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The amplifier effect: how Pin1 empowers mutant p53
Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations....
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262197/ https://www.ncbi.nlm.nih.gov/pubmed/22017796 http://dx.doi.org/10.1186/bcr2941 |
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author | Hu, Hai Wulf, Gerburg M |
author_facet | Hu, Hai Wulf, Gerburg M |
author_sort | Hu, Hai |
collection | PubMed |
description | Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. |
format | Online Article Text |
id | pubmed-3262197 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-32621972012-04-13 The amplifier effect: how Pin1 empowers mutant p53 Hu, Hai Wulf, Gerburg M Breast Cancer Res Viewpoint Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. BioMed Central 2011 2011-10-13 /pmc/articles/PMC3262197/ /pubmed/22017796 http://dx.doi.org/10.1186/bcr2941 Text en Copyright ©2011 BioMed Central Ltd |
spellingShingle | Viewpoint Hu, Hai Wulf, Gerburg M The amplifier effect: how Pin1 empowers mutant p53 |
title | The amplifier effect: how Pin1 empowers mutant p53 |
title_full | The amplifier effect: how Pin1 empowers mutant p53 |
title_fullStr | The amplifier effect: how Pin1 empowers mutant p53 |
title_full_unstemmed | The amplifier effect: how Pin1 empowers mutant p53 |
title_short | The amplifier effect: how Pin1 empowers mutant p53 |
title_sort | amplifier effect: how pin1 empowers mutant p53 |
topic | Viewpoint |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262197/ https://www.ncbi.nlm.nih.gov/pubmed/22017796 http://dx.doi.org/10.1186/bcr2941 |
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