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• W2043964688 abstract "Although it is well-established that p53 functions as a tumor suppressor gene, certain mutations exhibit gain-of-function activities that increase oncogenic transformation. We have found a common class of p53 missense mutation that exhibits a dominant, gain-of-function activity that generates genomic instability. Fibroblasts from Li–Fraumeni syndrome heterozygotes with such mutations generate polyploid cells when exposed to spindle depolymerizing agents. Expression of such mutant alleles in normal fibroblasts yields the same phenotype. This class of dominant, gain-of-function p53 mutation (p53 RSC , relaxed spindle checkpoint allele) does not require the transcriptional activation function of p53 for this behavior. Thus p53 mutations can contribute to progression of a cancer cell not only by absence of p53 tumor suppressor activity but also by the presence of an activity that promotes genetic instability." @default.
• W2043964688 created "2016-06-24" @default.
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• W2043964688 date "1998-04-28" @default.
• W2043964688 modified "2023-10-16" @default.
• W2043964688 title "An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control" @default.
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• W2043964688 doi "https://doi.org/10.1073/pnas.95.9.5166" @default.
• W2043964688 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/20232" @default.
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• W2043964688 hasPublicationYear "1998" @default.
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