tumor type. These teratocarcinoma cells undergo
p53–mediated apoptosis in response to DNA damage, which may explain the routine cures of human testicular tumors with combination chemotherapy. Access through your institution Buy or
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_TP53_: THE UNLUCKIEST OF GENES? Article Open access 23 October 2024 OF THE MANY CELLULAR RESPONSES ACTIVATED BY TP53, WHICH ONES ARE CRITICAL FOR TUMOUR SUPPRESSION? Article 08 April 2022
P53 REGULATES DIVERSE TISSUE-SPECIFIC OUTCOMES TO ENDOGENOUS DNA DAMAGE IN MICE Article Open access 21 March 2024 REFERENCES * Pottern, L. & Goedert, J. _Principles and Management of
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AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Molecular Biology, Princeton University, Princeton, New Jersey, 08540, USA Stuart G. Lutzker & Arnold J. Levine * The Cancer
Institute of New Jersey, Robert Wood Johnson Medical School, New Brunswick, New Jersey, 08901, USA Stuart G. Lutzker Authors * Stuart G. Lutzker View author publications You can also search
for this author inPubMed Google Scholar * Arnold J. Levine View author publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and
permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Lutzker, S., Levine, A. A functionally inactive p53 protein interatocarcinoma cells is activated by either DNA damage or cellular
differentiation. _Nat Med_ 2, 804–810 (1996). https://doi.org/10.1038/nm0796-804 Download citation * Received: 20 February 1996 * Accepted: 22 May 1996 * Published: 01 July 1996 * Issue
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