CHARACTERIZATION OF ABERRANT PHENOTYPES IN ACUTE MYELOBLASTIC-LEUKEMIA

Citation
A. Macedo et al., CHARACTERIZATION OF ABERRANT PHENOTYPES IN ACUTE MYELOBLASTIC-LEUKEMIA, Annals of hematology, 70(4), 1995, pp. 189-194
Citations number
24
Categorie Soggetti
Hematology
Journal title
ISSN journal
09395555
Volume
70
Issue
4
Year of publication
1995
Pages
189 - 194
Database
ISI
SICI code
0939-5555(1995)70:4<189:COAPIA>2.0.ZU;2-A
Abstract
The existence of leukemic-associated phenotypes has been suggested to be a valuable tool for the detection of minimal residual disease (MRD) in AML patients, as they would allow to distinguish leukemic blast ce lls from normal hematopoietic progenitors. The present study was desig ned to analyze in which proportion of AML patients the immunological d etection of MRD is feasible, based on the presence of aberrant phenoty pes that allow the distinction of leukemic from normal cells. For this purpose we have prospectively investigated the blast cells from 40 AM L patients at diagnosis with a large panel of MoAb in double and tripl e staining combinations analyzed at flow cytometry, in order to detect aberrant phenotypes on blast cells (lineage infidelity, antigenic ove rexpression, and asynchronous antigenic expression, as well as aberran t light-scatter pattern). In the analysis of the 40 AML cases more tha n one blast cell subset, distinguished by its different antigenic expr ession, was detected in 85% of the patients: five different phenotypic blast cell subsets were observed in six cases, four in 13 patients, t hree subsets in three cases, and two in 12 patients; only six cases sh owed a homogeneous phenotypical blast cell population. Twenty-nine of the 40 AML cases analyzed (73%) showed the existence of at least one a berrant phenotype: in 15 cases the myeloid blast cells co-expressed ly mphoid-associated antigens (CD2, CD5, CD7, and/or CD19) - lineage infi delity -; asynchronous antigen expression was detected in 25 patients (CD34 + CD56 +, CD34 + CD11b +, CD34 + CD14 +, CD117 + CD15 +, CD33 - CD13 +, CD13 - CD15 +, HLADR + CD15 + + +, HLADR - CD14 + CD11b + CD4 +); seven cases displayed antigen overexpression (CD13, CD33, CD15, or CD14); and in 13 patients leukemic cells had an abnormal FSC/SSC dist ribution according to their phenotype. These results suggest that immu nological methods for the detection of MRD based on the existence of a berrant phenotypes could be used in the majority of AML patients.