التفاصيل البيبلوغرافية
| العنوان: |
Obesity increases genomic instability at DNA repeat-mediated endogenous mutation hotspots |
| المؤلفون: |
Pallavi Kompella, Guliang Wang, Russell E. Durrett, Yanhao Lai, Celeste Marin, Yuan Liu, Samy L. Habib, John DiGiovanni, Karen M. Vasquez |
| المصدر: |
Nature Communications, Vol 15, Iss 1, Pp 1-18 (2024) |
| بيانات النشر: |
Nature Portfolio, 2024. |
| سنة النشر: |
2024 |
| المجموعة: |
LCC:Science |
| مصطلحات موضوعية: |
Science |
| الوصف: |
Abstract Obesity is associated with increased cancer risk, yet the underlying mechanisms remain elusive. Obesity-associated cancers involve disruptions in metabolic and cellular pathways, which can lead to genomic instability. Repetitive DNA sequences capable of adopting alternative DNA structures (e.g., H-DNA) stimulate mutations and are enriched at mutation hotspots in human cancer genomes. However, it is not known if obesity impacts DNA repeat-mediated endogenous mutation hotspots. We address this gap by measuring mutation frequencies in obese and normal-weight transgenic reporter mice carrying either a control human B-DNA- or an H-DNA-forming sequence (from a translocation hotspot in c-MYC in Burkitt lymphoma). Here, we discover that H-DNA-induced DNA damage and mutations are elevated in a tissue-specific manner, and DNA repair efficiency is reduced in obese mice compared to those on the control diet. These findings elucidate the impact of obesity on cancer-associated endogenous mutation hotspots, providing mechanistic insight into the link between obesity and cancer. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
2041-1723 |
| Relation: |
https://doaj.org/toc/2041-1723 |
| DOI: |
10.1038/s41467-024-50006-8 |
| URL الوصول: |
https://doaj.org/article/363ca44e435d4b4689a49fce09619af1 |
| رقم الانضمام: |
edsdoj.363ca44e435d4b4689a49fce09619af1 |
| قاعدة البيانات: |
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