p53 polymorphisms: cancer implications
By C. Whibley, P. Pharoah, M. Hollstein. Nature Reviews. Cancer, 2009
688 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/a3f229c52ca9b2e66af5c4cbfa4004141a584ab2
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- Varda Rotter
- Magali Olivier
- M. Hollstein
- Pierre Hainaut
- Victor E. Velculescu
- Bert Vogelstein
- Kenneth W. Kinzler
- K. Strebhardt
In Oncology
- Varda Rotter
- Magali Olivier
- M. Hollstein
- Pierre Hainaut
- Bert Vogelstein
- Kenneth W. Kinzler
- K. Strebhardt
- R. Brosh
Citations in the corpus
- TP53 mutations in human cancers: origins, consequences, and clinical use. (2010, background): “Third, TP53 is highly polymorphic in coding and noncoding regions and some of these polymorphisms have been shown to increase cancer susceptibility and to modify cancer phenotypes in TP53 mutation carriers (Whibley et al. 2009).”
- TP53 Variations in Human Cancers: New Lessons from the IARC TP53 Database and Genomics Data (2016, background): “These variants are considered as neutral, although some of them have been shown to be associated with cancer susceptibility [Whibley et al., 2009, Sagne et al., 2013].”
- Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments (2023, background): “P53 is a pivotal factor to mediate cell apoptosis, and the existence of gene mutation of P53 is prevalent in most cancer cells [204].”
- Cancer-specific High-throughput Annotation of Somatic Mutations: computational prediction of driver missense mutations (2009, background): “apoptosis (32) P53 is a tumor suppressor and is compromised in almost”
- TSGene: a web resource for tumor suppressor genes (2012, background): “The prominent role of protein-coding TSGs in cancer pathogenesis is highlighted by the frequent somatic mutations on gene TP53 in various cancer types with that frequency ranging from 5% to 80% (4,5).”
- When mutants gain new powers: news from the mutant p53 field (2009, background): “Therefore, tumour TP53 status should not be considered a binary variable, but rather as multi-parameter data, consisting of the type of mutation, the level and subcellular localization of the mutant protein, as well as the status of TP53 LOH, codon 72 single nucleotide polymorphis”
- Multifaceted polo-like kinases: drug targets and antitargets for cancer therapy (2010, background): “Normal functioning of p53 maintains the stability of the genome and is a potent barrier to cancer developmen”