title: Acute myeloid leukemias with chromosomal abnormalities involving the 21q22 region identified by their in vitro responsiveness to interleukin-5.
abstract: Among 52 patients diagnosed as acute myeloid leukemia (AML), nine cases were found in which interleukin-5 (IL-5) induced a proliferative response in the leukemic cells, as measured by the stimulation of DNA synthesis or colony formation in vitro. All cases (n = 7) with the cytogenetic abnormality t(8;21)(q22;q22) belonged to this group of IL-5 responders. Of the additional two cases, one had an apparently normal karyotype, but the other expressed a dicentric chromosome 21, an abnormality also involving the breakpoint region 21q22. The leukemic cells of the IL-5 responsive patients could also be stimulated to proliferate by IL-3, GM-CSF and G-CSF, and in some cases by IL-6 or M-CSF. Immunophenotypic analysis revealed the presence of the immature hematopoietic cell antigen CD34, the myelomonocytic maturation antigens CD13 and CD33, in association with the B-cell related surface marker CD19 on the leukemic cells. Immunoglobulin mu and T-cell receptor beta-genes in the leukemic cells were in germline configuration. Upon incubation in colony culture, clonogenic cells were capable of producing progeny showing eosinophilic or neutrophilic maturation following stimulation with IL-5 or G-CSF, respectively. It is concluded that IL-5 responsive AML represents a subgroup of leukemia with distinct immunotypic and cytogenetic features.
authors.affiliation: Department of Hematology, Dr Daniel den Hoed Cancer Center, Rotterdam, The Netherlands.
authors.forename: I
authors.initials: I
authors.lastname: Touw
authors.forename: J
authors.initials: J
authors.lastname: Donath
authors.forename: K
authors.initials: K
authors.lastname: Pouwels
authors.forename: C
authors.initials: C
authors.lastname: van Buitenen
authors.forename: P
authors.initials: P
authors.lastname: Schipper
authors.forename: V
authors.initials: V
authors.lastname: Santini
authors.forename: A
authors.initials: A
authors.lastname: Hagemeijer
authors.forename: B
authors.initials: B
authors.lastname: Löwenberg
authors.forename: R
authors.initials: R
authors.lastname: Delwel
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D002455:Cell Division / Q000187:drug effects; D002869:Chromosome Aberrations / Q000235:genetics / Q000276:immunology / Q000473:pathology; D025063:Chromosome Disorders; D002891:Chromosomes, Human, Pair 21; D005260:Female; D015322:Gene Rearrangement, B-Lymphocyte; D015329:Gene Rearrangement, T-Lymphocyte; D005803:Genes, Immunoglobulin; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007377:Interleukin-3 / Q000494:pharmacology; D015848:Interleukin-5 / Q000494:pharmacology*; D007951:Leukemia, Myeloid / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D008297:Male; D011948:Receptors, Antigen, T-Cell / Q000235:genetics; D014407:Tumor Cells, Cultured
chemical_list: D015703:Antigens, CD; D007377:Interleukin-3; D015848:Interleukin-5; D011948:Receptors, Antigen, T-Cell; D016179:Granulocyte Colony-Stimulating Factor; D016178:Granulocyte-Macrophage Colony-Stimulating Factor