Science advances · 2025
Distinctive molecular features of radiation-induced thyroid cancers.
СтатьяПоддержка NIH: внешняя программаResearch Support, N.I.H., IntramuralНазвание и аннотация: Перевод пока не подготовлен
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Karyadi Danielle M, Bogdanova Tetiana I, Milder Cato M, Hartley Stephen W, Lee Olivia W, Dean Michael, Drozdovitch Vladimir, Cahoon Elizabeth K, Masiuk Sergii, Chepurny Mykola, Zurnadzhy Liudmyla Yu, Vij Vibha, Kitahara Cari M, Thomas Gerry A, Woloschak Gayle E, Ramsden Dale A, Tronko Mykola D, Chanock Stephen J, Morton Lindsay M
Аннотация
Papillary thyroid carcinoma (PTC) incidence increased after childhood exposure to radioactive fallout from the Chornobyl accident. We investigated PTC genomic profiles to distinguish radiation-induced versus sporadic oncogenic drivers by modeling dose and molecular characteristics by driver category: BRAFV600E (n = 132), RAS mutation (n = 31), fusions generated from two breakpoints and <20 base pairs (bp) breakpoint gain/loss (Fusion2B<20bp; n = 63), or ≥3 breakpoints and ≥1000 bp breakpoint loss (n = 20). The frequency of Fusion2B<20bp-PTC increased with increasing thyroid radiation dose, whereas all others declined. Clonal small deletion counts increased with increasing radiation dose for Fusion2B<20bp-PTC (P = 5.1 × 10-4) but not other drivers (P > 0.08). Clonal clock mutational signatures, marking the age of tumor initiation, were associated with age at the accident for Fusion2B<20bp-PTC (P = 8.2 × 10-4) but not other drivers (P > 0.21). Together, these results support a causal role for ionizing radiation in Fusion2B<20bp-PTC as a group but not other drivers.