Abstract
Mutations of the AML1 gene are frequent molecular abnormalities in minimally differentiated acute myeloblastic leukemia (M0 AML), a rare type of AML. In this retrospective multicenter study, morphologic, immunophenotypical, cytogenetic, and molecular features of 59 de novo M0 AML cases were analyzed and correlated to AML1 mutations. Point mutations of AML1 gene were observed in 16 cases (27%). They were correlated with higher white blood cell (WBC) count (P =.001), greater marrow blast involvement (P =.03), higher incidence of immunoglobulin H/T-cell receptor (IgH/TCR) gene rearrangement (P <.0001), and with a borderline significant lower incidence of complex karyotypes. In the 59 patients, FLT3 mutations were the only significant prognostic factors associated with short survival.
Publication types
-
Multicenter Study
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adult
-
Aged
-
Aged, 80 and over
-
Bone Marrow / pathology
-
Core Binding Factor Alpha 2 Subunit
-
DNA-Binding Proteins / genetics*
-
Gene Rearrangement, T-Lymphocyte
-
Humans
-
Immunoglobulin Heavy Chains / genetics
-
Immunophenotyping
-
In Situ Hybridization, Fluorescence
-
Leukemia, Myeloid, Acute / genetics*
-
Leukemia, Myeloid, Acute / immunology
-
Leukemia, Myeloid, Acute / pathology
-
Leukocyte Count
-
Middle Aged
-
Point Mutation*
-
Prognosis
-
Proto-Oncogene Proteins / genetics
-
Receptor Protein-Tyrosine Kinases / genetics
-
Receptors, Antigen, T-Cell / genetics
-
Retrospective Studies
-
Survival Rate
-
Transcription Factors / genetics*
-
fms-Like Tyrosine Kinase 3
Substances
-
Core Binding Factor Alpha 2 Subunit
-
DNA-Binding Proteins
-
Immunoglobulin Heavy Chains
-
Proto-Oncogene Proteins
-
RUNX1 protein, human
-
Receptors, Antigen, T-Cell
-
Transcription Factors
-
FLT3 protein, human
-
Receptor Protein-Tyrosine Kinases
-
fms-Like Tyrosine Kinase 3