{"created":"2023-07-27T06:59:59.182506+00:00","id":59754,"links":{},"metadata":{"_buckets":{"deposit":"f0a4dec6-04c1-4016-afc7-78bba243d75c"},"_deposit":{"created_by":18,"id":"59754","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"59754"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00059754","sets":["2812:2813:2835"]},"author_link":["100925","21709"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"1999-12-07","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"2p.","bibliographicVolumeNumber":"1997 – 1998","bibliographic_titles":[{"bibliographic_title":"平成10(1998)年度 科学研究費補助金 基盤研究(C) 研究成果報告書概要"},{"bibliographic_title":"1998 Fiscal Year Final Research Report Summary","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"私は、膵液中のK-ras変異の検索が膵癌診断に有用であることを報告してきたが、p53分析を加えても陽性率は100%になるわけではなく、さらに特異性の高い遺伝子を分析の対象に加えることが望まれる.p16は、cyclin dependent kinase(CDK)インヒビターをコードする癌抑制遺伝子として注目され、膵癌培養細胞株では高頻度に不活性化されていると報告されている。\n手術ないしは剖検で得られた膵癌62例、嚢胞腺種8例、慢性膵炎20例、正常膵6例のパラフィン包埋切片に対してp16モノクローナル抗体(G175-405)を用いた免疫染色の検討では、膵癌で41.9%(26/62)にp16蛋白発現の欠失がみられ、膵癌は慢性膵炎に比較してp16蛋白発現の欠失が有意に高率であった(p<0.01)。さらに、膵癌の組織学的分化度でも、中.低分化度(G2,G3)は高分化度(G1)に比してp16蛋白発現の欠失は有意に高率であった(p<0.01)。しかし、膵癌の各臨床病理学的事項とp16蛋白発現の有無を比較しても有意差はみられなかった。\n一方、膵癌組織のp16免疫染色性すなわち蛋白発現の低下した領域をmicrodissection法にて区分し、DNAを抽出した。p16遺伝子の3つのエクソンに対応するプライマーを用いてPCRを行ない、homozygous deletionの有無を判定した。膵癌26例中エクソン1では5例(19.2%)に、エクソン2では6例(23.1%)にPCR産物の欠損が認められたが、エクソン3には認められず、合計すると26例中9例(34.6%)にhomozygous deletionが認められた。さらに、PCR産物が得られた17例については、PCR-SSCPによりp16の突然変異の有無を検索したが、明らかなmutationを認めたものはなかった。最近、p16蛋白発現低下の原因のひとつにCpG island領域のmethylationの関与が示唆されており、現在、p16のmethylationについても検索中である。また、ヒト膵液中のp16変異の検討については、正常膵管上皮が多量に含まれている膵液中では、homozygous deletionの検討は困難であることから、p16のmutationの有無につき検討を行っているが、現在のところ、明らかなp16mutation陽性症例はみられていない。","subitem_description_type":"Abstract"},{"subitem_description":"I have repoted that detection of K-ras mutations in pure pancreatic juice (PPJ) was useful for the diagnosis of pancreatic carcinoma (PCa). However, combination assay of K-rag and p53 mutations was not completely fulfiled for the diagnosis of PCa. Therefore, a new specific gene for PCa is needed for the supplemental diagnosis of PCa. p16 is a suppressor gene with the function of cyclin dependent kinase (CDK) inhibitor, and high incidence of p16 inactivation in PCa cell lines was recently reported.\nExpression of p1 6 gene product in human PCa was investigated in paraffin-embedded tissue using a monclonal antibody against p16 protein, clone G175-405, by means of immunohistochemical staining. All six cases of normal pancreas and all but 1 of 20 cases of chronic pancreatitis (CP) expressed p16 protein, whereas 41.9% (26 of 62) of PCas lost p16 expression. There was a significant difference between CP and PCa for frequency of the loss of p16 expression. (p< 0.01). Moreover loss of p16 protein in pancreatic malignancy was significantly associated with histological grade (G1 versus G2 and G3, p< 0.01) but not with sex, age, clinical stage, tumor location, or resectability. DNA was extracted using microdissection method from the 26 PCa tissues which show the loss of p16 expression by immunohistochemical staining. Incidence of homozygous deletion was found in 19.2% (5/26) in exon 1, 23.1% (6/26) in exon 2, 0% (0/26) in exon 3 ofpl6, and 34.6% (9126) in all by PCR with the corresponding primers. On the other hand, there was no mutaion of p1 6 gene about the remnant 17 PCa cases expressing PCR products by PCR-SSCP.Recently, methylation of CpG island is regarded as a cause of the loss of p16 expression and p16 methylation for PCa is now under investigation. It is very difficult to detect homozygous deletions of p16 in PPJ because an amount of exfoliated normal pancreatic epitheliums are present in PPJ.Therefore, mutation of p16 in PPJ obtained from patients with PCa is under investigation. At present, there has been no detectable mutations of p16 in PPJ.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:09670524, 研究期間(年度):1997 – 1998","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「膵癌におけるp16遺伝子異常の検索と膵液を用いたその臨床的応用 」課題番号09670524\n（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） \n（https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-09670524/096705241998kenkyu_seika_hokoku_gaiyo/）を加工して作成","subitem_description_type":"Other"}]},"item_9_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学がん研究所","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00066009","subitem_identifier_reg_type":"JaLC"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/search/?qm=30242564"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=30242564","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670524/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670524/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-09670524/096705241998kenkyu_seika_hokoku_gaiyo/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-09670524/096705241998kenkyu_seika_hokoku_gaiyo/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2022-05-27"}],"displaytype":"detail","filename":"CA-PR-WATANABE-H-kaken 1999-2p.pdf","filesize":[{"value":"91.1 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-WATANABE-H-kaken 1999-2p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/59754/files/CA-PR-WATANABE-H-kaken 1999-2p.pdf"},"version_id":"90fd1f73-f521-414b-85fe-fd84180a823e"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"膵癌におけるp16遺伝子異常の検索と膵液を用いたその臨床的応用","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"膵癌におけるp16遺伝子異常の検索と膵液を用いたその臨床的応用"},{"subitem_title":"p16 mutations in pancreatic cancer and its clinical application using pancreaitc juice","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2835"],"pubdate":{"attribute_name":"公開日","attribute_value":"2022-05-27"},"publish_date":"2022-05-27","publish_status":"0","recid":"59754","relation_version_is_last":true,"title":["膵癌におけるp16遺伝子異常の検索と膵液を用いたその臨床的応用"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T13:00:34.069961+00:00"}