Journal ArticleDOI
Gain of function mutations in p53.
Dirk P. Dittmer,Sibani Pati,Gerard P. Zambetti,Shelley Chu,Angelika K. Teresky,M Moore,Cathy A. Finlay,Arnold J. Levine +7 more
TLDR
These data demonstrate a gain of function associated with p53 mutations in addition to the loss of function shown previously to be associated with mutations in this tumour suppressor gene.Abstract:
We report that the expression of murine or human mutant p53 proteins in cells with no endogenous p53 proteins confers new or additional phenotypes upon these cells. Mutant p53 proteins expressed in cell lines lacking p53 resulted in either enhanced tumorigenic potential in nude mice ((10)3 cells) or enhanced plating efficiency in agar cell culture (human SAOS-2 cells). Also, mutant human p53 alleles, unlike the wild-type p53 protein, could also enhance the expression of a test gene regulated by the multi-drug resistance enhancer-promoter element. These data demonstrate a gain of function associated with p53 mutations in addition to the loss of function shown previously to be associated with mutations in this tumour suppressor gene.read more
Citations
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Journal ArticleDOI
p53, the Cellular Gatekeeper for Growth and Division
TL;DR: The author regrets the lack of citations for many important observations mentioned in the text, but their omission is made necessary by restrictions in the preparation of review manuscripts.
Journal ArticleDOI
p53: puzzle and paradigm.
Linda J. Ko,Carol Prives +1 more
TL;DR: Some of the key developments leading to the current state of knowledge in p53 research are presented and how they either shed light on or add to the complexities of p53 are discussed.
Journal ArticleDOI
Tumor spectrum analysis in p53-mutant mice.
Tyler Jacks,Lee Remington,Bart O. Williams,Earlene M. Schmitt,Shlomit Halachmi,Roderick T. Bronson,Robert A. Weinberg +6 more
TL;DR: It is reaffirm that p53 function is not required for normal mouse development and conclude that p 53 status can strongly influence tumor latency and tissue distribution.
Journal ArticleDOI
p53 mutations in cancer
TL;DR: Some of the emerging molecular mechanisms through which mutant p53 proteins can exert oncogenic functions, including invasion, metastasis, proliferation and cell survival, are highlighted.
Journal ArticleDOI
Clinical implications of the p53 tumor-suppressor gene
TL;DR: The p53 tumor-suppressor gene is the most striking example because it is mutated in about half of almost all types of cancer arising from a wide spectrum of tissues.
References
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Journal ArticleDOI
p53 mutations in human cancers
TL;DR: The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues as mentioned in this paper.
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The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53
TL;DR: It is demonstrated that the E6 proteins of the oncogenic HPVs that bind p53 stimulate the degradation of p53, which results in selective degradation of cellular proteins such as p53 with negative regulatory functions provides a novel mechanism of action for dominant-acting oncoproteins.
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The p53 tumour suppressor gene
TL;DR: The cell cycle is composed of a series of steps which can be negatively or postively regulated by various factors, chief among the negative regulators is the p53 protein, which can lead to cancer.
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The mdm-2 oncogene product forms a complex with the p53 protein and inhibits p53-mediated transactivation
TL;DR: A product of the mdm-2 oncogene forms a tight complex with the p53 protein, and the mDM-2oncogene can inhibit p53-mediated transactivation.
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Association of human papillomavirus types 16 and 18 E6 proteins with p53.
TL;DR: This study shows that the E6 protein of HPV-16 is capable of binding to the cellular p53 protein, providing further evidence that the human papillomaviruses, the adenovirus type 5, and SV40 may effect similar cellular pathways in transformation.