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Status |
Public on Oct 25, 2013 |
Title |
Novel kinase fusion oncogenes in post-Chernobyl radiation-induced pediatric thyroid cancers |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
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 PPARĪ³. 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 PPARĪ³-driven transcriptional program.
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Overall design |
Examination of transcriptome profiles and genetic somatic changes in thyroid cancer.
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Contributor(s) |
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 |
Citation(s) |
24135138 |
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Submission date |
Jul 13, 2013 |
Last update date |
May 15, 2019 |
Contact name |
Christopher E Mason |
E-mail(s) |
chm2042@med.cornell.edu
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Organization name |
Weill Cornell Medical College
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Department |
Physiology and Biophysics
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Lab |
Christopher Mason Lab
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Street address |
1305 York Ave
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City |
New York |
ZIP/Postal code |
10065 |
Country |
USA |
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Platforms (1) |
GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
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Samples (11)
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Relations |
BioProject |
PRJNA211959 |
SRA |
SRP027364 |