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Verfasst von:Kayser, Sabine [VerfasserIn]   i
 Levis, Mark J. [VerfasserIn]   i
 Schlenk, Richard Friedrich [VerfasserIn]   i
Titel:Midostaurin treatment in FLT3-mutated acute myeloid leukemia and systemic mastocytosis
Verf.angabe:Sabine Kayser, Mark J. Levis, Richard F. Schlenk
Umfang:13 S.
Fussnoten:Gesehen am 30.07.2018
Titel Quelle:Enthalten in: Expert review of clinical pharmacology
Jahr Quelle:2017
Band/Heft Quelle:10(2017), 11, S. 1177-1189
ISSN Quelle:1751-2441
Abstract:Introduction: A number of tyrosine kinase inhibitors (TKIs) have been developed that inhibit the constitutively activated kinase activity caused by activating tyrosine kinase mutations, such as FLT3 or KIT, thus interrupting signaling pathways. Currently, midostaurin is the only approved TKI as monotherapy for aggressive systemic mastocytosis (SM), SM with associated hematological neoplasm, or mast cell leukemia displaying a KIT mutation as well as in combination with standard intensive chemotherapy for adult patients with newly diagnosed FLT3-mutated acute myeloid leukemia (AML).Areas covered: We provide a concise review of the pharmacology, tolerability and clinical efficacy of midostaurin and emerging new treatment options for ASM and FLT3-mutated AML.Expert commentary: Currently, midostaurin is the only approved TKI in aggressive SM, SM with associated hematological neoplasm, or mast cell leukemia inducing responses including complete remissions. With regard to AML, midostaurin is the first drug to receive regulatory approval in this indication in the molecularly defined subgroup of AML with FLT3 mutations. By introduction of this new standard in AML with FLT3 mutations, the bare has been raised for future approvals of next generation FLT3 inhibitors which will be based increasingly on head to head comparisons with midostaurin.
DOI:doi:10.1080/17512433.2017.1387051
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Verlag: http://dx.doi.org/10.1080/17512433.2017.1387051
 Verlag: https://doi.org/10.1080/17512433.2017.1387051
 DOI: https://doi.org/10.1080/17512433.2017.1387051
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:157806466X
Verknüpfungen:→ Zeitschrift

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