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
Descripción
Sumario: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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