Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms
FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not pri...
Ausführliche Beschreibung
Autor*in: |
Haijiao Zhang [verfasserIn] Samantha Savage [verfasserIn] Anna Reister Schultz [verfasserIn] Daniel Bottomly [verfasserIn] Libbey White [verfasserIn] Erik Segerdell [verfasserIn] Beth Wilmot [verfasserIn] Shannon K. McWeeney [verfasserIn] Christopher A. Eide [verfasserIn] Tamilla Nechiporuk [verfasserIn] Amy Carlos [verfasserIn] Rachel Henson [verfasserIn] Chenwei Lin [verfasserIn] Robert Searles [verfasserIn] Hoang Ho [verfasserIn] Yee Ling Lam [verfasserIn] Richard Sweat [verfasserIn] Courtney Follit [verfasserIn] Vinay Jain [verfasserIn] Evan Lind [verfasserIn] Gautam Borthakur [verfasserIn] Guillermo Garcia-Manero [verfasserIn] Farhad Ravandi [verfasserIn] Hagop M. Kantarjian [verfasserIn] Jorge Cortes [verfasserIn] Robert Collins [verfasserIn] Daelynn R. Buelow [verfasserIn] Sharyn D. Baker [verfasserIn] Brian J. Druker [verfasserIn] Jeffrey W. Tyner [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2019 |
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Übergeordnetes Werk: |
In: Nature Communications - Nature Portfolio, 2016, 10(2019), 1, Seite 13 |
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Übergeordnetes Werk: |
volume:10 ; year:2019 ; number:1 ; pages:13 |
Links: |
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DOI / URN: |
10.1038/s41467-018-08263-x |
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Katalog-ID: |
DOAJ061547557 |
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10.1038/s41467-018-08263-x doi (DE-627)DOAJ061547557 (DE-599)DOAJ998f439604e74cef95464ecda676fa5a DE-627 ger DE-627 rakwb eng Haijiao Zhang verfasserin aut Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondary FLT3 mutations. Science Q Samantha Savage verfasserin aut Anna Reister Schultz verfasserin aut Daniel Bottomly verfasserin aut Libbey White verfasserin aut Erik Segerdell verfasserin aut Beth Wilmot verfasserin aut Shannon K. McWeeney verfasserin aut Christopher A. Eide verfasserin aut Tamilla Nechiporuk verfasserin aut Amy Carlos verfasserin aut Rachel Henson verfasserin aut Chenwei Lin verfasserin aut Robert Searles verfasserin aut Hoang Ho verfasserin aut Yee Ling Lam verfasserin aut Richard Sweat verfasserin aut Courtney Follit verfasserin aut Vinay Jain verfasserin aut Evan Lind verfasserin aut Gautam Borthakur verfasserin aut Guillermo Garcia-Manero verfasserin aut Farhad Ravandi verfasserin aut Hagop M. Kantarjian verfasserin aut Jorge Cortes verfasserin aut Robert Collins verfasserin aut Daelynn R. Buelow verfasserin aut Sharyn D. Baker verfasserin aut Brian J. Druker verfasserin aut Jeffrey W. Tyner verfasserin aut In Nature Communications Nature Portfolio, 2016 10(2019), 1, Seite 13 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:10 year:2019 number:1 pages:13 https://doi.org/10.1038/s41467-018-08263-x kostenfrei https://doaj.org/article/998f439604e74cef95464ecda676fa5a kostenfrei https://doi.org/10.1038/s41467-018-08263-x kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019 1 13 |
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10.1038/s41467-018-08263-x doi (DE-627)DOAJ061547557 (DE-599)DOAJ998f439604e74cef95464ecda676fa5a DE-627 ger DE-627 rakwb eng Haijiao Zhang verfasserin aut Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondary FLT3 mutations. Science Q Samantha Savage verfasserin aut Anna Reister Schultz verfasserin aut Daniel Bottomly verfasserin aut Libbey White verfasserin aut Erik Segerdell verfasserin aut Beth Wilmot verfasserin aut Shannon K. McWeeney verfasserin aut Christopher A. Eide verfasserin aut Tamilla Nechiporuk verfasserin aut Amy Carlos verfasserin aut Rachel Henson verfasserin aut Chenwei Lin verfasserin aut Robert Searles verfasserin aut Hoang Ho verfasserin aut Yee Ling Lam verfasserin aut Richard Sweat verfasserin aut Courtney Follit verfasserin aut Vinay Jain verfasserin aut Evan Lind verfasserin aut Gautam Borthakur verfasserin aut Guillermo Garcia-Manero verfasserin aut Farhad Ravandi verfasserin aut Hagop M. Kantarjian verfasserin aut Jorge Cortes verfasserin aut Robert Collins verfasserin aut Daelynn R. Buelow verfasserin aut Sharyn D. Baker verfasserin aut Brian J. Druker verfasserin aut Jeffrey W. Tyner verfasserin aut In Nature Communications Nature Portfolio, 2016 10(2019), 1, Seite 13 (DE-627)626457688 (DE-600)2553671-0 20411723 nnns volume:10 year:2019 number:1 pages:13 https://doi.org/10.1038/s41467-018-08263-x kostenfrei https://doaj.org/article/998f439604e74cef95464ecda676fa5a kostenfrei https://doi.org/10.1038/s41467-018-08263-x kostenfrei https://doaj.org/toc/2041-1723 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2110 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2019 1 13 |
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Haijiao Zhang @@aut@@ Samantha Savage @@aut@@ Anna Reister Schultz @@aut@@ Daniel Bottomly @@aut@@ Libbey White @@aut@@ Erik Segerdell @@aut@@ Beth Wilmot @@aut@@ Shannon K. McWeeney @@aut@@ Christopher A. Eide @@aut@@ Tamilla Nechiporuk @@aut@@ Amy Carlos @@aut@@ Rachel Henson @@aut@@ Chenwei Lin @@aut@@ Robert Searles @@aut@@ Hoang Ho @@aut@@ Yee Ling Lam @@aut@@ Richard Sweat @@aut@@ Courtney Follit @@aut@@ Vinay Jain @@aut@@ Evan Lind @@aut@@ Gautam Borthakur @@aut@@ Guillermo Garcia-Manero @@aut@@ Farhad Ravandi @@aut@@ Hagop M. Kantarjian @@aut@@ Jorge Cortes @@aut@@ Robert Collins @@aut@@ Daelynn R. Buelow @@aut@@ Sharyn D. Baker @@aut@@ Brian J. Druker @@aut@@ Jeffrey W. Tyner @@aut@@ |
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2019-01-01T00:00:00Z |
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clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms |
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Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms |
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FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondary FLT3 mutations. |
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FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondary FLT3 mutations. |
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FLT3 is commonly mutated in acute myeloid leukaemia and treatment with FLT3 inhibitors often ends with relapse. Here, the authors perform exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondary FLT3 mutations. |
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Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms |
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