Acute myeloid leukaemia M0: haematological, immunophenotypic and cytogenetic characteristics and their prognostic significance: an analysis in 241 patients

Abstract

Summary. Haematological, immunophenotypic and cytogenetic characteristics were analysed in 241 patients with acute myeloid leukaemia (AML) M0, including 58 children. Children , 3 years and adults between 60 and 70 years of age were most frequently affected. Immunophenotyping showed a heterogeneous phenotype. Anti-myeloperoxidase was positive in about half of the patients. Cytogenetic data were available from 129 (54%) patients. A normal karyotype was found in only 24%. Most of the abnormalities were unbalanced and the chromosomes 5, 7, 8 and 11 were the most frequently affected. Survival data were available from 152 treated patients (63%). The median overall survival for all patients was 10 months, 20 months for children (n 36), 10 months for the young adult group (n 50) and 7 months for the elderly patients (n 66) (P 0´09). Karyotype was not a prognostic factor influencing survival. AML M0 shows the immunological characteristics of early progenitor cells, but the expression of the different markers and cytogenetic abnormalities is heterogeneous. The prognosis is poor compared with other de novo AML and similar to that of AML with multilineage dysplasia or AML following myelodysplastic syndromes.

Flow cytometric maturity score as a novel prognostic parameter in patients with acute myeloid leukemia

“…In contrast, PML-RARA and NPM1 mutations had a higher frequency in the in the AML-ma group. These results are supported by previous studies, in which AML FAB M0 was associated an accumulation the same adverse chromosomal aberrations, a higher age and consequently a worse outcome [18][19][20]. Furthermore, also in recently published studies, a lower frequency of favorable molecular aberrations such as NPM1 and CEBPA has been described in the more immature AML subgroup AML FAB M0 [21].…”

Immunological classification of acute myeloblastic leukemias: relevance to patient outcome

“…The prognostic value of CD14 expression was independent of the FAB classification in the MD subset and had already been reported in such FAB subsets as M3 (22) or M0. (2) The imbalanced prognostic weight of CD7,-CD14, or CD34 expression in different immunological settings could explain the discrepancies previously observed when analyzing individually the prognostic value of these antigens expression. (19-21, 24-28, 30-39) The relation between the proposed immunological classification of AML and cytogenetic subsets remain to be determined.…”

“…The distance linkage between CD7 and the cluster CD13/ CD33/CD117 was larger than that observed between CD34 and the pan-myeloid antigens. Moreover, the frequency of CD7 expression decreased along granulomonocytic AML maturation from MB to ME (2), while the frequency of CD34 positivity was quite similar in all these AML subsets. This indicates that, as in normal myeloid differentiation, (15,16) CD7 is likely to be expressed in a small compartment of immature cells, while CD34 is expressed on a larger population of both immature and committed myeloid cells.…”

“…Immunophenotyping of blast cells has thus become an elective and useful tool to characterize the myeloid or lymphoid origin of blast cell populations. The use of more extensive panels further allows us to identify either undifferentiated acute leukemias (1,2) or acute leukemia entities expressing simultaneously several lineage antigens, defining multiphenotypic acute leukemia. (1,3) In lymphoid lineage-derived acute leukemia, extended immunophenotyping, moreover, allows to stratify distinct clinical and biological subsets, based on the hierarchy of antigen expression during the maturation of the normal cell counterparts of blast cells.…”

Inhibition of retinoic acid receptor signaling by Ski in acute myeloid leukemia

“…In our study, we were interested in the better molecular understanding of a clinical homogenous subgroup with a poor prognosis (AML with monosomy 7 or deletion 7q (À7/del7q)). [5][6][7][8] We analyzed samples from AML patients with À7/del7q, AML patients with normal karyotype (without FLT3 mutation) and normal bone marrow stem cells of healthy individuals, by gene expression profiling. Comparison of these three groups showed that the expression of SKI, a nuclear co-repressor of the HDAC complex, is highly upregulated in À7/del7q AML.…”