ログイン
言語:

WEKO3

  • トップ
  • ランキング
To
lat lon distance
To

Field does not validate



インデックスリンク

インデックスツリー

メールアドレスを入力してください。

WEKO

One fine body…

WEKO

One fine body…

アイテム

  1. Public
  2. 学位論文
  3. 博士論文2020.3~

SETD2 and miR-21 as therapeutic targets for NUT midline carcinoma

https://asahikawa-med.repo.nii.ac.jp/records/2000315
https://asahikawa-med.repo.nii.ac.jp/records/2000315
1b4ef7b7-4fd5-475a-ac11-2829ff9553ff
名前 / ファイル ライセンス アクション
K587 K587 Yoshida Nana_TD.pdf (716 KB)
Item type 学位論文 / Thesis or Dissertation_02(1)
公開日 2023-04-11
タイトル
タイトル SETD2 and miR-21 as therapeutic targets for NUT midline carcinoma
言語 en
言語
言語 eng
キーワード
言語 en
主題Scheme Other
主題 MicroR-21
キーワード
言語 en
主題Scheme Other
主題 Nuclear protein in testis midline carcinoma
キーワード
言語 en
主題Scheme Other
主題 SET domain-containing protein 2
キーワード
言語 en
主題Scheme Other
主題 WEE1 G2 checkpoint kinase
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_db06
資源タイプ doctoral thesis
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
その他(別言語等)のタイトル
その他のタイトル NUT midline carcinomaの新規治療におけるSETD2とmiR-21の検討
言語 ja
著者 吉田, 奈七

× 吉田, 奈七

ja 吉田, 奈七

ja-Kana ヨシダ, ナナ

en Yoshida, Nana

Search repository
bibliographic_information en : Journal of Cancer Science and Clinical Therapeutics

巻 6, 号 1, p. 129-135, 発行日 2022-03-01
ISSN
収録物識別子タイプ PISSN
収録物識別子 2637-5079
dissertation_number
学位授与番号 甲第587号
学位授与年月日
学位授与年月日 2023-03-24
学位名
言語 ja
学位名 博士(医学)
item_10_degree_grantor_32
言語 ja
学位授与機関名 旭川医科大学
item_10_description_33
内容記述タイプ Abstract
内容記述 Nuclear Protein in Testis (NUT) Midline Carcinoma (NMC) is a rare and highly aggressive tumor with the bromodomain containing 4 proteins (BRD4)-NUT (NUTM1) gene fusion. Few targeted therapies are available for NMC, and thus novel therapeutic targets are required. To the best of our knowledge, the present study was the first to report that SET domain-containing protein 2 (SETD2) deficiency and microRNA (miRNA/miR)-21 may serve as novel therapeutic targets for the treatment of NMC. First, Next-Generation Sequencing (NGS) identified a novel SETD2 mutation (p.Ser2382fs) in the NMC cell lines, HCC2429 and Ty82. Trimethylation of lysine 36 on histone H3 expression was depleted in the NMC cells, which was indicative of SETD2 loss. NMC cells were sensitive to the WEE1 G2 checkpoint kinase (WEE1) inhibitor, AZD1775, in the cancer cells with SETD2 deficiency. NMC cells that were resistant to Bromodomain and Extra-Terminal Motif (BET) inhibitors were next established, and these resistant cells were also sensitive to AZD1775. Subsequently, miRNA analysis revealed that miR-21 expression was increased in BET-inhibitor-resistant NMC cells. In addition, miR-21 regulated the proliferation of NMCs. The miR-21 inhibitor also suppressed the proliferation of BET-inhibitor-resistant cells. Additionally, a digital PCR assay was established to detect NUT gene rearrangements to identify patients with NMC. A total of 32 clinical samples were analyzed and one case of NMC was identified, in which the novel SETD2 mutation was detected. These data suggested that SETD2 loss and miR-21 may be therapeutic targets for treatment of NMC.
言語 en
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
戻る
0
views
See details
Views

Versions

Ver.1 2025-01-30 06:21:26.038161
Show All versions

Share

Mendeley Twitter Facebook Print Addthis

Cite as

エクスポート

OAI-PMH
  • OAI-PMH JPCOAR 2.0
  • OAI-PMH JPCOAR 1.0
  • OAI-PMH DublinCore
  • OAI-PMH DDI
Other Formats
  • JSON
  • BIBTEX

Confirm


Powered by WEKO3


Powered by WEKO3