The N676D and G697R mutations in the kinase domain of FLT3 confer resistance to the inhibitor AC220.
about
Targeting oncoprotein stability overcomes drug resistance caused by FLT3 kinase domain mutationsG-749, a novel FLT3 kinase inhibitor, can overcome drug resistance for the treatment of acute myeloid leukemia.Prospective identification of resistance mechanisms to HSP90 inhibition in KRAS mutant cancer cells.Predicting Chemotherapy Resistance in AML.The FLT3 and PDGFR inhibitor crenolanib is a substrate of the multidrug resistance protein ABCB1 but does not inhibit transport function at pharmacologically relevant concentrations.Kinase-targeted cancer therapies: progress, challenges and future directions.
P2860
The N676D and G697R mutations in the kinase domain of FLT3 confer resistance to the inhibitor AC220.
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2012 nî lūn-bûn
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2012年の論文
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2012年学术文章
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2012年学术文章
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2012年学术文章
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name
The N676D and G697R mutations ...... stance to the inhibitor AC220.
@ast
The N676D and G697R mutations ...... stance to the inhibitor AC220.
@en
type
label
The N676D and G697R mutations ...... stance to the inhibitor AC220.
@ast
The N676D and G697R mutations ...... stance to the inhibitor AC220.
@en
prefLabel
The N676D and G697R mutations ...... stance to the inhibitor AC220.
@ast
The N676D and G697R mutations ...... stance to the inhibitor AC220.
@en
P2860
P1433
P1476
The N676D and G697R mutations ...... istance to the inhibitor AC220
@en
P2093
Bram Sweron
Daphnie Pauwels
P2860
P304
P356
10.3324/HAEMATOL.2012.069781
P50
P577
2012-08-08T00:00:00Z