Recurrent Noncoding Mutations in Skin Cancers: UV Damage Susceptibility or Repair Inhibition as Primary Driver?

BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology
Steven A RobertsJohn J Wyrick

Abstract

Somatic mutations arising in human skin cancers are heterogeneously distributed across the genome, meaning that certain genomic regions (e.g., heterochromatin or transcription factor binding sites) have much higher mutation densities than others. Regional variations in mutation rates are typically not a consequence of selection, as the vast majority of somatic mutations in skin cancers are passenger mutations that do not promote cell growth or transformation. Instead, variations in DNA repair activity, due to chromatin organization and transcription factor binding, have been proposed to be a primary driver of mutational heterogeneity in melanoma. However, as discussed in this review here, recent studies indicate that chromatin organization and transcription factor binding also significantly modulate the rate at which UV lesions form in DNA. The authors propose that local variations in lesion susceptibility may be an important driver of mutational hotspots in melanoma and other skin cancers, particularly at binding sites for ETS transcription factors.

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Citations

Nov 15, 2019·Proceedings of the National Academy of Sciences of the United States of America·Sanjay PremiDouglas E Brash
Mar 28, 2021·The Journal of Biological Chemistry·Yuchao JiangAziz Sancar
Sep 7, 2021·The EMBO Journal·Smitha SivapragasamJohn J Wyrick

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