Oncogenic mutations of the p53 tumor suppressor: the demons of the guardian of the genome.
By Alex Sigal, Varda Rotter. Cancer Research, 2000
777 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/3299ac969db6a3cabff32a236631ab5a1127c612
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Citations in the corpus
- Modeling the therapeutic efficacy of p53 restoration in tumors. (2006, background): “Iacopetta, 2006; Sigal and Rotter, 2000 ), we found no evidence for dominant-negative p53 mutations in Em-myc; p53KI/null lymphomas, perhaps reflecting the fact that in”
- Mutations in the p53 Tumor Suppressor Gene: Important Milestones at the Various Steps of Tumorigenesis. (2011, background): “It is well established that p53 inactivation and mutant p53 expression can grant cells with additive growth and survival advantages, such as increased proliferation, evasion of apoptosis, and chemoresistance.(16,18) In an effort to further study the mechanisms that underlie the role of mutant p53 at”
- Hallmarks of cancer: the next generation. (2011, unknown): “In addition, the accumulation of mutations can be accelerated by compromising the surveillance systems that normally monitor genomic integrity and force genetically damaged cells into either senescence or apoptosis (Jackson and Bartek, 2009; Kastan, 2008; Sigal and Rotter, 2000).”
- When mutants gain new powers: news from the mutant p53 field (2009, background): “Moreover, these mutations usually confer the mutant protein with a dominant-negative activity over the remaining wild-type allele, a mechanism that involves hetero-oligomerization of the mutant protein with the wild-type protei”
- Live or let die: the cell's response to p53 (2002, background): “In addition to the dominant-negative inactivation of wild-type p53, there is evidence that some of the tumour-associated mutant p53 proteins acquire new transforming functions that contribute to tumour developmen”
- Mutant p53 drives invasion by promoting integrin recycling. (2009, background): “However, there is also clear evidence that mutant p53 proteins acquire a transforming activity that is independent of wild-type p53 and so constitutes a gain of function (Sigal and Rotter, 2000).”
- Mutant p53: one name, many proteins. (2012, background): “Conformational (or class II) mutants, typified by p53-R175H, are those missense mutations that disrupt the structure of the p53 protein on either a local or global level (Sigal and Rotter 2000; Soussi and Lozano 2005).”
- p53 in health and disease (2007, background): “In addition, mutant forms of p53 acquire novel transcriptional activities that are also likely to contribute to the enhanced malignant potential of cells that express these protein”
- MuSiC: Identifying mutational significance in cancer genomes (2012, background): “MuSiC also helps us confirm the importance of mutations in the P53 DNA-binding domain (Sigal and Rotter 2000).”
- Mutant p53 gain-of-function in cancer. (2010, background): “In principle, emergence of a p53 mutation within a cell might have three, not mutually exclusive, types of outcome (Michalovitz et al. 1991; Sigal and Rotter 2000; Weisz et al. 2007b).”
- Awakening guardian angels: drugging the p53 pathway (2009, background): “These mutations usually confer the mutant protein with a dominant-negative activity over the remaining wild-type allele, a mechanism that involves hetero-oligomerization of the mutant protein with the wild-type protei”