Abstract
DNA repair is a key mechanism in maintaining genomic stability: repair deficiencies increase DNA damage and mutations that lead to several diseases, including cancer. We extracted DNA from peripheral blood mononuclear cells (PBMCs) of 48 pancreatic adenocarcinoma cases and 48 healthy controls to determine relative levels of nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) damage by QPCR. All participants were never smokers and between the ages of 60 and 69. Average levels among cases were compared to controls using a rank sum test, and logistic regression adjusted for potential confounding factors (age, sex, and diabetes mellitus). Cases had less DNA damage, with a significant decrease in mtDNA damage (P-value=0.03) and a borderline significant decrease in nDNA damage (P=0.08). Across samples, we found mtDNA abundance was higher among non-diabetics compared to diabetics (P=0.04). Our results suggest that patients with pancreatic adenocarcinoma have less DNA damage in their PBMCs, and that having diabetes, a known pancreatic cancer risk factor, is associated with lower levels of mtDNA abundance.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1220-1226 |
| Number of pages | 7 |
| Journal | Molecular Carcinogenesis |
| Volume | 54 |
| Issue number | 10 |
| DOIs | |
| State | Published - Oct 1 2015 |
| Externally published | Yes |
Bibliographical note
Publisher Copyright:© 2015 Wiley Periodicals, Inc.
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- DNA damage
- Pancreatic cancer
- QPCR
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