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Absence of G‐CSF receptors and absent response to G‐CSF in childhood Burkitt's lymphoma and B‐ALL cells
Author(s) -
Tomeczkowski Jörg,
Yakisan Elif,
Wieland Britta,
Reiter Alfred,
Welte Karl,
Sykora KarlWalter
Publication year - 1995
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1995.tb08414.x
Subject(s) - northern blot , microbiology and biotechnology , biology , cell culture , receptor , burkitt's lymphoma , messenger rna , gene , biochemistry , genetics
The expression of the granulocyte colony‐stimulating factor (G‐CSF) receptor in childhood Burkitt's lymphoma (BL) cells, and the mitogenic effect of G‐CSF on these cells, was studied in a panel of 13 Epstein‐Barr virus (EBV) positive and negative BL cell lines derived from nine children. G‐CSF receptor mRNA expression was investigated by Northern blot analysis and reverse transcriptase polymerase chain reaction (RT‐PCR). Binding of G‐CSF to BL cell lines was measured by chemical crosslinking of 125 I‐G‐CSF, and proliferation by thymidine incorporation. Inducibility of the G‐CSF receptor was studied by stimulation with interleukin‐1β, tumour necrosis factor‐α, Staphylococcus aureus Cowan A, anti‐human IgM, phorbol myristate acetate, calcium ionophore A23187, and by infection in vitro by immortalizing and non‐immortalizing strains of EBV. BL cell lines, unstimulated or stimulated by biological reagents or EBV infection, did not bind radioionated G‐CSF in crosslinking experiments. No stimulation by recombinant human G‐CSF was observed in 3 H‐thymidine incorporation assays. No G‐CSF receptor mRNA was detected by Northern blot analysis or RT‐PCR in BL cell lines. It is concluded that G‐CSF plays no direct stimulatory role in the growth of these malignant B‐cells, making a deleterious influence of G‐CSF in the clinical treatment situation unlikely.