Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 2041-4889

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant ; volume:9 ; number:2 ; day:22 ; month:1 ; year:2018 ; pages:1-16 ; date:2.2018
Cell death & disease ; 9, Heft 2 (22.1.2018), 1-16, 2.2018

Classification: Biowissenschaften, Biologie

Creator: Jin, Bei

Contributor: Wang, Chengyan
Shen, Yingying
Pan, Jingxuan
SpringerLink (Online service)

DOI: 10.1038/s41419-017-0075-7

URN: urn:nbn:de:1111-201804135464

Rights: Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:49 AM CEST

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Jin, Bei
Wang, Chengyan
Shen, Yingying
Pan, Jingxuan
SpringerLink (Online service)

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Importance of early and deeper responses to long-term survival in CML patients: Implications of BCR-ABL testing in management of CML in Indian setting

Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment

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Initial decline of BCR-ABL transcript levels as early prognostic marker for patients with chronic myeloid leukemia (CML) treated with imatinib

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KU-CHEN # CML

Priapism in CML

Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy

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Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl

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Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant

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Other Objects (12)

Phosphorylation of Beclin 1 by BCR-ABL suppresses autophagy in CML

Importance of early and deeper responses to long-term survival in CML patients: Implications of BCR-ABL testing in management of CML in Indian setting

Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment

CML

SP.1

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KU-CHEN # CML

Priapism in CML

Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl

Targeted Therapy for CML

Phosphorylation of Beclin 1 by BCR-ABL suppresses autophagy in CML

Importance of early and deeper responses to long-term survival in CML patients: Implications of BCR-ABL testing in management of CML in Indian setting

Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment

CML

SP.1

Initial decline of BCR-ABL transcript levels as early prognostic marker for patients with chronic myeloid leukemia (CML) treated with imatinib

KU-CHEN # CML

Priapism in CML

Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy

Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

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Targeted Therapy for CML

Phosphorylation of Beclin 1 by BCR-ABL suppresses autophagy in CML

Importance of early and deeper responses to long-term survival in CML patients: Implications of BCR-ABL testing in management of CML in Indian setting

Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment

CML

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Initial decline of BCR-ABL transcript levels as early prognostic marker for patients with chronic myeloid leukemia (CML) treated with imatinib

KU-CHEN # CML

Priapism in CML

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Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen

Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl

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