Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype

In this issue, the Gabrielli laboratory and collaborators address the bulky CPD lesions created in DNA when UV joins two adjacent pyrimidines (thymine or cytosine), leading to skin cancers such as melanoma (Pavey S et al. (2019) Mol Oncol). Our understanding of postreplication repair mechanisms for...

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Detalles Bibliográficos
Autores principales: Brash, Douglas E., Seidman, Michael M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Commentary
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6944110/
https://www.ncbi.nlm.nih.gov/pubmed/31821728
http://dx.doi.org/10.1002/1878-0261.12612
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author Brash, Douglas E.
Seidman, Michael M.
author_facet Brash, Douglas E.
Seidman, Michael M.
author_sort Brash, Douglas E.
collection PubMed
description In this issue, the Gabrielli laboratory and collaborators address the bulky CPD lesions created in DNA when UV joins two adjacent pyrimidines (thymine or cytosine), leading to skin cancers such as melanoma (Pavey S et al. (2019) Mol Oncol). Our understanding of postreplication repair mechanisms for bulky lesions has lagged, and the newly reported predominance of translational control in the UV response has important implications. Image taken from https://www.flickr.com/photos/atul666/2059154608 by brx0, licensed under CC BY‐SA 2.0. https://doi.org/10.1002/1878-0261.12601 [Image: see text]
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spelling pubmed-69441102020-01-07 Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype Brash, Douglas E. Seidman, Michael M. Mol Oncol Commentary In this issue, the Gabrielli laboratory and collaborators address the bulky CPD lesions created in DNA when UV joins two adjacent pyrimidines (thymine or cytosine), leading to skin cancers such as melanoma (Pavey S et al. (2019) Mol Oncol). Our understanding of postreplication repair mechanisms for bulky lesions has lagged, and the newly reported predominance of translational control in the UV response has important implications. Image taken from https://www.flickr.com/photos/atul666/2059154608 by brx0, licensed under CC BY‐SA 2.0. https://doi.org/10.1002/1878-0261.12601 [Image: see text] John Wiley and Sons Inc. 2019-12-31 2020-01 /pmc/articles/PMC6944110/ /pubmed/31821728 http://dx.doi.org/10.1002/1878-0261.12612 Text en © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Commentary
Brash, Douglas E.
Seidman, Michael M.
Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype
title Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype
title_full Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype
title_fullStr Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype
title_full_unstemmed Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype
title_short Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype
title_sort defective postreplication repair of uv photoproducts in melanoma: a mutator phenotype
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6944110/
https://www.ncbi.nlm.nih.gov/pubmed/31821728
http://dx.doi.org/10.1002/1878-0261.12612
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