DVOŘÁK, Petr, Aleš HAMPL, D. DVOŘÁKOVÁ, M. DOUBEK, J. FAITOVÁ, L. PACHOLÍKOVÁ and J. MAYER. Increased expression of fibroblast growth factor receptor 3 in CD34+ BCR-ABL+ cells from patients with chronic myeloid leukemia. Leukemia. 2003, vol. 17, No 12, p. 2418-2425. ISSN 0887-6924.
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Basic information
Original name Increased expression of fibroblast growth factor receptor 3 in CD34+ BCR-ABL+ cells from patients with chronic myeloid leukemia
Authors DVOŘÁK, Petr, Aleš HAMPL, D. DVOŘÁKOVÁ, M. DOUBEK, J. FAITOVÁ, L. PACHOLÍKOVÁ and J. MAYER.
Edition Leukemia, 2003, 0887-6924.
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 5.116
Organization unit Faculty of Science
Keywords in English cells
Tags cells
Changed by Changed by: prof. Ing. Petr Dvořák, CSc., učo 47260. Changed: 1/2/2006 13:45.
Abstract
Previously, we showed that expression of myeloma-associated (proto)oncogene fibroblast growth factor receptor 3 (FGFR-3) is increased in white blood cells from patients with chronic myeloid leukemia (CML). The abnormal expression was returned back to the normal levels as soon as these patients reconstituted their hematopoiesis following transplantation of allogeneic peripheral blood stem cells. The aims of this study were: (1) to define population(s) of cells overexpressing FGFR-3, and (2) to determine the expression of FGFR-3 during the clinical course of the disease. We show that the vast majority of FGFR-3 transcripts as well as FGFR-3 protein arise from CD34+ BCR-ABL+ cells. Although increased levels of FGFR-3 were found in majority of late chronic phase patients treated with interferon alpha or hydroxyurea, the expression of FGFR-3 was always lowered following treatment with BCR-ABL tyrosine kinase inhibitor STI571. Compared to unstimulated cells, high levels of FGFR-3 were also identified in CD34+ cells from granulocyte colony-stimulating factor-mobilized blood stem cell harvests from healthy donors, suggesting a potential growth factor-dependent basis for elevated expression of FGFR-3 in CML. These findings have implications for the involvement of FGFR-3 in malignant hematopoiesis and depict FGFR-3 tyrosine kinase in CD34+ leukemic cells as a possible target for tyrosine kinase inhibitors.
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