p53 and human cancer: the first ten thousand mutations.

By Pierre Hainaut, M. Hollstein. Advances in Cancer Research, 2000

1,035 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/55e2f508f8132397f0439dd106155dc7d23d7d6b

How researchers see this paper

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

In Biotechnology

1. D. Meek
2. Magali Olivier
3. Varda Rotter
4. R. Brosh
5. Pierre Hainaut
6. W. Gu
7. Moshe Oren
8. Scott W. Lowe

In Molecular Biology

1. Magali Olivier
2. Varda Rotter
3. Pierre Hainaut
4. W. Gu
5. M. Hollstein
6. D. Meek
7. Moshe Oren
8. R. Brosh

In Oncology

1. Magali Olivier
2. Varda Rotter
3. Pierre Hainaut
4. W. Gu
5. M. Hollstein
6. D. Meek
7. Moshe Oren
8. Peter J. Campbell

Citations in the corpus

• TP53 mutations in human cancers: functional selection and impact on cancer prognosis and outcomes (2007, background): “…to nucleotide substitutions at highly mutable CpG dinucleotides, at codons encoding residues that play essential structural and chemical roles in the contact between the p53 protein and specific DNA sequences that constitute the p53 response elements (p53-RE) (Hainaut and Hollstein, 2000).”
• Impact of mutant p53 functional properties on TP53 mutation patterns and tumor phenotype: lessons from recent developments in the IARC TP53 database (2007, background): “Somatic TP53 gene alterations are frequent in most human cancers [Hainaut and Hollstein, 2000], ranging from 5 to 80% depending on the type, stage, and etiology of tumors.”
• Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis. (2006, background): “More than 50% of sporadic tumors harbor somatic mutations of the p53 gene, and germline p53 mutations that confer a high familial risk of cancer are associated with Li-Fraumeni patients (Hussain and Harris, 1999; Hainaut and Hollstein, 2000 ).”
• Tumour suppression by p53: a role for the DNA damage response? (2009, background): “This barrier is disabled during the pathogenesis of most, if not all, human cancers, either through sporadic TP53 mutation”
• Mutations in the p53 Tumor Suppressor Gene: Important Milestones at the Various Steps of Tumorigenesis. (2011, background): “Unlike the majority of tumor suppressor genes, such as RB, APC, or BRCA1, which are usually inactivated during cancer progression by deletions or truncating mutations, the TP53 gene in human tumors is often found to undergo missense mutations, in which a single nucleotide is substituted by another.(”
• Mutational signatures associated with tobacco smoking in human cancer (2016, background): “Many human cancers have a somatic mutation in the TP53 gene and thus catalogues of TP53 mutations compiled two decades ago enabled early exploration of these signatures ( 10 ).”
• 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).”
• Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers (2002, background): “G to T transversions have been described as a molecular signature of tobacco smoke mutagens in smokingassociated lung cancers (Greenblatt et al., 1994; Hainaut and Hollstein, 2000).”
• Tumor suppressive functions of p53. (2009, background): “The DNA-binding domain of the p53 protein is a “hot spot” for mutation, as the majority of tumor-associated mutations in p53 occur within this region (Hainaut and Hollstein 2000).”
• The IARC TP53 database: New online mutation analysis and recommendations to users (2002, background): “Most TP53 mutations abrogate p53 transcriptional activity and result in the loss of its anti-proliferative properties [Hainaut and Hollstein, 2000].”