Takeaway
- Indoor radon exposure was associated with significantly higher tumor mutation burden (TMB) in patients with lung adenocarcinoma and no smoking history.
- The mutational signature was associated with defective DNA mismatch repair.
Why this matters
- Indoor radon exposure or residential radon is the second most common cause of lung cancer.
Study design
- 41 patients with lung adenocarcinoma with no smoking history who lived in the same home for ≥2 years before diagnosis.
- Funding: Korean Ministry of Environment; National Research Foundation.
Key results
- Mean TMB/megabase was significantly higher in patients with high exposure to radon (>48 Bq/m3) vs those with low radon exposure (≤48 Bq/m3; 4.94 Mb vs 2.62 Mb; P=.01).
- No differences in radon concentrations between patients with and without EGFR mutations.
- Recurrence rates were similar between high and low radon exposure groups.
- There were significant protein-protein interactions (PPI) between genes involved in DNA damage and repair (PPI enrichment, P<.001 in patients with high radon exposure.>
- High radon exposure was associated with tumors with more mutated genes involved in DNA damage and repair (P<.01>
Limitations
- Small sample size and all-Korean cohort.
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