title: Immunophenotype distinction between acute promyelocytic leukaemia and CD15- CD34- HLA-DR- acute myeloid leukaemia with nucleophosmin mutations.
abstract: Acute promyelocytic leukaemia (APL) is a unique clinicobiologic entity that can be successfully treated with All-trans Retinoic Acid ATRA-based regimens. Some cases of acute myeloid leukaemia (AML) with nucleophosmin (NPM) mutations have an immunophenotype that is similar to APL. The objective of the study is to compare antigenic expression in a group of APL patients with that in AML patients with NPM mutations and an APL-like immunophenotype (CD15- CD34- HLA-DR-). A consecutive series of 40 APL and 12 NPM patients with an APL-like phenotype were included in the study. Immunophenotypic patterns were investigated by multiparametric flow cytometry. Promyelocytic leukaemia-retinoic acid receptor-α transcript type, NPM and FLT3 mutations were investigated using conventional methods. Statistically significant differences were found between APL and NPM-mutated AML in CD33, CD13, CD2 and CD110 reactivity. CD2 expression was absent in every patient with NPM-mutated AML. In addition, mean fluorescence intensity and the coefficient of variation (cv) of CD33 and CD13 showed statistical differences between the two groups for CD33 (p = 0.007) and a trend to significance for CD13 (p = 0.05). Furthermore, among 45 evaluable patients, CD110 expression statistically differentiates between the two groups: [2/33 (6%) in the APL group and 8/12 (66.6%) in the NPM-mutated AML (p = 0.014)]. However, these traits were subtle, raising the possibility of practical diagnostic challenges. In conclusion, CD110 and CD33 reactivity may be useful to distinguish APL from NPM-mutated AML with CD15, CD34 and HLA-DR negativity. Nevertheless, cytogenetic and molecular characterization is necessary to establish the accurate diagnosis of AML.
authors.affiliation: Department of Laboratory of Hematology, Institute of Biomedical Research, IIB Sant Pau, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.
authors.forename: Angela
authors.initials: A
authors.lastname: Ferrari
authors.forename: Elena
authors.initials: E
authors.lastname: Bussaglia
authors.forename: Josep
authors.initials: J
authors.lastname: Úbeda
authors.forename: Luca
authors.initials: L
authors.lastname: Facchini
authors.forename: Anna
authors.initials: A
authors.lastname: Aventin
authors.forename: Jorge
authors.initials: J
authors.lastname: Sierra
authors.forename: Josep F
authors.initials: JF
authors.lastname: Nomdedéu
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis*; D018952:Antigens, CD34 / Q000032:analysis; D000951:Antigens, Neoplasm / Q000032:analysis*; D003937:Diagnosis, Differential; D005434:Flow Cytometry; D005647:Fucosyltransferases / Q000032:analysis; D006684:HLA-DR Antigens / Q000032:analysis*; D006801:Humans; D016130:Immunophenotyping; D015470:Leukemia, Myeloid, Acute / Q000175:diagnosis* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D015473:Leukemia, Promyelocytic, Acute / Q000175:diagnosis* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D016256:Lewis X Antigen / Q000032:analysis; D009363:Neoplasm Proteins / Q000235:genetics*; D009687:Nuclear Proteins / Q000235:genetics*; D000090243:Nucleophosmin; D051562:Proto-Oncogene Proteins c-bcr / Q000235:genetics; D053628:Receptors, Thrombopoietin / Q000032:analysis; D051941:fms-Like Tyrosine Kinase 3 / Q000235:genetics
chemical_list: D015703:Antigens, CD; D018952:Antigens, CD34; D000951:Antigens, Neoplasm; D006684:HLA-DR Antigens; D016256:Lewis X Antigen; C000716967:NPM1 protein, human; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D053628:Receptors, Thrombopoietin; D000090243:Nucleophosmin; C082218:MPL protein, human; C066693:FUT4 protein, human; D005647:Fucosyltransferases; C497970:FLT3 protein, human; D051941:fms-Like Tyrosine Kinase 3; C496613:BCR protein, human; D051562:Proto-Oncogene Proteins c-bcr