Hochschulschrift
Remarkable leukemogenic potency of the novel FLT3-N676K mutant
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
Hannover, Medizinische Hochschule Hannover, Dissertation, 2016
- Schlagwort
-
Krebs
Onkologie
- Ereignis
-
Veröffentlichung
- (wo)
-
Hannover
- (wer)
-
Bibliothek der Medizinischen Hochschule Hannover
- (wann)
-
2016
- Urheber
- Beteiligte Personen und Organisationen
-
Li, Zhixiong
Neuhoff, Nils Freiherr von
Klinik für Hämatologie, Hämostaseologie, Onkologie und Stammzelltransplantation der Medizinischen Hochschule Hannover
Institut für Experimentelle Hämatologie der Medizinischen Hochschule Hannover
- URN
-
urn:nbn:de:gbv:354-2016122926
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
2025-08-14T10:51:18+0200
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.
Objekttyp
- Hochschulschrift
Beteiligte
- Huang, Kezhi
- Li, Zhixiong
- Neuhoff, Nils Freiherr von
- Klinik für Hämatologie, Hämostaseologie, Onkologie und Stammzelltransplantation der Medizinischen Hochschule Hannover
- Institut für Experimentelle Hämatologie der Medizinischen Hochschule Hannover
- Bibliothek der Medizinischen Hochschule Hannover
Entstanden
- 2016
Ähnliche Objekte (12)
Leukemogenic potency of the high affinity neurotrophin receptors and FLT3-ITD
Inhibitors of class I HDACs and of FLT3 combine synergistically against leukemia cells with mutant FLT3
A remarkable change in inhibition potency and selectivity of isofagomine by simple N-modification
The role of GAB2 in FLT3-ITD mutant acute myeloid leukemia
Actin cytoskeleton deregulation confers midostaurin resistance in FLT3-mutant acute myeloid leukemia
Non-canonical FLT3 alterations reveal novel germline FLT3 variants leading to somatic gene rescue mutations
Gilteritinib: a novel FLT3 inhibitor for acute myeloid leukemia
GNF-7, a novel FLT3 inhibitor, overcomes drug resistance for the treatment of FLT3‑ITD acute myeloid leukemia
The RET receptor tyrosine kinase promotes AML through protection of mutant FLT3 from autophagic degradation
Abnormal Localization and Accumulation of FLT3-ITD, a Mutant Receptor Tyrosine Kinase Involved in Leukemogenesis
Remarkable inscriptions
Remarkable effect
Leukemogenic potency of the high affinity neurotrophin receptors and FLT3-ITD
Inhibitors of class I HDACs and of FLT3 combine synergistically against leukemia cells with mutant FLT3
A remarkable change in inhibition potency and selectivity of isofagomine by simple N-modification
The role of GAB2 in FLT3-ITD mutant acute myeloid leukemia
Actin cytoskeleton deregulation confers midostaurin resistance in FLT3-mutant acute myeloid leukemia
Non-canonical FLT3 alterations reveal novel germline FLT3 variants leading to somatic gene rescue mutations
Gilteritinib: a novel FLT3 inhibitor for acute myeloid leukemia
GNF-7, a novel FLT3 inhibitor, overcomes drug resistance for the treatment of FLT3‑ITD acute myeloid leukemia
The RET receptor tyrosine kinase promotes AML through protection of mutant FLT3 from autophagic degradation
Abnormal Localization and Accumulation of FLT3-ITD, a Mutant Receptor Tyrosine Kinase Involved in Leukemogenesis
Remarkable inscriptions
Remarkable effect
Leukemogenic potency of the high affinity neurotrophin receptors and FLT3-ITD
Inhibitors of class I HDACs and of FLT3 combine synergistically against leukemia cells with mutant FLT3
A remarkable change in inhibition potency and selectivity of isofagomine by simple N-modification
The role of GAB2 in FLT3-ITD mutant acute myeloid leukemia
Actin cytoskeleton deregulation confers midostaurin resistance in FLT3-mutant acute myeloid leukemia
Non-canonical FLT3 alterations reveal novel germline FLT3 variants leading to somatic gene rescue mutations
Gilteritinib: a novel FLT3 inhibitor for acute myeloid leukemia
GNF-7, a novel FLT3 inhibitor, overcomes drug resistance for the treatment of FLT3‑ITD acute myeloid leukemia
The RET receptor tyrosine kinase promotes AML through protection of mutant FLT3 from autophagic degradation
Abnormal Localization and Accumulation of FLT3-ITD, a Mutant Receptor Tyrosine Kinase Involved in Leukemogenesis
Remarkable inscriptions