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Abstract
DNA repair phenotype can be measured in blood and may be a potential biomarker of cancer risk. We conducted a systematic review and meta-analysis of epidemiological studies of DNA repair phenotype and cancer through March 2021. We used random-effects models to calculate pooled odds ratios (ORs) of cancer risk for those with the lowest DNA repair capacity compared with those with the highest capacity. We included 55 case–control studies that evaluated 12 different cancers using 10 different DNA repair assays. The pooled OR of cancer risk (all cancer types combined) was 2.92 (95% Confidence Interval (CI) 2.49, 3.43) for the lowest DNA repair. Lower DNA repair was associated with all studied cancer types, and pooled ORs (95% CI) ranged from 2.02 (1.43, 2.85) for skin cancer to 7.60 (3.26, 17.72) for liver cancer. All assays, except the homologous recombination repair assay, showed statistically significant associations with cancer. The effect size ranged from 1.90 (1.00, 3.60) for the etoposide-induced double-strand break assay to 5.06 (3.67, 6.99) for the γ-H2AX assay. The consistency and strength of the associations support the use of these phenotypic biomarkers; however large-scale prospective studies will be important for understanding their use related to age and screening initiation.
Highlights
DNA repair phenotype can be measured in blood and may be a potential biomarker of cancer risk
All studies used a case–control study design and most used blood collected at the time of cancer diagnosis; only two studies were nested case–control studies using blood collected before cancer diagnosis[8,9]
The first nested-case control study was by Sigurdson et al.[8] and used three DNA repair assays: comet assay, host cell reactivation assay and mutagen sensitivity assay in blood collected between 0.3 and 6 years before lung cancer[8]
Summary
DNA repair phenotype can be measured in blood and may be a potential biomarker of cancer risk. We conducted a systematic review and meta-analysis of epidemiological studies of DNA repair phenotype and cancer through March 2021. DNA repair capacity can be assessed either with genomic/proteomic approaches or with phenotypic approaches[5]. A concern with genomic/proteomic approaches is that mammalian DNA damage repair mechanisms are extraordinarily complex. In humans it involves ~ 450 genes in 13 different pathways including 7 core and 6 associated pathways, with over half the proteins interacting with other proteins from different pathways (Fig. 1)[6]; it follows that any specific genomic or proteomic methodology is unlikely to reflect overall DNA repair capacity. Phenotype biomarkers with the risk of cancer by conducting a meta-analysis from all epidemiological studies published through March 2021
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