EXPRESSION OF P56(LCK) IN B-CELL NEOPLASIAS

The protooncogene p56(lck) is considered to participate in malignant t ransformation of lymphoid cells. In order to evaluate the role of this tyrosine kinase in B cell neoplasias, we investigated the expression of p56(lck) by Western blot analysis. In 12/16 Burkitt's lymphoma deri ved cell lines, 3/3 lymphoblastoid cell lines, 1/6 Hodgkin's disease d erived cell lines, and 10/10 freshly isolated chronic lymphocytic leuk emia cells constitutive expression of the protein was detected. Protei n tyrosine kinase assays detected a catalytic active form of p56(lck) in all p56(lck) expressing samples. Stimulation experiments of the dif ferent cell Lines and primary tumour cells by the phorbol ester TPA an d the B-cell specific stimulation with SAC/anti-IgM respectively indic ated a change of the expression level in comparison with the unstimula ted cells and, a higher molecular weight species of the protein tyrosi ne kinase p56(lck) was observed. This was probably due to hyperphospho rylation of p56(lck). No correlation between an infection with the Eps tein-Barr virus and the expression of p56(lck) was found in the cell L ines used and in primary tumour cells. Inhibition of p56(lck) activity by the specific inhibitor 4-amino-6-hydroxyflavone revealed a decreas e of proliferation of the T-cell line Jurkat, but not of the Burkitt's lymphoma cell lines. In the analysed cell lines we found a reduction of the kinase activity of p56(lck) Of approximately 70%. These results suggest that lck may contribute to the maintenance of the transformat ion of the analysed B cell neoplasias but that lck does not support a model for an initial event in B cell transformation.