{"created":"2023-05-15T16:49:20.928147+00:00","id":26765,"links":{},"metadata":{"_buckets":{"deposit":"53787c00-7bd1-45d4-85ff-4579a0104b17"},"_deposit":{"created_by":6,"id":"26765","owners":[6],"pid":{"revision_id":0,"type":"depid","value":"26765"},"status":"published"},"_oai":{"id":"oai:nagasaki-u.repo.nii.ac.jp:00026765","sets":["25:26"]},"author_link":["118566","118565"],"item_2_biblio_info_6":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2021-05-05","bibliographicIssueDateType":"Issued"},"bibliographicPageEnd":"i77","bibliographicPageStart":"i71","bibliographicVolumeNumber":"62","bibliographic_titles":[{"bibliographic_title":"Journal of radiation research"}]}]},"item_2_description_4":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"There has been little understanding of the molecular pathogenesis of pediatric thyroid cancers. Most of them are histologically classified as papillary thyroid carcinoma (PTC). Ionizing radiation is the most important environmental factor to inducePTC, especially in children.Particularly, radiation-related pediatricPTCs after theChernobyl accident provided invaluable information. In addition, the recent accumulation of sporadic pediatric PTC cases, partly due to advances in diagnostic imaging, has also provided insight into their general pathogenesis. In PTC development, basically two types of genetic alterations, fusion oncogenes,mainly RET/PTC, and a point mutation,mainly BRAFV600E, are thought to play a key role as driver oncogenes. Their frequencies vary depending on patient age. The younger the age, the more prevalent the fusion oncogenes are. Higher incidence of fusion ncogenes was also observed in cases exposed to radiation. In short, fusion oncogenes are associated with both age and radiation and are not evidence of radiation exposure.The type of driver oncogene is shifted toward BRAFV600E during adolescence in sporadic PTCs. However, until about this age, fusion oncogenes seem to still confer dominant growth advantages, which may lead to the higher discovery rate of the fusion oncogenes. It has been postulated that RET/PTC in radiation-induced PTC is generated by ionizing radiation; however, there is an interesting hypothesis that thyroid follicular cell clones with pre-existing RET/PTC were already present, and radiation may play a role as a promoter/progressor but not initiator.Telomerase reverse transcriptase gene (TERT) promotermutations,which are the strongestmarker of tumor aggressiveness in adult PTC cases, have not been detected in pediatric cases; however, TERT expression without the mutations may play a role in tumor aggressiveness. In this paper, the recent information regarding molecular findings in sporadic and radiation-associated pediatric PTCs is summarized.","subitem_description_type":"Abstract"}]},"item_2_description_63":{"attribute_name":"引用","attribute_value_mlt":[{"subitem_description":"Journal of radiation research, 62, pp. i71-i77; 2021","subitem_description_type":"Other"}]},"item_2_publisher_33":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Oxford University Press"}]},"item_2_relation_12":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.1093/jrr/rraa096","subitem_relation_type_select":"DOI"}}]},"item_2_rights_13":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"© The Author(s) 2020. Published by Oxford University Press on behalf of The Japanese Radiation Research Society and Japanese Society for Radiation Oncology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/bync/ 4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com"}]},"item_2_source_id_7":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"1349-9157","subitem_source_identifier_type":"ISSN"}]},"item_2_version_type_16":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Mitsutake, Norisato"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Saenko, Vladimir"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2021-10-11"}],"displaytype":"detail","filename":"JRR62_i71.pdf","filesize":[{"value":"309.0 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"JRR62_i71.pdf","url":"https://nagasaki-u.repo.nii.ac.jp/record/26765/files/JRR62_i71.pdf"},"version_id":"968965b0-fc35-49fc-8325-e8dc6c54556b"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"Molecular pathogenesis of pediatric thyroid carcinoma","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Molecular pathogenesis of pediatric thyroid carcinoma"}]},"item_type_id":"2","owner":"6","path":["26"],"pubdate":{"attribute_name":"公開日","attribute_value":"2021-10-11"},"publish_date":"2021-10-11","publish_status":"0","recid":"26765","relation_version_is_last":true,"title":["Molecular pathogenesis of pediatric thyroid carcinoma"],"weko_creator_id":"6","weko_shared_id":-1},"updated":"2023-05-15T20:12:20.006621+00:00"}