{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360004236369090816.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1158/1078-0432.ccr-12-1777"}},{"identifier":{"@type":"URI","@value":"https://aacrjournals.org/clincancerres/article-pdf/19/6/1422/2298021/1422.pdf"}},{"identifier":{"@type":"PMID","@value":"23382113"}},{"identifier":{"@type":"NAID","@value":"20001443728"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Combination of Ponatinib with Hedgehog Antagonist Vismodegib for Therapy-Resistant BCR-ABL1–Positive Leukemia"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title>\n                  <jats:p>Purpose: The Hedgehog signaling pathway is a key regulator of cell growth and differentiation during development. Whereas the Hedgehog pathway is inactive in most normal adult tissues, Hedgehog pathway reactivation has been implicated in the pathogenesis of several neoplasms including BCR-ABL1–positive leukemia. The clear link between the Hedgehog pathway and BCR-ABL1–positive leukemia led to an effort to identify small molecules to block the pathway.</jats:p>\n                  <jats:p>Experimental Design: We investigated the combined effects of vismodegib and ponatinib, a pan-ABL1 kinase inhibitor, in nonobese diabetic/severe-combined immunodeficiency (NOD/SCID) repopulating T315I BCR-ABL1–positive cells in vitro and in vivo.</jats:p>\n                  <jats:p>Results: We observed that combination with vismodegib and ponatinib helps to eliminate therapy-resistant NOD/SCID repopulating T315I BCR-ABL1–positive cells. The percentage of CD19-positive leukemia cells in peripheral blood was significantly lower in vismodegib + ponatinib–treated mice than that of the vehicle or ponatinib alone (P &lt; 0.001). Spleen weights were also lower in vismodegib + ponatinib–treated mice than in ponatinib alone (P &lt; 0.05). Overall tumor burden, as assessed by BCR-ABL mRNA from bone marrow cells, was significantly lower in vismodegib + ponatinib–treated mice than in ponatinib alone (P &lt; 0.005). We also found that vismodegib significantly reduced BCR-ABL1–positive leukemia cell self-renewal in vitro as well as during serial transplantation in vivo.</jats:p>\n                  <jats:p>Conclusions: The combination with a Smo inhibitor and ABL1 tyrosine kinase inhibitors may help eliminate therapy-resistant T315I BCR-ABL1–positive leukemia cells. Our preclinical results indicate that vismodegib has potential as an important option for controlling minimal residual cells in BCR-ABL1–positive leukemia. Clin Cancer Res; 19(6); 1422–32. ©2012 AACR.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381412896274645249","@type":"Researcher","foaf:name":[{"@value":"Seiichiro Katagiri"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381412896274645248","@type":"Researcher","foaf:name":[{"@value":"Tetsuzo Tauchi"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1420001326231592960","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"40366109"},{"@type":"NRID","@value":"1000040366109"}],"foaf:name":[{"@value":"Seiichi Okabe"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381412896274645380","@type":"Researcher","foaf:name":[{"@value":"Yosuke Minami"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381412896274645376","@type":"Researcher","foaf:name":[{"@value":"Shinya Kimura"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381412896274645378","@type":"Researcher","foaf:name":[{"@value":"Taira Maekawa"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381412896274645377","@type":"Researcher","foaf:name":[{"@value":"Tomoki Naoe"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381412896274645383","@type":"Researcher","foaf:name":[{"@value":"Kazuma Ohyashiki"}],"jpcoar:affiliationName":[{"@value":"Authors' Affiliations: 1First Department of Internal Medicine, Tokyo Medical University, Shinjuku-ku, Tokyo; 2Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya; 3Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga; and 4Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Faculty of Medicine, Kyoto University, Kyoto, Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"10780432"},{"@type":"EISSN","@value":"15573265"}],"prism:publicationName":[{"@value":"Clinical Cancer Research"}],"dc:publisher":[{"@value":"American Association for Cancer Research (AACR)"}],"prism:publicationDate":"2013-03-14","prism:volume":"19","prism:number":"6","prism:startingPage":"1422","prism:endingPage":"1432"},"reviewed":"false","url":[{"@id":"https://aacrjournals.org/clincancerres/article-pdf/19/6/1422/2298021/1422.pdf"}],"createdAt":"2013-01-14","modifiedAt":"2022-06-11","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Pyridines","dc:title":"Pyridines"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Cycle","dc:title":"Cell Cycle"},{"@id":"https://cir.nii.ac.jp/all?q=Fusion%20Proteins,%20bcr-abl","dc:title":"Fusion Proteins, bcr-abl"},{"@id":"https://cir.nii.ac.jp/all?q=Imidazoles","dc:title":"Imidazoles"},{"@id":"https://cir.nii.ac.jp/all?q=Mice,%20SCID","dc:title":"Mice, SCID"},{"@id":"https://cir.nii.ac.jp/all?q=Pyridazines","dc:title":"Pyridazines"},{"@id":"https://cir.nii.ac.jp/all?q=Mice","dc:title":"Mice"},{"@id":"https://cir.nii.ac.jp/all?q=Drug%20Resistance,%20Neoplasm","dc:title":"Drug Resistance, Neoplasm"},{"@id":"https://cir.nii.ac.jp/all?q=Leukemia,%20Myelogenous,%20Chronic,%20BCR-ABL%20Positive","dc:title":"Leukemia, Myelogenous, Chronic, BCR-ABL Positive"},{"@id":"https://cir.nii.ac.jp/all?q=Antineoplastic%20Combined%20Chemotherapy%20Protocols","dc:title":"Antineoplastic Combined Chemotherapy Protocols"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Anilides","dc:title":"Anilides"},{"@id":"https://cir.nii.ac.jp/all?q=Hedgehog%20Proteins","dc:title":"Hedgehog Proteins"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Proliferation","dc:title":"Cell Proliferation"},{"@id":"https://cir.nii.ac.jp/all?q=Signal%20Transduction","dc:title":"Signal Transduction"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000782141227264","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"23112507"},{"@type":"JGN","@value":"JP23112507"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PUBLICLY-23112507/"}],"notation":[{"@language":"ja","@value":"骨髄低酸素環境における骨髄腫幹細胞の解析と治療標的分子同定"}]},{"@id":"https://cir.nii.ac.jp/crid/1040000782156544384","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"23501312"},{"@type":"JGN","@value":"JP23501312"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23501312/"}],"notation":[{"@language":"ja","@value":"Ｈｅｄｇｅｈｏｇによる白血病幹細胞維持の分子メカニズム"},{"@language":"en","@value":"Targeting Hedgehog in a CML Stem Cell Pathway"}]},{"@id":"https://cir.nii.ac.jp/crid/1040000782235096448","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"25112706"},{"@type":"JGN","@value":"JP25112706"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PUBLICLY-25112706/"}],"notation":[{"@language":"ja","@value":"骨髄低酸素環境における骨髄腫幹細胞維持分子を標的とした新規治療開発"}]},{"@id":"https://cir.nii.ac.jp/crid/1040000782259917440","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"25461412"},{"@type":"JGN","@value":"JP25461412"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25461412/"}],"notation":[{"@language":"ja","@value":"急性骨髄性白血病の微小環境における治療抵抗性機序の解明および克服療法の基礎研究"},{"@language":"en","@value":"Circumventing resistance at bone marrow microenvironment in acute myeloid leukemia"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282257089342848","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"22390192"},{"@type":"JGN","@value":"JP22390192"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22390192/"}],"notation":[{"@language":"ja","@value":"分子標的治療における残存・耐性化機序の解明と克服に向けた基礎研究"},{"@language":"en","@value":"Basic research aimed at understanding and overcoming of the primary and secondary resistance in molecular target therapy"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282257177066368","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"24390244"},{"@type":"JGN","@value":"JP24390244"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24390244/"}],"notation":[{"@language":"ja","@value":"ＣＭＬ幹細胞の特異的代謝経路と転写因子制御を標的とした新規治療法の開発"},{"@language":"en","@value":"Novel therapeutics targeting the specified metabolic pathway and transcription factor related to stem cells of  chronic myelogenous leukemia"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282257199618176","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"24659461"},{"@type":"JGN","@value":"JP24659461"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24659461/"}],"notation":[{"@language":"ja","@value":"薬物刺激間葉系幹細胞を用いたＤｕａｌ　Ｓｔｅｍ　Ｃｅｌｌ　Ｔｈｅｒａｐｙの開発"},{"@language":"en","@value":"Dual Stem Cell Therapy with Pharmacologically-Stimulated Mesenchymal Stem Cells"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360011144006161408","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"The controversial role of the Hedgehog pathway in normal and malignant hematopoiesis"}]},{"@id":"https://cir.nii.ac.jp/crid/1360011145474467072","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Small Molecule Inhibition of GDC-0449 Refractory Smoothened Mutants and Downstream Mechanisms of Drug Resistance"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292619680281984","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Comparison of imatinib, dasatinib, nilotinib and INNO-406 in imatinib-resistant cell lines"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292620378219904","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Pharmacokinetic Dose-Scheduling Study of Hedgehog Pathway Inhibitor Vismodegib (GDC-0449) in Patients with Locally Advanced or Metastatic Solid Tumors"}]},{"@id":"https://cir.nii.ac.jp/crid/1360292620972017280","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Hedgehog regulates cell growth and proliferation by inducing Cyclin D and Cyclin E"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567181954203136","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"The Hedgehog inhibitor suppresses the function of monocyte-derived dendritic cells from patients with advanced cancer under hypoxia"}]},{"@id":"https://cir.nii.ac.jp/crid/1360567184436754816","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Effects of the Hedgehog Inhibitor GDC-0449, Alone or in Combination with Dasatinib, on BCR-ABL-Positive Leukemia Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360574094204981632","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Human GLI2 and GLI1 are part of a positive feedback mechanism in Basal Cell Carcinoma"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848658384050048","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Combined effects of novel heat shock protein 90 inhibitor NVP-AUY922 and nilotinib in a random mutagenesis screen"}]},{"@id":"https://cir.nii.ac.jp/crid/1360855570707125888","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Pharmacokinetics of Hedgehog Pathway Inhibitor Vismodegib (GDC-0449) in Patients with Locally Advanced or Metastatic Solid Tumors: the Role of Alpha-1-Acid Glycoprotein Binding"}]},{"@id":"https://cir.nii.ac.jp/crid/1361137043582973056","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Normal and leukaemic stem cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1361137044101184768","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based Resistance"}]},{"@id":"https://cir.nii.ac.jp/crid/1361418520002530816","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Clinical Experience With Hedgehog Pathway Inhibitors"}]},{"@id":"https://cir.nii.ac.jp/crid/1361699994220770816","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"The output of Hedgehog signaling is controlled by the dynamic association between Suppressor of Fused and the Gli proteins"}]},{"@id":"https://cir.nii.ac.jp/crid/1361981468331282560","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Hedgehog signalling is essential for maintenance of cancer stem cells in myeloid leukaemia"}]},{"@id":"https://cir.nii.ac.jp/crid/1361981468717603584","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Hedgehog pathway activation in chronic myeloid leukemia: A promise for a novel combination therapeutic approach?"}]},{"@id":"https://cir.nii.ac.jp/crid/1361981470039956864","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Targeting the Hedgehog Pathway in Cancer: Can the Spines Be Smoothened?"}]},{"@id":"https://cir.nii.ac.jp/crid/1361981470365003520","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"A Member of Forkhead Transcription Factor FKHRL1 Is a Downstream Effector of STI571-induced Cell Cycle Arrest in BCR-ABL-expressing Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544418702178432","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Establishment of a new Philadelphia chromosome−positive acute lymphoblastic leukemia cell line (SK-9) with T315I mutation"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544420099628544","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"<i>Smoothened</i>\n                    Mutation Confers Resistance to a Hedgehog Pathway Inhibitor in Medulloblastoma"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544420145677568","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Activation of the hedgehog-signaling pathway in human cancer and the clinical implications"}]},{"@id":"https://cir.nii.ac.jp/crid/1362544420513449088","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Hedgehog signaling in animal development: paradigms and principles"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825893612513792","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Expansion of Bcr-Abl-Positive Leukemic Stem Cells Is Dependent on Hedgehog Pathway Activation"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825894700900096","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Irrespective of CD34 expression, lineage‐committed cell fraction reconstitutes and re‐establishes transformed Philadelphia chromosome‐positive leukemia in NOD / SCID / IL‐2Rγc<sup>−/−</sup> mice"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825895318471936","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Summing up cancer stem cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1362825896235252480","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Inhibition of the Hedgehog Pathway in Advanced Basal-Cell Carcinoma"}]},{"@id":"https://cir.nii.ac.jp/crid/1363388844347929856","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Treatment of Medulloblastoma with Hedgehog Pathway Inhibitor GDC-0449"}]},{"@id":"https://cir.nii.ac.jp/crid/1363388845424943488","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Clonal evolution in cancer"}]},{"@id":"https://cir.nii.ac.jp/crid/1363388845843972736","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Targeting hedgehog in hematologic malignancy"}]},{"@id":"https://cir.nii.ac.jp/crid/1363388846119570816","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Phase I Trial of Hedgehog Pathway Inhibitor Vismodegib (GDC-0449) in Patients with Refractory, Locally Advanced or Metastatic Solid Tumors"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670318702257664","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"The Crosstalk of mTOR/S6K1 and Hedgehog Pathways"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670319842799744","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Activity of a novel G-quadruplex-interactive telomerase inhibitor, telomestatin (SOT-095), against human leukemia cells: involvement of ATM-dependent DNA damage response pathways"}]},{"@id":"https://cir.nii.ac.jp/crid/1363951794534306048","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Coupling between p210bcr-abl and Shc and Grb2 adaptor proteins in hematopoietic cells permits growth factor receptor-independent link to ras activation pathway."}]},{"@id":"https://cir.nii.ac.jp/crid/1363951795667753600","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"BCR-ABL signal transduction"}]},{"@id":"https://cir.nii.ac.jp/crid/1363951796295752448","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Pharmacokinetic–Pharmacodynamic Analysis of Vismodegib in Preclinical Models of Mutational and Ligand-Dependent Hedgehog Pathway Activation"}]},{"@id":"https://cir.nii.ac.jp/crid/1364233270662677760","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Molecular Pathways: BCR-ABL"}]},{"@id":"https://cir.nii.ac.jp/crid/1371412896274645257","@type":"Product","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Role foe E2F1 in p210 BCR-ABL downstream regulation of c-myc transcription initiation. Studies in murine myeloid cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205036941440","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Novel therapeutic approach of Ph-positive leukemia: combination of tyrosine kinase inhibitors with other targeted drugs"},{"@language":"ja","@value":"Ph陽性白血病の新規治療の試み：ABLチロシンキナーゼ阻害薬と分子標的薬との併用"},{"@language":"ja-Kana","@value":"Ph ヨウセイ ハッケツビョウ ノ シンキ チリョウ ノ ココロミ : ABL チロシンキナーゼ ソガイヤク ト ブンシ ヒョウテキヤク ト ノ ヘイヨウ"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1158/1078-0432.ccr-12-1777"},{"@type":"CIA","@value":"20001443728"},{"@type":"KAKEN","@value":"PRODUCT-21354348"},{"@type":"KAKEN","@value":"PRODUCT-14002788"},{"@type":"KAKEN","@value":"PRODUCT-14002787"},{"@type":"KAKEN","@value":"PRODUCT-14920062"},{"@type":"KAKEN","@value":"PRODUCT-15082298"},{"@type":"KAKEN","@value":"PRODUCT-13357459"},{"@type":"KAKEN","@value":"PRODUCT-14575993"},{"@type":"KAKEN","@value":"PRODUCT-14790808"},{"@type":"KAKEN","@value":"PRODUCT-14575952"},{"@type":"OPENAIRE","@value":"doi_dedup___::51bc864a42627aed66795d27d61871b5"},{"@type":"CROSSREF","@value":"10.1016/j.bbrc.2013.05.057_references_DOI_ZHJoKBWRTTKHwOKXIhTQun084gs"}]}