Author/Authors :
Dehbi، Hind نويسنده Genetics and Molecular Pathology Laboratory, Medical School of Casablanca, Hassan II University, Casablanca, Morocco , , Kassogue، Yaya نويسنده Genetics and Molecular Pathology Laboratory, Medical School of Casablanca, Hassan II University, Casablanca, Morocco , , Nasserddine، Sanaa نويسنده Genetics and Molecular Pathology Laboratory, Medical School of Casablanca, Hassan II University, Casablanca, Morocco , , Quessar، Asma نويسنده Department of Onco-Hematology, Ibn Rochd University Hospital, Casablanca, Morocco , , Nadifi، Sellama نويسنده Genetics and Molecular Pathology Laboratory, Medical School of Casablanca, Hassan II University, Casablanca, Morocco ,
Abstract :
Background: According to numerous studies, FMS-like tyrosine kinase 3, internal
tandem duplication, and the D835 mutation are associated with a poor prognostic clinical
outcome in acute myeloid leukemia patients. Detection of the FMS-like tyrosine
kinase 3 mutation in patients who present with normal karyotype acute myeloid
leukemia helps in both the understanding of the disease and the treatment of patients.
This study evaluates the incidence of FMS-like tyrosine kinase 3-internal tandem
duplication and FMS-like tyrosine kinase 3-D835 mutation in newly diagnosed patients
with normal karyotype acute myeloid leukemia.
Methods: This study looked at 33 new cases who presented with normal karyotype
acute myeloid leukemia at diagnosis. We collected peripheral blood samples from patients
at diagnosis. FMS-like tyrosine kinase 3-internal tandem duplication mutation was
detected using polymerase chain reaction and FMS-like tyrosine kinase 3-D835
mutation by restriction fragment length polymorphism after polymerase chain reaction.
Results: FMS-like tyrosine kinase 3-internal tandem duplication mutation was found
in 18% (6/33) of all patients and in 30% (6/20) of patients over 30 years of age. FMSlike
tyrosine kinase 3-internal tandem duplication mutation was most common with
M2 (50%), M5 (33.3%), and M0 (16.7%). FMS-like tyrosine kinase 3-D835 mutation
was detected in one patient (3%) that had M2. No significant association was found
between FMS-like tyrosine kinase 3 mutation and age, sex, white blood cell count,
platelets, or blasts percentage.
Conclusion: Most of FMS-like tyrosine kinase 3 mutations were found in patients
older than 30 years. The frequency observed in this work is comparable with that
observed in the literature. No pediatric case of FMS-like tyrosine kinase 3 mutation
was found in this study. A large scale study is needed to confirm our findings and to
further appreciate the prognostic value of FMS-like tyrosine kinase 3 mutation among
Moroccan patients.