- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1476-5551
- Extent
-
Online-Ressource
- Language
-
Englisch
- Notes
-
online resource.
- Bibliographic citation
-
Targeting FLT3 mutations in AML: review of current knowledge and evidence ; volume:33 ; number:2 ; day:16 ; month:1 ; year:2019 ; pages:299-312 ; date:2.2019
Leukemia ; 33, Heft 2 (16.1.2019), 299-312, 2.2019
- Creator
- Contributor
-
SpringerLink (Online service)
- DOI
-
10.1038/s41375-018-0357-9
- URN
-
urn:nbn:de:101:1-2019031120055666730462
- Rights
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 11:01 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Daver, Naval
- Schlenk, Richard Friedrich
- Russell, Nigel H.
- Levis, Mark J.
- SpringerLink (Online service)
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Investigation of AML-specific FLT3 mutations – from next generation diagnostics to combined targeted therapy
BCL-2 inhibition synergizes with dual targeting of FLT3 and AXL in FLT3 wildtype AML via downregulation of MCL-1
Chimeric antigen receptor (CAR)-modified T cells targeting FLT3 in acute myeloid leukemia (AML)
GATA1 epigenetic deregulation contributes to the development of AML with NPM1 and FLT3-ITD cooperating mutations
CCL5 mediates target-kinase independent resistance to FLT3 inhibitors in FLT3-ITD-positive AML
FLT3 inhibitors as MRD-guided salvage treatment for molecular failure in FLT3 mutated AML
Distinct Metabolic features differentiating FLT3-ITD AML from FLT3-WT childhood Acute Myeloid Leukemia
Study of HOTAIR LncRNA in AML patients in context to FLT3-ITD and NPM1 mutations status
Dendritic cell dysfunctions in AML patients with FLT3 ITD mutations
Dendritic Cell dysfunctions in AML patients with FLT3 ITD mutations
Significance of targeting DNMT3A mutations in AML
FLT3-ITD regulated miRs in AML
Investigation of AML-specific FLT3 mutations – from next generation diagnostics to combined targeted therapy
BCL-2 inhibition synergizes with dual targeting of FLT3 and AXL in FLT3 wildtype AML via downregulation of MCL-1
Chimeric antigen receptor (CAR)-modified T cells targeting FLT3 in acute myeloid leukemia (AML)
GATA1 epigenetic deregulation contributes to the development of AML with NPM1 and FLT3-ITD cooperating mutations
CCL5 mediates target-kinase independent resistance to FLT3 inhibitors in FLT3-ITD-positive AML
FLT3 inhibitors as MRD-guided salvage treatment for molecular failure in FLT3 mutated AML
Distinct Metabolic features differentiating FLT3-ITD AML from FLT3-WT childhood Acute Myeloid Leukemia
Study of HOTAIR LncRNA in AML patients in context to FLT3-ITD and NPM1 mutations status
Dendritic cell dysfunctions in AML patients with FLT3 ITD mutations
Dendritic Cell dysfunctions in AML patients with FLT3 ITD mutations
Significance of targeting DNMT3A mutations in AML
FLT3-ITD regulated miRs in AML
Investigation of AML-specific FLT3 mutations – from next generation diagnostics to combined targeted therapy
BCL-2 inhibition synergizes with dual targeting of FLT3 and AXL in FLT3 wildtype AML via downregulation of MCL-1
Chimeric antigen receptor (CAR)-modified T cells targeting FLT3 in acute myeloid leukemia (AML)
GATA1 epigenetic deregulation contributes to the development of AML with NPM1 and FLT3-ITD cooperating mutations
CCL5 mediates target-kinase independent resistance to FLT3 inhibitors in FLT3-ITD-positive AML
FLT3 inhibitors as MRD-guided salvage treatment for molecular failure in FLT3 mutated AML
Distinct Metabolic features differentiating FLT3-ITD AML from FLT3-WT childhood Acute Myeloid Leukemia