Rowlands · Annals of oncology : official journal of the European Society for Medical Oncology 2024 · meta-analysis of case-control studies · n=414341

Population-based germline breast cancer gene association studies and meta-analysis to inform wider mainstream testing.

Cited 39 times in the scientific literature.

Level 3 - non-randomized controlled study

Meta-analysis of population-based case-control studies

PubMed 38986768 · doi:10.1016/j.annonc.2024.07.244 · record verified 2026-08-26

What was done

Weighted meta-analysis was carried out for three population-based case-control studies (BRIDGES, CARRIERS, and UK Biobank) comprising 101,397 women with breast cancer and 312,944 women without breast cancer. The authors quantified pathogenic variant (PV) frequencies and disease associations across 37 putative breast cancer susceptibility genes in unselected, population-type breast cancer cases and subtypes.

What was found

Pathogenic variant frequencies in cases and pooled odds ratios (ORs) were: - BRCA1: OR 8.73 (95% CI 7.47-10.20), carrier frequency 1 in 101 - BRCA2: OR 5.68 (95% CI 5.13-6.30), carrier frequency 1 in 68 - PALB2: OR 4.30 (95% CI 3.68-5.03), carrier frequency 1 in 187 - CHEK2: OR 2.40 (95% CI 2.21-2.62), carrier frequency 1 in 73 (stronger in estrogen receptor-positive disease) - ATM: OR 2.16 (95% CI 1.93-2.41), carrier frequency 1 in 132 (stronger in estrogen receptor-positive disease) - RAD51C: OR 1.53 (95% CI 1.29-2.04), carrier frequency 1 in 913 - RAD51D: OR 1.76 (95% CI 1.29-2.41), carrier frequency 1 in 1079 - BARD1: OR 2.34 (95% CI 1.85-2.97), carrier frequency 1 in 672 (higher in triple-negative cases) Syndromic genes showed very low PV frequencies in cases: TP53 (1 in 1844; OR 3.62, 95% CI 1.98-6.61), STK11 (1 in 11,525; OR 1.60, 95% CI 0.48-5.30), CDH1 (1 in 2668), PTEN (1 in 3755), and NF1 (1 in 1470).

Why it matters

As germline genetic testing expands to unselected breast cancer patients in mainstream oncology clinics, these population-level metrics help define which genes provide sufficient diagnostic yield and clinical validity to include on routine testing panels.

Limits

The abstract does not report the racial or ancestral breakdown of the pooled cohorts, which are historically heavily European-predominant. Due to extremely low mutation rates, several syndromic genes (such as STK11) had wide confidence intervals crossing unity. Specific effect estimates were not provided in the abstract for all 37 evaluated genes.

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