Deficiency of myeloperoxidase and abnormal chromosome 1 occurs in variant (HL60) promyelocytes.
Maturation of normal polymorphonuclear neutrophils is characterized by successive periods of granule synthesis, a process which frequently is abnormal in leukemia. Recently, the human leukemic cell line HL60, displaying a promyelocytic phenotype, has been used to study granulocyte maturation. We describe a variant line of HL60, called HL60-A7, resulting from growth in actinomycin D, which contains atypical large azurophilic granules deficient in myeloperoxidase. The products of in-vitro translation of A7 RNA contained less than 5% of the immunoreactive MPO found in the parent line. Electrophoresis of plasma membrane polypeptides radioiodinated by the lactoperoxidase technique revealed several differences. Karyotypic analysis identified a consistent chromosome 1q+ abnormality which was not found in any of the parental cells examined. This constellation of differences between HL60 and HL60-A7, i.e. MPO deficiency, abnormal granule morphology, cell surface changes, and further cytogenetic abnormalities, may point to a common site sensitive to altered regulation in some leukemic promyelocytes.
D002478:Cells, Cultured; D002869:Chromosome Aberrations; D002900:Chromosomes, Human, 1-3; D006098:Granulocytes / Q000201:enzymology*; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000201:enzymology / Q000235:genetics / Q000473:pathology*; D009195:Peroxidase / Q000096:biosynthesis / Q000172:deficiency*; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000378:metabolism
D012333:RNA, Messenger; D009195:Peroxidase