Literature DB >> 3422031

HL-60 cell line was derived from a patient with FAB-M2 and not FAB-M3.

W T Dalton1, M J Ahearn, K B McCredie, E J Freireich, S A Stass, J M Trujillo.   

Abstract

The leukemia from which the human cell line HL-60 was derived was classified in 1976 as acute progranulocytic leukemia (APL), although it was recognized to show a number of atypical features. In the ensuing 10 years, the concept of APL and its integral association with t(15;17) has evolved, and the concept of APL as a morphologically recognizable entity has become embodied in the term French-American-British classification M3 (FAB-M3). It is now recognized that not every case of leukemia with a high proportion of progranulocytes can be classified as FAB-M3. We reviewed the light and ultrastructural morphology of the original diagnostic material from this case, and we report that the leukemia from which HL-60 was derived does not conform to the currently recognized entity of FAB-M3 and is more appropriately classified as an acute myeloblastic leukemia with maturation, FAB-M2.

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Mesh:

Year:  1988        PMID: 3422031

Source DB:  PubMed          Journal:  Blood        ISSN: 0006-4971            Impact factor:   22.113


  56 in total

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3.  Granulocytic sarcoma with expression of CD30.

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4.  Transcriptomes reflect the phenotypes of undifferentiated, granulocyte and macrophage forms of HL-60/S4 cells.

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Review 5.  The HL60 cell line: a model system for studying human myeloid cell differentiation.

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7.  Correlation of differentiation-inducing activity of retinoids on human leukemia cell lines HL-60 and NB4.

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8.  Equitoxic doses of 5-azacytidine and 5-aza-2'deoxycytidine induce diverse immediate and overlapping heritable changes in the transcriptome.

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9.  Pulsed-field gel electrophoresis analysis of retinoic acid receptor-alpha and promyelocytic leukemia rearrangements. Detection of the t(15;17) translocation in the diagnosis of acute promyelocytic leukemia.

Authors:  Y H Xiao; W H Miller; R P Warrell; E Dmitrovsky; A D Zelenetz
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10.  Granulocyte colony-stimulating factor inhibits CXCR4/SDF-1α signaling and overcomes stromal-mediated drug resistance in the HL-60 cell line.

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