Biallelic DICER1 mutations in sporadic pleuropulmonary blastoma.

نویسندگان

  • Masafumi Seki
  • Kenichi Yoshida
  • Yuichi Shiraishi
  • Teppei Shimamura
  • Yusuke Sato
  • Riki Nishimura
  • Yusuke Okuno
  • Kenichi Chiba
  • Hiroko Tanaka
  • Keisuke Kato
  • Motohiro Kato
  • Ryoji Hanada
  • Yuko Nomura
  • Myoung-Ja Park
  • Toshiaki Ishida
  • Akira Oka
  • Takashi Igarashi
  • Satoru Miyano
  • Yasuhide Hayashi
  • Seishi Ogawa
  • Junko Takita
چکیده

Pleuropulmonary blastoma (PPB) is a rare pediatric malignancy whose pathogens are poorly understood. Recent reports suggest that germline mutations in the microRNA-processing enzyme DICER1 may contribute to PPB development. To investigate the genetic basis of this cancer, we performed whole-exome sequencing or targeted deep sequencing of multiple cases of PPB. We found biallelic DICER1 mutations to be very common, more common than TP53 mutations also found in many tumors. Somatic ribonuclease III (RNase IIIb) domain mutations were identified in all evaluable cases, either in the presence or absence of nonsense/frameshift mutations. Most cases had mutated DICER1 alleles in the germline with or without an additional somatic mutation in the remaining allele, whereas other cases displayed somatic mutations exclusively where the RNase IIIb domain was invariably affected. Our results highlight the role of RNase IIIb domain mutations in DICER1 along with TP53 inactivation in PPB pathogenesis.

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منابع مشابه

Biallelic DICER1 mutations in sporadic pleuropulmonary blastoma Running title Biallelic DICER1 mutations in sporadic PPB

Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan; Laboratory of Sequence Data Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan; Division of Pediatric Hematology and Oncology, Ibaraki Children’s Hospital, Mito, Ibaraki, Japan; Department of Hematology/Oncology, Saitama Children’s Medical Center, Saitama, Saitama,...

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Molecular and Cellular Pathobiology Biallelic DICER1 Mutations in Sporadic Pleuropulmonary Blastoma

Pleuropulmonary blastoma (PPB) is a rare pediatric malignancy whose pathogens are poorly understood. Recent reports suggest that germline mutations in the microRNA-processing enzyme DICER1 may contribute to PPB development. To investigate the genetic basis of this cancer, we performed whole-exome sequencing or targeted deep sequencing of multiple cases of PPB. We found biallelic DICER1 mutation...

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Temporal order of RNase IIIb and loss-of-function mutations during development determines phenotype in pleuropulmonary blastoma / syndrome: a unique variant DICER1

Pleuropulmonary blastoma (PPB) is the most frequent pediatric lung tumor and often the first indication of a pleiotropic cancer predisposition, DICER1 syndrome, comprising a range of other individually rare, benign and malignant tumors of childhood and early adulthood. The genetics of -associated DICER1 tumorigenesis are unusual in that tumors typically bear neomorphic missense mutations at on...

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Germline mutations in identified breast cancer susceptibility genes account for less than 20% of Chinese familial breast cancers. Dicer is an essential component of the microRNA-producing machinery; germline mutations of DICER1 have been confirmed in familial pleuropulmonary blastoma, ovarian sex cord-stromal tumors, and other cancers. Low expression of DICER1 is frequently detected in breast c...

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Temporal order of RNase IIIb and loss-of-function mutations during development determines phenotype in DICER1 syndrome: a unique variant of the two-hit tumor suppression

Pleuropulmonary blastoma (PPB) is the most frequent pediatric lung tumor and often the first indication of a pleiotropic cancer predisposition, DICER1 syndrome, comprising a range of other individually rare, benign and malignant tumors of childhood and early adulthood. The genetics of -associated DICER1 tumorigenesis are unusual in that tumors typically bear neomorphic missense mutations at on...

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عنوان ژورنال:
  • Cancer research

دوره 74 10  شماره 

صفحات  -

تاریخ انتشار 2014