Normal karyotype acute myeloid leukemia with the CD7+ CD15+ CD34+ HLA-DR + immunophenotype is a clinically distinct entity with a favorable outcome.
Recently, the presence of CEBPA mutation was identified as an important prognostic factor for normal karyotype (NK) acute myeloid leukemia (AML). Because AML with CEBPA mutation is closely associated with CD7, CD15, CD34, and HLA-DR expression, we investigated the prognostic implications of CD7+ CD15+ CD34+ HLA-DR + immunophenotype in NK-AML. We analyzed the immunophenotype of 329 patients with NK-AML from the Japan Adult Leukemia Study Group (JALSG) AML97 population. NK-AML with the CD7+ CD15+ CD34+ HLA-DR + immunophenotype was classified as the CEBPA type, and NK-AML that did not meet this criterion was considered as the non-CEBPA type. The influence of the CEBPA status on event-free survival (EFS) and overall survival (OS) was assessed using log-rank test and a multivariate Cox proportional hazard regression model. Furthermore, the surface antigen expression profile in AML according to the CEBPA mutation status (monoallelic or biallelic) was also investigated. Of the 329 NK-AML patients that were studied, 39 and 243 were classified as having CEBPA and non-CEBPA type NK-AML, respectively. Patients with CEBPA type NK-AML had significantly better EFS and OS than those with non-CEBPA type NK-AML. Multivariate analysis showed that the CEBPA type and white blood cell (WBC) counts of >20 × 10(9)/L were independent prognostic factors for EFS and OS. Moreover, NK-AML with the biallelic CEBPA mutation was more closely associated with CD34 positivity than that with the monoallelic CEBPA mutation. NK-AML with the CD7+ CD15+ CD34+ HLA-DR + immunophenotype is a clinically discrete entity, and this may have a possible role in risk stratification.
Department of Hematology and Rheumatology, Nihon University School of Medicine, 30-1 Oyaguchi Kamicho, Itabashi-ku, Tokyo, 173-8610, Japan, iriyama.noriyoshi@nihon-u.ac.jp.
Noriyoshi
N
Iriyama
Norio
N
Asou
Yasushi
Y
Miyazaki
Shunichiro
S
Yamaguchi
Shinya
S
Sato
Toru
T
Sakura
Tomoya
T
Maeda
Hiroshi
H
Handa
Masatomo
M
Takahashi
Shigeki
S
Ohtake
Yoshihiro
Y
Hatta
Hisashi
H
Sakamaki
Sumihisa
S
Honda
Tomohiko
T
Taki
Masafumi
M
Taniwaki
Shuichi
S
Miyawaki
Kazunori
K
Ohnishi
Yukio
Y
Kobayashi
Tomoki
T
Naoe
D000293:Adolescent; D000328:Adult; D000368:Aged; D018952:Antigens, CD34 / Q000032:analysis; D019011:Antigens, CD7 / Q000032:analysis; D000964:Antimetabolites, Antineoplastic / Q000627:therapeutic use; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics; D003561:Cytarabine / Q000627:therapeutic use; D005260:Female; D005647:Fucosyltransferases / Q000032:analysis; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D016130:Immunophenotyping; D053208:Kaplan-Meier Estimate; D059785:Karyotype; D007621:Karyotyping; D015470:Leukemia, Myeloid, Acute / Q000145:classification / Q000188:drug therapy / Q000235:genetics*; D007958:Leukocyte Count; D016256:Lewis X Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D015337:Multicenter Studies as Topic / Q000706:statistics & numerical data; D016016:Proportional Hazards Models; D016032:Randomized Controlled Trials as Topic / Q000706:statistics & numerical data; D012189:Retrospective Studies; D018570:Risk Assessment; D016896:Treatment Outcome; D055815:Young Adult
D018952:Antigens, CD34; D019011:Antigens, CD7; D000964:Antimetabolites, Antineoplastic; D022762:CCAAT-Enhancer-Binding Proteins; C515848:CEBPA protein, human; D006684:HLA-DR Antigens; D016256:Lewis X Antigen; D003561:Cytarabine; C066693:FUT4 protein, human; D005647:Fucosyltransferases