title: Cytogenetic profile of minimally differentiated (FAB M0) acute myeloid leukemia: correlation with clinicobiologic findings.
abstract: Cytogenetic data were studied in 26 patients with de novo acute myeloid leukemia (AML) with minimal myeloid differentiation, corresponding to the M0 subtype of the French-American-British classification, in correlation with cytoimmunologic and clinical findings. Clonal abnormalities were detected in 21 cases (80.7%), 12 of which had a complex karyotype. Partial or total monosomy 5q and/or 7q was found, either as the sole aberration or in all abnormal metaphases, in 11 patients; in 8 cases, additional chromosome changes were present, including rearrangements involving 12p12-13 and 2p12-15 seen in 3 cases each. Five patients had trisomy 13 as a possible primary chromosome change; in 5 cases, nonrecurrent chromsome abnormalities were observed. Comparison of these findings with chromosome data from 42 patients with AML-M1 shows that abnormal karyotypes, complex karyotypes, unbalanced chromosome changes (-5/5q- and/or -7/7q- and +13) were observed much more frequently in AML-M0 than in AML-M1. Patients with abnormalities of chromosome 5 and/or 7 frequently showed trilineage myelodysplasia and low white blood cell count. Despite their relatively young age, complete remission was achieved in 4 of 11 patients only. Patients with +13 were elderly males with frequent professional exposure to myelotoxic agents. Unlike patients with clonal abnormalities, most AML-M0 patients with normal karyotype showed 1% to 2% peroxidase-positive blast cells at light microscopy and frequently achieved CR. It is concluded that (1) AML-M0 shows a distinct cytogenetic profile, partially recalling that of therapy-related AML, (2) different cytogenetic groups of AML-M0 can be identified showing characteristic clinicobiologic features, and (3) chromosome rearrangements may partially account for the unfavorable outcome frequently observed in these patients.
authors.affiliation: Institute of Haematology, University of Ferrara, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Cuneo
authors.forename: A
authors.initials: A
authors.lastname: Ferrant
authors.forename: J L
authors.initials: JL
authors.lastname: Michaux
authors.forename: M
authors.initials: M
authors.lastname: Boogaerts
authors.forename: H
authors.initials: H
authors.lastname: Demuynck
authors.forename: A
authors.initials: A
authors.lastname: Van Orshoven
authors.forename: A
authors.initials: A
authors.lastname: Criel
authors.forename: M
authors.initials: M
authors.lastname: Stul
authors.forename: P
authors.initials: P
authors.lastname: Dal Cin
authors.forename: J
authors.initials: J
authors.lastname: Hernandez
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D001853:Bone Marrow / Q000473:pathology; D002869:Chromosome Aberrations; D006801:Humans; D016130:Immunophenotyping; D007621:Karyotyping; D007951:Leukemia, Myeloid / Q000235:genetics* / Q000276:immunology / Q000401:mortality / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D016019:Survival Analysis
chemical_list: D015703:Antigens, CD