When mutants gain new powers: news from the mutant p53 field

By R. Brosh, Varda Rotter. Nature Reviews. Cancer, 2009

1,178 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/4669112296232f5d96415632bfd849d52c58d686

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Citations in the corpus

Mutant p53 gain-of-function in cancer. (2010, background): “…2005; Weisz et al. 2007a), Egr1 (Weisz et al. 2004), cyclin A, cyclin B1, cdk1, cdc25C (Di Agostino et al. 2006), calmodulin 2 (Knaup and Roemer 2004), hTERT (Scian et al. 2004a), stathmin (Singer et al. 2007), and Galectin-3 (Lavra et al. 2009) (see Brosh and Rotter 2009 for comprehensive review).”
Overexpressed of RAD51 suppresses recombination defects: a possible mechanism to reverse genomic instability (2010, background): “It is important to note that TP53 mutations are very heterogeneous (4,30), and only a few mutant versions, other than the TP53 homozygous deletion, have been tested for their effects on upregulating RAD51 expression.”
Mutant p53 drives invasion by promoting integrin recycling. (2009, background): “As described previously (Cantor et al., 2007), H1299 cells are tumorigenic in this model, with primary tumors arising after 30 days.”
Mutant p53 Disrupts Mammary Acinar Morphogenesis via the Mevalonate Pathway (2012, positive): “Transcriptional regulation by mutant p53 may occur in many cases through interactions with other sequence-specific transcription factors binding to their cognate sites (Brosh and Rotter, 2009).”
Driver mutations in TP53 are ubiquitous in high grade serous carcinoma of the ovary (2010, background): “What is particularly unusual about HGPSC is an almost total reliance on mutation TP53 itself for pathway inactivation, perhaps reflecting the requirement of certain tissues for neomorphic mutations for their transformation [1].”
The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer. (2010, background): “One possible explanation for their prevalence is that mutant p53 proteins can act dominantly, forming complexes with and inhibiting normal p53 or the related p63 and p73 proteins (Brosh and Rotter, 2009).”
Mutations in the p53 Tumor Suppressor Gene: Important Milestones at the Various Steps of Tumorigenesis. (2011, background): “This term refers to the acquisition of oncogenic properties by the mutant protein, compared with the mere inactivation of the protein.(18,19) Both the DN and GOF effects may play a significant role in the positive selection of missense mutations in TP53 during tumorigenesis.”
Mutant p53: one name, many proteins. (2012, background): “Just as wild-type p53 primarily functions as a transcription factor, mutant p53 proteins have been shown to transactivate myriad genes involved in many different aspects of tumorigenesis (Strano et al. 2007; Weisz et al. 2007b; Brosh and Rotter 2009).”