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Distinctive molecular features of radiation-induced thyroid cancers
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DOI：10.1126/sciadv.adw7680.png)
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Abstract
En 中文
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.
Keywords:
radiation-induced thyroid cancer
papillary thyroid carcinoma
genomic profiles
Fusion2B<20bp
BRAFV600E
RAS mutation
Journal
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