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E-GEOD-48850 - Novel kinase fusion oncogenes in post-Chernobyl radiation-induced pediatric thyroid cancers

Released on 25 October 2013, last updated on 25 August 2017
Homo sapiens
Samples (11)
Protocols (1)
Exposure to ionizing radiation during childhood markedly increases the risk of developing papillary thyroid cancer. We identified non-overlapping somatic driver mutations in all 26 cases of post-Chernobyl thyroid cancers we studied through candidate gene assays and next generation RNA-sequencing. We found that 22/26 harbored fusion oncogenes arising primarily through intrachromosomal rearrangements. Altogether 23/26 of the oncogenic drivers identified in this cohort aberrantly activate MAPK signaling, including the two novel somatic rearrangements ETV6-NTRK3 and AGK-BRAF. Two other tumors harbored distinct fusions leading to overexpression of the nuclear receptor PPARγ. A lower prevalence of fusion oncogenes was found in a cohort of pediatric thyroid cancers from children from the same geographical regions that were not exposed to radiation. Radiation-induced thyroid cancers are a paradigm of tumorigenesis driven by fusion oncogenes that activate MAPK signaling or, less frequently, a PPARγ-driven transcriptional program. Examination of transcriptome profiles and genetic somatic changes in thyroid cancer.
Experiment type
RNA-seq of coding RNA 
Christopher Mason <>, Adriana Heguy, Agnes Viale, Christopher E Mason, Cristina Montero-Conde, Francesca Voza, Geraldine A Thomas, James A Fagin, Jeffrey A Knauf, Julio C Ricarte-Filho, Maria E Garcia-Rendueles, Sheng Li, Tetyana Bogdanova
Identification of kinase fusion oncogenes in post-Chernobyl radiation-induced thyroid cancers. Ricarte-Filho JC, Li S, Garcia-Rendueles ME, Montero-Conde C, Voza F, Knauf JA, Heguy A, Viale A, Bogdanova T, Thomas GA, Mason CE, Fagin JA. , PMID:24135138
Exp. designProtocolsVariablesProcessedSeq. reads
Investigation descriptionE-GEOD-48850.idf.txt
Sample and data relationshipE-GEOD-48850.sdrf.txt
Additional data (1)