Combined corticosteroid/granulocyte colony-stimulating factor (G-CSF) therapy in the treatment of severe congenital neutropenia unresponsive to G-CSF: Activated glucocorticoid receptors synergize with G-CSF signals

Experimental Hematology

Volumn 28, Issue 12, 2000, Pages 1381-1389

  Dror, Yigal ^a   Ward, Alister C ^b   Touw, Ivo P ^b   Freedman, Melvin H ^a  

^a HOSPITAL FOR SICK CHILDREN   (Canada)

^b ERASMUS UNIVERSITY ROTTERDAM   (Netherlands)

Author keywords

Glucocorticoids; Granulocyte colony stimulating factor; Kostmann's disease; Neutropenia; Receptor

Indexed keywords

CD34 ANTIGEN; DEXAMETHASONE; ERYTHROPOIETIN; GLUCOCORTICOID RECEPTOR; GRANULOCYTE COLONY STIMULATING FACTOR; HYDROCORTISONE; INTERLEUKIN 3; STAT5 PROTEIN; STEM CELL FACTOR;

APOPTOSIS; ARTICLE; BONE MARROW CELL; CASE REPORT; CHILD; CONGENITAL DISORDER; CYTOGENETICS; DRUG EFFECT; FEMALE; GRANULOPOIESIS; HEMATOPOIESIS; HUMAN; HUMAN CELL; MONONUCLEAR CELL; NEUTROPENIA; POINT MUTATION; PRIORITY JOURNAL;

ADRENAL CORTEX HORMONES; ANTIGENS, CD34; APOPTOSIS; BONE MARROW CELLS; CELL DIVISION; CELLS, CULTURED; DEXAMETHASONE; DNA-BINDING PROTEINS; FEMALE; GLUCOCORTICOIDS; GRANULOCYTE COLONY-STIMULATING FACTOR; HEMATOPOIESIS; HUMANS; HYDROCORTISONE; INFANT, NEWBORN; MILK PROTEINS; NEUTROPENIA; NEUTROPHILS; POINT MUTATION; RECEPTORS, GRANULOCYTE COLONY-STIMULATING FACTOR; STAT5 TRANSCRIPTION FACTOR; STROMAL CELLS; TRANS-ACTIVATORS;

MURINAE;

EID: 0034536402     PISSN: 0301472X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0301-472X(00)00544-0     Document Type: Article

References (52)

1. Infantile genetic agranulocytosis
2. Granulopoiesis in severe congenital neutropenia
3. Granulopoiesis in patients with congenital neutropenia
4. Infantile genetic agranulocytosis. A review with presentation of ten new cases
5. Stimulation of Stat5 by granulocyte colony-stimulating factor (G-CSF) is modulated by two distinct cytoplasmic regions of the G-CSF receptor
6. Frequency of point mutations in the gene for the G-CSF receptor patients with chronic neutropenia undergoing G-CSF therapy
7. Abnormal responses of myeloid progenitor cells to recombinant human colony-stimulating factors in congenital neutropenia
8. Differential effects of granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in children with severe congenital neutropenia
9. Effects of recombinant human granulocyte colony-stimulating factor on neutropenia in patients with congenital agranulocytosis
10. A randomized controlled phase III trial of recombinant human granulocyte colony-stimulating factor (Filgrastim) for treatment of severe chronic neutropenia
11. Hemopoietic cell growth factors and their receptors
12. Granulocyte colony-stimulating factor and its receptor
13. Mice lacking granulocyte colony-stimulating factor have chronic neutropenia, granulocyte and macrophage progenitor cell deficiency, and impaired neutrophil mobilization
14. Impaired production and increased apoptosis of neutrophils in granulocyte colony-stimulating factor receptor-deficient mice
15. Expression cloning of a receptor for murine granulocyte colony-stimulating factor
16. Purification and characterization of the receptor for murine granulocyte colony-stimulating factor
17. Tyrosine kinase JAK1 is associated with the granulocyte colony-stimulating factor receptor and both become tyrosine phosphorylated after receptor activation
18. Tyrosine residues in the granulocyte colony-stimulating receptor (G-CSF-R) mediate G-CSF-induced differentiation of murine myeloid leukemic (M1) cells
19. Rapid activation of the STAT3 transcription factor by granulocyte colony-stimulating factor
20. Multiple signaling pathways induced by granulocyte colony-stimulating factor involving activation of JAKs, STAT5, and/or STAT3 are required for regulation of three distinct classes of immediate early genes
21. Tryptophan 650 of human granulocyte colony-stimulating factor (G-CSF) receptor, implicated in the activation of JAK2, is also required for G-CSF-mediated activation of signaling complexes of the p21ras route
22. The membrane-distal cytoplasmic region of human granulocyte colony-stimulating factor receptor is required for STAT3 but not STAT1 homodimer formation
23. Aberrant activation of JAK/STAT pathway components in response to G-CSF, interferon-α/β and interferon-γ in NFS-60 cells
24. Jak1 plays an essential role for receptor phosphorylation and Stat activation in response to granulocyte colony-stimulating factor
25. Tyrosine-dependent and independent mechanisms of STAT3 activation by the human granulocyte colony-stimulating factor (G-CSF) receptor are differentially utilized depending on G-CSF concentration
26. Defective internalization and sustained activation of truncated granulocyte colony-stimulating factor receptor found in severe congenital neutropenia/acute myeloid leukemia
27. Steroid hormone receptors; many actors in search of a plot
28. The nuclear receptor superfamily; the second decade
29. Molecular mechanisms of action of steroid/thyroid receptor superfamily members
30. Nuclear factor RIP 140 modulates transcriptional activation by the estrogen receptor
31. Glucocorticoids and protein kinase A coordinately modulate transcription factor recruitment at a glucocorticoid-responsive unit
32. Inhibition of mouse GATA-1 function by the glucocorticoid receptor; possible mechanism of steroid inhibition of erythroleukemia cell differentiation
33. Negative cross-talk between RelA and the glucocorticoid receptor; a possible mechanism for the antiinflammatory action of glucocorticoids
34. Functional interactions between Stat5 and the glucocorticoid receptor
35. Characterization of Stat5a and Stat5b homodimers and heterodimers and their association with the glucocorticoid receptor in mammary cells
36. The glucocorticoid receptor is a key regulator of the decision between self-renewal and differentiation in erythroid progenitors
37. Novel point mutation in the extracellular domain of the granulocyte colony-stimulating factor (G-CSF) receptor in a case of severe congenital neutropenia hyporesponsive to G-CSF treatment
38. Cytogenetic analysis of hematological malignant diseases
39. Shwachman-Diamond syndrome is an inherited pre-leukemic bone marrow failure disorder with aberrant hematologic progenitors and faulty marrow microenvironment
40. Demonstration of permanent factor-dependent multipotential (erythroid/neutrophil/basophil) hematopoietic progenitor cell lines
41. Naturally occurring dominant negative variants of Stat5
42. Glucocorticoids inhibit apoptosis of human neutrophils
43. Stat5a and Stat5b proteins have essential and nonessential, or redundant, roles in cytokine responses
44. Glucocorticoids inhibit IL-4 and mitogen-induced IL-4R α chain expression by different posttranscriptional mechanisms
45. Expression of EVI1 in myelodysplastic syndromes and other hematologic malignancies without 3q26 translocations
46. Thrombopoietin is not responsible for the thrombocytosis observed in patients with acute myeloid leukemias and the 3q21q26 syndrome
47. The t(3;21) fusion product, AML1/Evi-1, interacts with smad3 and blocks transforming growth factor-β-mediated growth inhibition of myeloid cells
48. Identification of translocational breakpoints within the intron region before the last coding exon (exon 12) of the EVI1 gene in two cases of CML-BC with inv(3)(q21q26)
49. EVI-1 gene expression in myeloid clonogenic cells from juvenile myelomonocytic leukemia (JMML)
50. Expression of the Evi-1 gene in haemopoietic cells of children with juvenile myelomonocytic leukaemia and normal donors
51. Abnormal expression of Evi-1 gene in human leukemias