{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["11(34)"],"submitter":["Karyadi DM"],"pubmed_abstract":["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."],"journal":["Science advances"],"pagination":["eadw7680"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12372901"],"repository":["biostudies-literature"],"pubmed_title":["Distinctive molecular features of radiation-induced thyroid cancers."],"pmcid":["PMC12372901"],"pubmed_authors":["Bogdanova TI","Vij V","Karyadi DM","Masiuk S","Chanock SJ","Morton LM","Kitahara CM","Ramsden DA","Zurnadzhy LY","Tronko MD","Lee OW","Chepurny M","Milder CM","Drozdovitch V","Woloschak GE","Thomas GA","Cahoon EK","Dean M","Hartley SW"],"additional_accession":[]},"is_claimable":false,"name":"Distinctive molecular features of radiation-induced thyroid cancers.","description":"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.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-05-08T10:48:11.147Z","creation":"2026-04-07T23:47:50.14Z"},"accession":"S-EPMC12372901","cross_references":{"pubmed":["40845117"],"doi":["10.1126/sciadv.adw7680"]}}