TP53 mutations in human cancers: origins, consequences, and clinical use.

By Magali Olivier, M. Hollstein, Pierre Hainaut. Cold Spring Harbor Perspectives in Biology, 2010

2,062 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/d8b6301d21e2159255023ec34b02c859359b9e03

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Moshe Oren
2. Vladimir N Uversky
3. Varda Rotter

In Molecular Biology

1. Varda Rotter
2. Moshe Oren
3. Xun Zhang
4. Vladimir N Uversky
5. A. Klibanski
6. Yunli Zhou
7. A. Keith Dunker
8. Lukasz Kurgan

In Oncology

1. Varda Rotter
2. Moshe Oren
3. Vladimir N Uversky

Citations in the corpus

• Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, neutral): “[26] Olivier M, Hollstein M, Hainaut P.”
• MEG3 noncoding RNA: a tumor suppressor (2012, background): “MEG3 functionally interacts with tumor suppressor p53 The p53 (TP53) gene is mutated in most human cancers and has been subject to intensive investigation and review (see reviews Olivier et al. (2010) and Soussi (2011)).”
• Signatures of mutational processes in human cancer (2013, neutral): “Signature 1A/Bcontributesrelativelysimilarnumbersofmutationstomostcancer caseswhereasothersignaturescontributeoverwhelmingnumbersof mutationstosomecancersamplesbutveryfewtoothersofthesame cancerclass,forexample,signatures2,3,4,6,7,9,10,11,13(Fig.4).”
• Mutant p53 gain-of-function in cancer. (2010, background): “This does not necessarily imply that cancers with p53 mutations will be more refractory to therapy (see Olivier et al. 2010).”
• Genomic and Molecular Landscape of DNA Damage Repair Deficiency across The Cancer Genome Atlas (2018, neutral): “…mutations may promote these consequences through simple loss of function, as well as by altering transcription or through dominant-negative, gain-of-function mechanisms (Bouaoun et al., 2016; Kastenhuber and Lowe, 2017; Olivier et al., 2010; Pfister and Prives, 2017; Stracquadanio et al., 2016).”
• p53 Proteoforms and Intrinsic Disorder: An Illustration of the Protein Structure–Function Continuum Concept (2016, background): “Germline mutations were reported for more than 660 families, where they cause Li–Fraumeni syndrome (LFS) and Li–Fraumeni-like syndrome (LFL), which are a familial clustering of early onset tumors, such as adrenal cortical carcinomas, brain tumors, breast cancers, and sarcomas [232,233].”