Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1423-0380
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
online resource.
- Erschienen in
-
Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment ; day:21 ; month:7 ; year:2016 ; pages:1-12
Tumor biology ; (21.7.2016), 1-12
- Urheber
-
Oaxaca, Derrick M.
- Beteiligte Personen und Organisationen
-
Yang-Reid, Sun Ah
Ross, Jeremy A.
Rodriguez, Georgialina
Staniswalis, Joan G.
Kirken, Robert A.
SpringerLink (Online service)
- DOI
-
10.1007/s13277-016-5179-7
- URN
-
urn:nbn:de:1111-2016072310056
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
14.08.2025, 10:49 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Oaxaca, Derrick M.
- Yang-Reid, Sun Ah
- Ross, Jeremy A.
- Rodriguez, Georgialina
- Staniswalis, Joan G.
- Kirken, Robert A.
- SpringerLink (Online service)
Ähnliche Objekte (12)
Phosphorylation of Beclin 1 by BCR-ABL suppresses autophagy in CML
The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification
Initial decline of BCR-ABL transcript levels as early prognostic marker for patients with chronic myeloid leukemia (CML) treated with imatinib
Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy
Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant
Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen
Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells
Bcr-Abl tyrosine kinase inhibitors- current status
BCR/ABL positive thrombocythemia: a diagnostic dilemma
Hemmung von Bcr-Abl durch Imatinib führt zu einer Cisplatin-Sensitivierung und zu einer modulierten p53-Funktion bei Bcr-Abl-positiven Zellen
Coexistence of P190 and P210 BCR/ABL transcripts in chronic myeloid leukemia blast crisis resistant to imatinib
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
Phosphorylation of Beclin 1 by BCR-ABL suppresses autophagy in CML
The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification
Initial decline of BCR-ABL transcript levels as early prognostic marker for patients with chronic myeloid leukemia (CML) treated with imatinib
Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy
Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant
Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen
Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells
Bcr-Abl tyrosine kinase inhibitors- current status
BCR/ABL positive thrombocythemia: a diagnostic dilemma
Hemmung von Bcr-Abl durch Imatinib führt zu einer Cisplatin-Sensitivierung und zu einer modulierten p53-Funktion bei Bcr-Abl-positiven Zellen
Coexistence of P190 and P210 BCR/ABL transcripts in chronic myeloid leukemia blast crisis resistant to imatinib
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
Phosphorylation of Beclin 1 by BCR-ABL suppresses autophagy in CML
The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification
Initial decline of BCR-ABL transcript levels as early prognostic marker for patients with chronic myeloid leukemia (CML) treated with imatinib
Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy
Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant
Molecular mechanisms in Bcr-Abl positive cells : = Molekulare Mechanismen in Bcr-Abl positiven Zellen
Combined targeting of GPX4 and BCR-ABL tyrosine kinase selectively compromises BCR-ABL+ leukemia stem cells
Bcr-Abl tyrosine kinase inhibitors- current status
BCR/ABL positive thrombocythemia: a diagnostic dilemma
Hemmung von Bcr-Abl durch Imatinib führt zu einer Cisplatin-Sensitivierung und zu einer modulierten p53-Funktion bei Bcr-Abl-positiven Zellen
Coexistence of P190 and P210 BCR/ABL transcripts in chronic myeloid leukemia blast crisis resistant to imatinib