Details

Autor(en) / Beteiligte

• Morton, Lindsay M
• Karyadi, Danielle M
• Stewart, Chip
• Bogdanova, Tetiana I
• Dawson, Eric T
• Steinberg, Mia K
• Dai, Jieqiong
• Hartley, Stephen W
• Schonfeld, Sara J
• Sampson, Joshua N
• Maruvka, Yosef E
• Kapoor, Vidushi
• Ramsden, Dale A
• Carvajal-Garcia, Juan
• Perou, Charles M
• Parker, Joel S
• Krznaric, Marko
• Yeager, Meredith
• Boland, Joseph F
• Hutchinson, Amy
• Hicks, Belynda D
• Dagnall, Casey L
• Gastier-Foster, Julie M
• Bowen, Jay
• Lee, Olivia
• Machiela, Mitchell J
• Cahoon, Elizabeth K
• Brenner, Alina V
• Mabuchi, Kiyohiko
• Drozdovitch, Vladimir
• Masiuk, Sergii
• Chepurny, Mykola
• Zurnadzhy, Liudmyla Yu
• Hatch, Maureen
• Berrington de Gonzalez, Amy
• Thomas, Gerry A
• Tronko, Mykola D
• Getz, Gad
• Chanock, Stephen J

Titel

Radiation-related genomic profile of papillary thyroid carcinoma after the Chernobyl accident

Ist Teil von

• Science (American Association for the Advancement of Science), 2021-05, Vol.372 (6543)

Ort / Verlag

United States: The American Association for the Advancement of Science

Erscheinungsjahr

2021

Quelle

American Association for the Advancement of Science

Beschreibungen/Notizen

• The 1986 Chernobyl nuclear power plant accident increased papillary thyroid carcinoma (PTC) incidence in surrounding regions, particularly for radioactive iodine ( I)-exposed children. We analyzed genomic, transcriptomic, and epigenomic characteristics of 440 PTCs from Ukraine (from 359 individuals with estimated childhood I exposure and 81 unexposed children born after 1986). PTCs displayed radiation dose-dependent enrichment of fusion drivers, nearly all in the mitogen-activated protein kinase pathway, and increases in small deletions and simple/balanced structural variants that were clonal and bore hallmarks of nonhomologous end-joining repair. Radiation-related genomic alterations were more pronounced for individuals who were younger at exposure. Transcriptomic and epigenomic features were strongly associated with driver events but not radiation dose. Our results point to DNA double-strand breaks as early carcinogenic events that subsequently enable PTC growth after environmental radiation exposure.