{"created":"2023-05-15T09:02:56.458757+00:00","id":3823,"links":{},"metadata":{"_buckets":{"deposit":"4eb95517-c60f-4f6d-8669-8b6a9a38c44d"},"_deposit":{"created_by":3,"id":"3823","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"3823"},"status":"published"},"_oai":{"id":"oai:hirosaki.repo.nii.ac.jp:00003823","sets":["557:561:656"]},"author_link":["11084","13849","11090","11094","13841","13847","13856","13850","13857","14463","14450","13855","11088","14468","14449","14448","11093","13846","14451","13840","13858","13848","14461","11086","13843","14472","14460","14445","13853","14471","11085","14447","14473","14459","11089","14464"],"item_3_alternative_title_21":{"attribute_name":"その他のタイトル","attribute_value_mlt":[{"subitem_alternative_title":"Novel In-Frame Deletion of GATA1 Observed in Pediatric Acute Megakaryoblastic Leukemia without Down Syndrome"}]},"item_3_alternative_title_22":{"attribute_name":"タイトル（ヨミ）","attribute_value_mlt":[{"subitem_alternative_title":"ヒ ダウンショウ ショウニ キュウセイ キョカク ガキュウセイ ハッケツビョウ ニ ミトメラレタ シンキ GATA1 インフレーム ヘンイ"}]},"item_3_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2014-09-30","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"2-4","bibliographicPageEnd":"237","bibliographicPageStart":"227","bibliographicVolumeNumber":"65","bibliographic_titles":[{"bibliographic_title":"弘前医学"}]}]},"item_3_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"ダウン症児は巨核芽球性白血病（DS－AMKL）のリスクが高い．DS－AMKL ではほぼ全例でGATA1 遺伝子変異があり，N末端領域を欠くGATA1s だけが発現する．非ダウン症例 （non－DS－AMKL）にはこの変異は稀である．最近我々は，19例中1例のnon－DS－AMKL にインフレーム欠失を見出した．患児は出生時より白血球増多を認め，生後1 ヶ月時にAMKL と診断された．芽球の核型は46,XY であった．変異確認の際，第3 エクソンのスプライシングを起こす別の欠失を認め，両変異は同アレルに座位していた．この変異体（#135）の転写活性化能は60%に減弱していた．完全長GATA1 発現レトロウィルスの導入でDS－AMKL 細胞株KPAM1 の増殖が著しく抑制されたが，GATA1s や#135では緩やかな抑制だった．これらの結果は#135変異体がnon－DS－AMKL 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