Increased expression of the differentiation-defective granulocyte colony-stimulating factor receptor mRNA isoform in acute myelogenous leukemia

S. M. White, E. D. Ball, W. Christopher Ehmann, A. S. Rao, D. J. Tweardy

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Granulocyte colony-stimulating factor (G-CSF) critically affects all stages of granulopoiesis by activating a signaling cascade initiated by dimerization of its receptor (G-CSFR). Five human G-CSFR isoforms have been identified (classes I-V). A quantitative polymerase chain reaction (Q-PCR) technique was used to examine the expression of these five isoforms in normal and leukemic myeloid cells. We demonstrated that neutrophils expressed predominantly the class I isoform and low levels of class IV isoform (IV/I = 0.037 ± 0.005). No expression of the class II, class III, or class V isoform was detected. In contrast, all AML cell lines and acute myelogenous leukemia (AML) patient samples expressed increased relative amounts of the class IV isoform (IV/I = 0.047-0.350). When compared to normal immature myeloid cells, as represented by the CD34+ fraction of adult bone marrow (ABM) cells, three of eight AML cell lines and three of six AML patient samples expressed significantly increased levels of the class IV isoform relative to class I. This suggests that the increase in the relative expression of the class IV isoform seen in a considerable portion of AML cell samples is related to their leukemic phenotype. Given the inability of the class IV G-CSFR to drive myeloid maturation, the relative increase in class IV expression in AML cells may contribute to their aberrant response to G-CSF.

Original languageEnglish (US)
Pages (from-to)899-906
Number of pages8
JournalLeukemia
Volume12
Issue number6
DOIs
StatePublished - Jan 1 1998

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Granulocyte Colony-Stimulating Factor Receptors
RNA Isoforms
Acute Myeloid Leukemia
Protein Isoforms
Granulocyte Colony-Stimulating Factor
Myeloid Cells
Cell Line
Dimerization
Bone Marrow Cells
Neutrophils
Phenotype
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Hematology
  • Cancer Research
  • Anesthesiology and Pain Medicine

Cite this

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title = "Increased expression of the differentiation-defective granulocyte colony-stimulating factor receptor mRNA isoform in acute myelogenous leukemia",
abstract = "Granulocyte colony-stimulating factor (G-CSF) critically affects all stages of granulopoiesis by activating a signaling cascade initiated by dimerization of its receptor (G-CSFR). Five human G-CSFR isoforms have been identified (classes I-V). A quantitative polymerase chain reaction (Q-PCR) technique was used to examine the expression of these five isoforms in normal and leukemic myeloid cells. We demonstrated that neutrophils expressed predominantly the class I isoform and low levels of class IV isoform (IV/I = 0.037 ± 0.005). No expression of the class II, class III, or class V isoform was detected. In contrast, all AML cell lines and acute myelogenous leukemia (AML) patient samples expressed increased relative amounts of the class IV isoform (IV/I = 0.047-0.350). When compared to normal immature myeloid cells, as represented by the CD34+ fraction of adult bone marrow (ABM) cells, three of eight AML cell lines and three of six AML patient samples expressed significantly increased levels of the class IV isoform relative to class I. This suggests that the increase in the relative expression of the class IV isoform seen in a considerable portion of AML cell samples is related to their leukemic phenotype. Given the inability of the class IV G-CSFR to drive myeloid maturation, the relative increase in class IV expression in AML cells may contribute to their aberrant response to G-CSF.",
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Increased expression of the differentiation-defective granulocyte colony-stimulating factor receptor mRNA isoform in acute myelogenous leukemia. / White, S. M.; Ball, E. D.; Ehmann, W. Christopher; Rao, A. S.; Tweardy, D. J.

In: Leukemia, Vol. 12, No. 6, 01.01.1998, p. 899-906.

Research output: Contribution to journalArticle

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