p53 mutations in cancer

By P. Muller, Karen H. Vousden. Nature Cell Biology, 2013

1,660 citations recorded by the source corpus.

In the past fifteen years, it has become apparent that tumour-associated p53 mutations can provoke activities that are different to those resulting from simply loss of wild-type tumour-suppressing p53 function. Many of these mutant p53 proteins acquire oncogenic properties that enable them to promote invasion, metastasis, proliferation and cell survival. Here we highlight some of the emerging molecular mechanisms through which mutant p53 proteins can exert these oncogenic functions.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/3f75caca2b1ae32d8535be2402af43294695af44

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

1. P. Muller
2. M. Guo
3. Haolan Wang
4. Yongheng Chen
5. Hudie Wei
6. T. Soussi
7. Ming Tan
8. John N. Weinstein

In Oncology

1. P. Muller
2. Ming Tan
3. Jianrong Lu
4. Qingsong Cai
5. M. Guo
6. Haolan Wang
7. Yongheng Chen
8. Hudie Wei

Citations in the corpus

• The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism (2014, background): “Tumor-derived mutant p53 can drive tumor survival, invasion, and metastasis [77].”
• Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “73,74 In the exogenous apoptotic pathway, p53 induces the expression of the death receptors Fas/Fas ligand and KILLER/DR5 located on the cell membrane, which activates caspase 8 and leads to apoptosis.”
• Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas (2019, background): “While cell culture studies indicate the mutant p53 protein can behave in a dominant negative fashion to inactivate wildtype p53 protein (Muller and Vousden, 2013)(Giacomelli et al.”
• Mutant p53 in Cancer: New Functions and Therapeutic Opportunities (2014, background): “…T24 endogenous Zhu et al., 2013 R175Hd H1299 stable/transient Fontemaggi et al., 2009 Y220S fibroblasts stable/transient Capponcelli et al., 2005 Cell Survival V157F Hs578T endogenous Braicu et al., 2013 C194T T47D endogenous Lim et al., 2009 P223L/V274F DU-145 endogenous Zhu et al., 2011”
• The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. (2017, neutral): “While wild-type TP53 is normally a rapidly degraded protein, mutant forms of TP53 are stabilized and accumulate to high levels in tumor cells (Muller and Vousden, 2013).”
• Exosomes in Cancer Development, Metastasis and Drug Resistance: A Comprehensive Review (2013, neutral): “Its critical role in normal cell physiology is highlighted by the fact that in >50 % of tumors, p53 is found either mutated or lost [86].”
• Combination therapy in combating cancer (2017, background): “However, if tumour suppressor genes are mutated, accumulation of damaged DNA and inhibition of cell cycle arrest contribute to increasingly rapid proliferation rates and a more aggressive cancer [185].”