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Recurrent homozygous deletion of DROSHA and microduplication of PDE4DIP in pineoblastoma.

Matija SnuderlKasthuri KannanElke PfaffShiyang WangJames M StaffordJonathan SerranoAdriana HeguyKarina RayArline FaustinOlga AminovaIgor DolgalevStacie L StapletonDavid ZagzagLuis A ChiribogaSharon L GardnerJeffrey H WisoffJohn G GolfinosDavid CapperVolker HovestadtMarc K RosenblumDimitris G PlacantonakisSarah E LeBoeufThales Y PapagiannakopoulosLukas ChavezSama AhsanCharles G EberhartStefan M PfisterDavid T W JonesMatthias A Karajannis
Published in: Nature communications (2018)
Pineoblastoma is a rare and highly aggressive brain cancer of childhood, histologically belonging to the spectrum of primitive neuroectodermal tumors. Patients with germline mutations in DICER1, a ribonuclease involved in microRNA processing, have increased risk of pineoblastoma, but genetic drivers of sporadic pineoblastoma remain unknown. Here, we analyzed pediatric and adult pineoblastoma samples (n = 23) using a combination of genome-wide DNA methylation profiling and whole-exome sequencing or whole-genome sequencing. Pediatric and adult pineoblastomas showed distinct methylation profiles, the latter clustering with lower-grade pineal tumors and normal pineal gland. Recurrent variants were found in genes involved in PKA- and NF-κB signaling, as well as in chromatin remodeling genes. We identified recurrent homozygous deletions of DROSHA, acting upstream of DICER1 in microRNA processing, and a novel microduplication involving chromosomal region 1q21 containing PDE4DIP (myomegalin), comprising the ancient DUF1220 protein domain. Expresion of PDE4DIP and DUF1220 proteins was present exclusively in pineoblastoma with PDE4DIP gain.
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