Mutagen Sensitivity, Apoptosis, and Polymorphism in DNA Repair as Measures of Prostate Cancer Risk
Abstract
Prostate cancer is the most common lethal tumor among US males but etiology of the disease remains unknown. We hypothesize that low DNA repair contributes to increased risk of having prostate cancer. To evaluate the hypothesis, we conducted a case-control study of prostate cancer evaluating association of mutagen sensitivity phenotype with cancer risk. We established a repository of fully annotated specimen of 63 prostate cancer cases and 109 controls frequency matched on age and race. We created a sample repository consisting of serum, plasma, buffy coat, urine, toenail clipping and saliva. We also created a computerized database of the samples in Microsoft Access. We developed assays for mutagen sensitivity, comet assay, and apoptosis in white blood cells exposed to bleomycin and ionizing radiation to evaluate DNA repair capacity. We evaluated mutagen sensitivity in 95 subjects and determined that mean breaks in lymphocytes exposed to bleomycin are significantly higher (p<0.001) in prostate cancer cases (mean=1.1; SD=0.3) than controls (mean=0.7; SD=0.3).This pilot study fills important gaps in our understanding of prostate cancer etiology and produces new hypotheses which can be tested in an expanded prostate cancer study.
Document Details
- Document Type
- Technical Report
- Publication Date
- Feb 01, 2006
- Accession Number
- ADA471725
Entities
People
- Radoslav Goldman
Organizations
- Georgetown University