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Detection of DNA damage in peripheral blood mononuclear cells from pancreatic cancer patients
Author(s) -
Jansen Rick J.,
FonsecaWilliams Sharon,
Bamlet William R.,
AyalaPeña Sylvette,
Oberg Ann L.,
Petersen Gloria M.,
TorresRamos Carlos A.
Publication year - 2015
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.22189
Subject(s) - dna damage , biology , peripheral blood mononuclear cell , mitochondrial dna , pancreatic cancer , confounding , diabetes mellitus , cancer , dna repair , medicine , adenocarcinoma , nuclear dna , oncology , gastroenterology , dna , immunology , cancer research , gene , genetics , endocrinology , in vitro
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. © 2014 Wiley Periodicals, Inc.