Defective differentiation of myeloid and plasmacytoid dendritic cells in advanced cancer patients is not normalized by tyrosine kinase inhibition of the vascular endothelial growth factor receptor
| Autor: | G. Giaccone, Bart C. Kuenen, R.J. Scheper, Klaas Hoekman, T.D. de Gruijl, A.J.M. van den Eertwegh, Anita G.M. Stam, H. van Cruijsen |
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| Přispěvatelé: | Internal medicine, Pathology |
| Rok vydání: | 2007 |
| Předmět: |
lcsh:Immunologic diseases. Allergy
Adult Male medicine.medical_specialty Myeloid Article Subject Cellular differentiation Immunology Population Biology chemistry.chemical_compound Gefitinib Internal medicine Neoplasms Antineoplastic Combined Chemotherapy Protocols medicine Immunology and Allergy Humans Myeloid Cells Epidermal growth factor receptor education Protein Kinase Inhibitors Aged education.field_of_study Cancer Cell Differentiation General Medicine Dendritic Cells Middle Aged medicine.disease Flow Cytometry Vascular endothelial growth factor Endocrinology medicine.anatomical_structure Receptors Vascular Endothelial Growth Factor chemistry Cancer research biology.protein Quinazolines Female lcsh:RC581-607 Tyrosine kinase medicine.drug Research Article |
| Zdroj: | Clinical and Developmental Immunology Van Cruijsen, H, Hoekman, K, Stam, A G M, Van Den Eertwegh, A J M, Kuenen, B C, Scheper, R J, Giaccone, G & De Gruijl, T D 2007, ' Defective differentiation of myeloid and plasmacytoid dendritic cells in advanced cancer patients is not normalized by tyrosine kinase inhibition of the vascular endothelial growth factor receptor ', Clinical and Developmental Immunology, vol. 2007, 17315 . https://doi.org/10.1155/2007/17315 Clinical and Developmental Immunology, Vol 2007 (2007) Clinical and Developmental Immunology, 2007:17315. Hindawi Publishing Corporation |
| ISSN: | 1740-2530 1740-2522 |
| DOI: | 10.1155/2007/17315 |
| Popis: | Tumor-derived vascular endothelial growth factor (VEGF) has previously been identified as a causative factor in the disturbed differentiation of myeloid dendritic cells (DC) in advanced cancer patients. Here, we investigated the potential of vascular endothelial growth factor receptor (VEGFR) tyrosine kinase (TK) inhibition to overcome this defective DC differentiation. To this end, peripheral blood DC (PBDC) precursor and subset frequencies were measured in 13 patients with advanced cancer before and after treatment with AZD2171, a TK inhibitor (TKI) of VEGFR, coadministered with gefitinib, and an epidermal growth factor receptor (EGFR) TKI. Of note, not only myeloid DC but also plasmacytoid DC frequencies were significantly reduced in the blood of the cancer patients prior to treatment, as compared to healthy controls. Moreover, besides an accumulated population of immature myeloid cells (ImC), a population of myeloid suppressor cells (MSC) was significantly increased. Upon systemic VEGFR TK inhibition, DC frequencies did not increase, whereas the rate of circulating MSC showed a slight, but not significant, decrease. In conclusion, TK inhibition of VEGFR with AZD2171 does not restore the defective PBDC differentiation observed in advanced cancer patients. |
| Databáze: | OpenAIRE |
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