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Functionally deficient differentiation of hl-60 promyelocytic leukemia cells induced by phorbol myristate acetate

  • Peter E. Newburger
  • , Robert D. Baker
  • , Susan L. Hansen
  • , Robert A. Duncan
  • , Joel S. Greenberger
  • Harvard University
  • Boston Children's Hospital

Research output: Contribution to journalArticlepeer-review

46 Scopus citations

Abstract

The human promyelocytic leukemia cell line HL-60 undergoes terminal myeloid differentiation in vitro in response to a wide variety of chemicals. The tumor promoter phorbol myristate acetate induces these cells to develop macrophage-like morphology, adherence, and enzymatic characteristics. The present study confirms those observations and further documents the induction, by 16 nM phorbol myristate acetate, of 5’-nucleotidase activity, another human macrophage marker enzyme. However, more importantly, functional studies show that phorbol myristate acetate-induced HL-60 cells fail to increase above base line uninduced levels of hexose monophosphate shunt activity, superoxide generation, nitroblue tetrazolium reduction, bacterial ingestion, or complement secretion. These cells therefore possess some macrophage-like properties but do not meet several important functional criteria of macrophage identity.

Original languageEnglish
Pages (from-to)1861-1865
Number of pages5
JournalCancer Research
Volume41
Issue number5
StatePublished - May 1 1981

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