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Incidence and prognosis of c‐KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias
Author(s) -
Care Rory S.,
Valk Peter J. M.,
Goodeve Anne C.,
AbuDuhier Faisel M.,
GeertsmaKleinekoort Wendy M. C.,
Wilson Giu A.,
Gari Mamdooh A.,
Peake Ian R.,
Löwenberg Bob,
Reilly John T.
Publication year - 2003
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2003.04362.x
Subject(s) - core binding factor , exon , mutation , myeloid , medicine , myeloid leukaemia , cancer research , gene , biology , genetics , transcription factor
Summary. DNA from 110 adult de novo acute myeloid leukaemia (AML) patients exhibiting either inv(16) ( n = 63) or t(8;21) ( n = 47) was screened for mutations in the c‐ KIT (exon 8 and Asp816) and FLT3 (ITD and Asp835) genes. c‐ KIT exon 8 mutations were found in 15/63 (23·8%) inv(16) patients and 1/47 (2·1%) t(8;21) patients. c‐ KIT Asp816 mutations were present in 5/63 (7·9%) inv(16) AML and 5/47 (10·6%) t(8;21) AML. FLT3 mutations were identified in five patients (7·9%) with inv(16) and three patients (5·6%) with t(8;21) AML. All mutations were mutually exclusive; 40% of inv(16) AML patients possessed either a c‐ KIT or FLT3 mutation. c‐ KIT exon 8 mutations were shown to be a significant factor adversely affecting relapse rate.